ライフサイエンスコーパス: diabetic subject

1 pared with individuals with GRS </=5 (30% of diabetic subjects).

2 tic retinopathy screening examinations among diabetic subjects.

3 line in best corrected EVA after dilation in diabetic subjects.

4 gulatory response seen in tightly controlled diabetic subjects.

5 e biopsies in 7 lean, 8 obese, and 14 type 2 diabetic subjects.

6 selection criterion for bariatric surgery in diabetic subjects.

7 ability of control aTreg to suppress Teff of diabetic subjects.

8 f glycogenolysis in both the nondiabetic and diabetic subjects.

9 s have shown that suppression is impaired in diabetic subjects.

10 issue explants obtained from nondiabetic and diabetic subjects.

11 intrinsic to the Treg or Teff compartment of diabetic subjects.

12 by insulin, but this process is defective in diabetic subjects.

13 rophin and FBG and insulin resistance in non-diabetic subjects.

14 ed to control sugar intake, such as obese or diabetic subjects.

15 ere also approximately twofold higher in the diabetic subjects.

16 ed to activate autoreactive CTLs from type 1 diabetic subjects.

17 myocardial infarction is abnormally high in diabetic subjects.

18 contribute to cognitive deficits observed in diabetic subjects.

19 enhanced in islets from recent-onset type 1 diabetic subjects.

20 e macular edema and improve visual acuity in diabetic subjects.

21 ng lymph nodes (PLN) of T1D patients and non-diabetic subjects.

22 ratio, FBG, HbA1C, HOMA-IR and TG in the non-diabetic subjects.

23 tions did not show any additional benefit in diabetic subjects.

24 ately twofold with no impairment in obese or diabetic subjects.

25 ess to physiological hyperglycemia in type 2 diabetic subjects.

26 lin resistance in muscle of obese and type 2 diabetic subjects.

27 pivotal role in exaggerating brain damage in diabetic subjects.

28 impaired glucose tolerance (IGT), and type 2 diabetic subjects.

29 ove basal is reduced 57% in obese and 65% in diabetic subjects.

30 der difference in CAC was not significant in diabetic subjects.

31 ET-1 constrictor tone among obese and type 2 diabetic subjects.

32 p between particle size and calcification in diabetic subjects.

33 rinsulinemic-euglycemic clamp in nine type 2 diabetic subjects.

34 ctivation in skeletal muscle of obese type 2 diabetic subjects.

35 ne on adiponectin levels in lean, obese, and diabetic subjects.

36 in-resistant obese subjects and obese type 2 diabetic subjects.

37 o that there was no sex difference in CAC in diabetic subjects.

38 nt, obese glucose-tolerant, and obese type 2 diabetic subjects.

39 inhibits eating in healthy, overweight, and diabetic subjects.

40 e MAP kinase pathway was normal in obese and diabetic subjects.

41 cohort of 100 healthy control and 50 type 1 diabetic subjects.

42 both at fast and after OGTT mainly in type 2 diabetic subjects.

43 tubes from normal glucose tolerant or type 2 diabetic subjects.

44 he reverse SI pattern was observed in type 1 diabetic subjects.

45 d between normal glucose tolerant and type 2 diabetic subjects.

46 ples collected from normal, prediabetic, and diabetic subjects.

47 ce of the metabolic abnormalities present in diabetic subjects.

48 elate with midperipheral retinal ischemia in diabetic subjects.

49 NGF for the prevention of cardiomyopathy in diabetic subjects.

50 e expression was similar in obese and type 2 diabetic subjects.

51 hepatic 11beta-HSD1 activity in obese type 2 diabetic subjects.

52 likely to be most effective in obese type 2 diabetic subjects.

53 o hypoglycemia in intensively treated type 1 diabetic subjects.

54 in Tregs and total CD4(+) T-cells of type 1 diabetic subjects.

55 on and accelerated cardiovascular disease in diabetic subjects.

