ライフサイエンスコーパス: hyperglycemic

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

2 Polg-Akita and Akita male mice were equally hyperglycemic.

3 All patients with prediabetes were hyperglycemic.

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

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

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

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

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

11 Using the hyperglycemic and euglycemic clamp, we demonstrated impa

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

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

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

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

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

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

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

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

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

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

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

23 e glucose intolerant, insulin-resistant, and hyperglycemic, and these metabolic defects worsened with

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

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

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

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

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

29 of the STZ-treated RhoB-null animals became hyperglycemic, as opposed to 61% of the wild-type contro

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

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

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

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

34 h both lowered by two-thirds in ZF rats made hyperglycemic by 60% Px.

35 and their control littermates were rendered hyperglycemic by streptozotocin administration.

36 e transplanted beneath the kidney capsule of hyperglycemic C57BL/6 mice, and treatment of recipients

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

38 the reduced oxidative stress in heat-shocked hyperglycemic cells down-regulates Glut-1 and glucose up

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

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

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

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

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

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

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

46 travenous glucose tolerance test (IVGTT) and hyperglycemic clamp characterized the insulinotropic eff

47 rements, and hyperinsulinemic-euglycemic and hyperglycemic clamp experiments were performed in RLIP76

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

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

50 In vivo studies using the IVGTT and the hyperglycemic clamp in Sprague Dawley rats demonstrate i

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

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

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

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

55 ciation measuring insulin sensitivity by the hyperglycemic clamp technique.

56 Insulin sensitivity was assessed using the hyperglycemic clamp technique.

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

58 ulin secretion rates (ISR) measured during a hyperglycemic clamp with either GLP-1 receptor blockade

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

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

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

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

63 n littermates (ZCL rats) before and during a hyperglycemic clamp.

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

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

66 Hyperglycemic clamps confirmed an increase in insulin se

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

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

69 Hyperglycemic clamps were performed in 14 severely obese

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

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

72 animals to succumb to acute pancreatitis and hyperglycemic coma.

73 Moreover, ROS generation in the hyperglycemic condition was also reduced in heat-shocked

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

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

76 Hyperglycemic conditions also attenuated mTORC1 signalin

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

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

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

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

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

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

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

84 Hyperglycemic conditions for up to 3 days reduced cell n

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

86 Finally, to test whether hyperglycemic conditions impair the immunomodulatory act

87 Hyperglycemic conditions impaired the T cell inhibitory

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

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

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

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

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

93 and wound healing, which are repressed under hyperglycemic conditions through the AR polyol pathway.

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

95 In contrast, cells exposed to hyperglycemic conditions were sensitized to the inhibito

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

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

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

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

100 Under hyperglycemic conditions, siah-1 formed a complex with G

101 Under hyperglycemic conditions, sirolimus impaired human aorti

102 tocrine IGF-1 occur equally in euglycemic or hyperglycemic conditions, suggesting that reduced RUNX2

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

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

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

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

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

108 defects observed during late gestation under hyperglycemic conditions.

109 ith previously published data obtained under hyperglycemic conditions.

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

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

112 w function of RPCs, and its regulation under hyperglycemic conditions.

113 th inhibition and hypertrophy of HRMCs under hyperglycemic conditions.

114 performed in Muller cell cultures exposed to hyperglycemic conditions.

115 fter 10 h of exposure of cells in culture to hyperglycemic conditions.

116 identified miR-93 as a signature microRNA in hyperglycemic conditions.

117 and HL60 neutrophil-like cells were grown in hyperglycemic conditions.

118 g siah-1 promotes Muller cell survival under hyperglycemic conditions.

119 pe 2 diabetes mellitus in direct relation to hyperglycemic conditions.

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

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

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

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

124 rization and limited insulin secretion under hyperglycemic conditions.

125 cose, particularly with prolonged culture in hyperglycemic conditions.

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

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

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

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

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

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

132 Hyperglycemic culture conditions rendered pericytes more

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

134 nd C/EBPalpha was observed at 48-72 h in the hyperglycemic cultures, and cyclin D3 and C/EBPalpha wer

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

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

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

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

139 ivators of PPARgamma include lipids and anti-hyperglycemic drugs such as thiazolidinediones (TZDs).

140 Rats that were hyperglycemic during tPA infusion had diffusely increase

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

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

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

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

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

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

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

148 We hypothesize that, in hyperglycemic endothelial cells, mitochondrial ROS produ

149 lencing of CSE exacerbated ROS production in hyperglycemic endothelial cells.

150 e (H(2)S) homeostasis in the pathogenesis of hyperglycemic endothelial dysfunction.