56 tence of FOXP3 expression in Tregs of type 1 diabetic subjects.

57 ansport chain activity was reduced in type 2 diabetic subjects (0.017 +/- 0.003 vs. 0.034 +/- 0.007 u

58 .32 +/- 0.02 vs 0.30 +/- 0.02; P < 0.05) and diabetic subjects (0.33 +/- 0.03 vs 0.31 +/- 0.02; P < 0

59 ificantly improved in both normotolerant and diabetic subjects (1.46 +/- 0.22 vs 1.37 +/- 0.55 mmol.m

60 ESEARCH DESIGN AND For this study, 22 type 1 diabetic subjects (11 men and 11 women, age 27 +/- 2 yea

61 AGE) content on inflammatory mediators of 24 diabetic subjects: 11 in a 2-week crossover and 13 in a

62 Of 2122 diabetic subjects, 18 (0.85%) were diagnosed with pancre

63 Thirty-three (13 diabetic and 20 non-diabetic) subjects, 20 to 39 weeks gestation, participat

64 Similar results were obtained among type 2 diabetic subjects (202 case and 114 control subjects).

65 st, hepatic glycogen concentration in type 1 diabetic subjects (215 +/- 23 mmol/l) was significantly

66 alues for BMI that were similar in obese and diabetic subjects (23.7+/-0.7, 33.2+/-0.8, and 31.8+/-0.

67 lucose disposal rate (R(d)) was lower in the diabetic subjects (3.4 +/- 0.5 mg. kg(-1). min(-1)) than

68 Ps in a case-control study made up of type 1 diabetic subjects (324 case subjects with diabetic nephr

69 he first-phase insulin response was lower in diabetic subjects (329.1 +/- 39.6 vs. 91.3 +/- 34.1 pmol

70 hundred sixteen nondiabetic subjects and 111 diabetic subjects (33 type I and 78 type II) were recrui

71 the obese (33.5 +/- 4.7 microg/l) and type 2 diabetic subjects (54.9 +/- 6.3 microg/l) than in the le

72 he Penn Diabetes Heart Study (N = 611 type 2 diabetic subjects, 71.4% men) and the Study of Inherited

73 PLTP activity was also higher in diabetic subjects (96 AU) than in nondiabetic subjects (

74 duced activity of hCD59 in erythrocytes from diabetic subjects, a finding consistent with glycation i

75 ished RCTs including periodontal therapy for diabetic subjects, a metabolic outcome, an untreated con

76 a lower risk for cardiovascular events among diabetic subjects (adjusted HR=0.49, 95% CI=0.25 to 0.94

77 rates, and muscle functions in eight type 2 diabetic subjects after withdrawing all treatments for 2

78 biopsy from 22 lean, 20 obese, and 20 type 2 diabetic subjects (ages 35+/-1, 42+/-2, and 52+/-2 years

79 reasing age in both nondiabetic subjects and diabetic subjects, along with an increasing variation in

80 Obese and type 2 diabetic subjects also had lower IkappaBalpha content, a

81 However, after the exclusion of diabetic subjects, an improvement in the insulinogenic i

82 In a case-control study of 1,161 type 2 diabetic subjects and 1,174 control Finns who are normal

83 t study from 2005 to 2011 among 1.25 million diabetic subjects and 1.25 million nondiabetic subjects

84 nducted a case-control study in 2,158 type 2 diabetic subjects and 2,574 control subjects and a famil

85 qPCR analysis of swab specimens from 30 diabetic subjects and 30 control subjects showed no diff

86 In a further cohort of 327 type 2 diabetic subjects and 357 normoglycemic control subjects

87 irculating RBCs ranged from 39 to 56 days in diabetic subjects and 38 to 60 days in nondiabetic contr

88 We found that 5 of 13 type 1 diabetic subjects and 4 of 6 antibody-positive relatives

89 for a protective effect (odd ratios, 25 for diabetic subjects and 8.5 for nondiabetic subjects).