151 nitric-oxide synthase (eNOS) is enhanced in hyperglycemic endothelium, potentially due to dissociati

152 Hyperglycemic enhancement of necroptosis depends upon gl

153 These results indicate that hyperglycemic environment induces proliferation of adult

154 evelopment in a normoglycemic or chronically hyperglycemic environment, with >50% of engrafted NRG-Ak

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

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

157 Hyperglycemic-euglycemic clamp studies and glucose toler

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

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

160 5-anhydroglucitol (1,5-AG) is a biomarker of hyperglycemic excursions associated with diabetic compli

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

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

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

164 Gcgr(+/+) mice became hyperglycemic (>500 mg/dL), hyperketonemic, polyuric, an

165 carbonyl metabolites were found to change in hyperglycemic HAECs.

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

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

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

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

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

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

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

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

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

175 In the presence of hyperglycemic-hyperinsulinemia in ZDF, reduced glycogeni

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

177 absence of fructose but in the presence of a hyperglycemic-hyperinsulinemic challenge including porta

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

179 A hyperglycemic-hyperinsulinemic clamp was established in

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

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

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

183 In hyperglycemic-hyperlipidemic kidneys, the accumulation o

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

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

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

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

188 red mean blood glucose (5.8 vs. 8.4 mmol/L), hyperglycemic index (0.8 vs. 3.2 mmol/L), and glycemic p

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

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

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

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

193 Cancer cells exposed to hyperglycemic insults acquire permanent aggressive trait

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

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

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

197 he pathogenesis of seizures that result from hyperglycemic ischemia.

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

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

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

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

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

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

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

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

206 Incubation of Mz-ChA-1 cells in hyperglycemic medium caused an increase in the InsP(3)-d

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

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

209 66(Shc) is the key effector driving vascular hyperglycemic memory in diabetes.

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

211 mmatory genes after glycemia is normalized ("hyperglycemic memory").

212 al molecular mechanism for the phenomenon of hyperglycemic memory.

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

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

215 Obese, hyperglycemic mice display hepatic insulin resistance, b

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

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

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

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

220 In hyperglycemic mice, alpha-dicarbonyl glucose metabolites

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

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

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

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

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

226 The same mechanism might occur in hyperglycemic mice.

227 mcitabine in hypoglycemic mice compared with hyperglycemic mice.

228 8-OHdG and mtDNA damage despite the adverse hyperglycemic milieu.

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

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

231 In contrast, hyperglycemic MPCCs displayed significant hepatic lipid

232 ges significantly ameliorated hyperlipidemic-hyperglycemic nephropathy.

233 confirmed by 100% diabetes reversal in newly hyperglycemic NOD mice and 100% indefinite survival of s

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

235 BALB/c islets transplanted into hyperglycemic NOD mice under prolonged mATG+CTLA4-Ig tre

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

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

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

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

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

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

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

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

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

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

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

247 aportal fructose infusion in the presence of hyperglycemic-normoinsulinemia.

248 This was followed by a 2-h hyperglycemic-normoinsulinemic control period, during wh

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

250 patients were hospitalized with AMI and were hyperglycemic on admission (glucose level > or = 140 mg/

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

252 However, hyperglycemic oxidative stress derived from NADPH oxidas

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

254 act on survival, particularly in nondiabetic hyperglycemic patients.

255 sulin therapy to normalize glucose levels in hyperglycemic patients.

256 sulin in response to glucose and corrected a hyperglycemic phenotype in two mouse models of type 1 an

257 served in this study are consistent with the hyperglycemic phenotype.

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

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

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

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

262 present in glomeruli of kidney sections from hyperglycemic rats 4 weeks after streptozotocin treatmen

263 The hyperglycemic rats also showed increased superoxide form

264 We transplanted hyperglycemic rats intraportally with 2500 ferucarbotran

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

266 atoma expansion in both diabetic and acutely hyperglycemic rats, whereas injection of bradykinin, pla

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

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

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

270 Moreover, this hyperglycemic response is reproduced by selective activa

271 Neither the hyperglycemic response to 2DG nor feeding elicited by me

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 alone did not reduce glucoprivic feeding or hyperglycemic responses, compared with responses of ntRN

276 Hyperglycemic RhoB(-/-) mice had fewer signs of nephropa

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

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

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

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

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

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

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

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

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

286 dification has been observed in diabetic and hyperglycemic states.

287 ation is a component of the VSMC response to hyperglycemic stress that results in an enhanced respons

288 RLIP76 was induced by oxidative or hyperglycemic stress; the concomitant increase in insuli

289 However, inhibition of AR reverses hyperglycemic suppression of RUNX2.

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

291 or conventional therapy aimed at preventing hyperglycemic symptoms.

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

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

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

295 a normal glucose tolerance and only 7% were hyperglycemic, whereas 53% of wild-type mice had stable

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

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

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

299 Hyperglycemic WT mice demonstrated dilated cardiomyopath

300 pancreatectomy rats (Px), normoglycemic and hyperglycemic Zucker fatty (ZF) rats, and mouse islets i