90 entration was increased (P < 0.05) in type 2 diabetic subjects and correlated with increased C18:1 an

91 ependent transcription, is decreased in both diabetic subjects and family history-positive nondiabeti

92 FOXO1 in human adipocytes obtained from non-diabetic subjects and from patients with T2D.

93 tion of IGRP-reactive T cells in both type 1 diabetic subjects and healthy subjects and recent report

94 oxidoreductase activity was lowest in type 2 diabetic subjects and highest in the lean volunteers (le

95 ls (EPCs) and platelets from nondiabetic and diabetic subjects and in human microvascular endothelial

96 e disposal rate in nondiabetic versus type 2 diabetic subjects and in the latter group after 1 year o

97 iopsies from hip or ankle were obtained from diabetic subjects and incubated for 9 days in the absenc

98 that the acute insulin response is absent in diabetic subjects and lower in impaired than in normal g

99 lasma ceramide levels are elevated in type 2 diabetic subjects and may contribute to insulin resistan

100 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP

101 omized to hyperinsulinemic-euglycemic (n = 6 diabetic subjects and n = 8 control subjects) or hypogly

102 tes to endothelium from normotriglyceridemic diabetic subjects and of decreased monocyte activity and

103 -controlled crossover design to eight type 2 diabetic subjects and seven age- and BMI-matched healthy

104 te metabolism in five well-controlled type 1 diabetic subjects and six nondiabetic control subjects u

105 Data collected from four previously untested diabetic subjects and the other eye of eight previous su

106 ed [(18)F]FDG uptake, decreased threefold in diabetic subjects and twofold in nondiabetic subjects (P

107 etes risk and protection in Caucasian type 2 diabetic subjects are associated with lower (P = 0.007)

108 Since diabetic subjects are characterized by a prothrombotic a

109 Compared with nondiabetic subjects, type 2 diabetic subjects are metabolically inflexible with impa

110 However, most type 2 diabetic subjects are obese (BMI >30 kg/m(2)), and exerc

111 tic islets transplanted into immunocompetent diabetic subjects are rapidly lost to apoptotic or lytic

112 glucose production was twice as high in the diabetic subjects as in control subjects (0.70 +/- 0.05

113 U progressively increased (P < 0.001) in the diabetic subjects as insulin increased from approximatel

114 A and G971R IRS1 variants in 971 U.K. type 2 diabetic subjects ascertained for strong family history

115 ncentration, SGU was lower (P < 0.01) in the diabetic subjects at all insulin concentrations tested.

116 test this hypothesis, we studied nine type 2 diabetic subjects before and after 2 weeks of treatment

117 ed signs of retinal dysfunction over time in diabetic subjects before or early in the course of retin

118 is reduced 26% in obese subjects and 62% in diabetic subjects (both comparisons P < 0.001).

119 novel variant, R176C, was identified in one diabetic subject but did not cosegregate with diabetes w

120 -positive cells were present in retinas from diabetic subjects but absent in those from nondiabetic s

121 mbda/zeta protein amount is decreased 46% in diabetic subjects but is normal in obese nondiabetic sub

122 x was augmented by BQ123 in obese and type 2 diabetic subjects but not in L subjects (P = 0.04), sugg

123 pression was significantly reduced in type 2 diabetic subjects but not in obese subjects.

124 l of Candida carriage was seen in 44% of the diabetic subjects but only in 28% of the nondiabetic con

125 ter whole-body amino acid turnover in type 2 diabetic subjects, but leucine nitrogen flux, transamina

126 (percent time asleep) was 77 +/- 18% in the diabetic subjects, but only 26 +/- 8% (P = 0.0109) in th

127 reduces cardiovascular end points of type 2 diabetic subjects by actions that cannot solely be attri

128 A were measured before and after dilation in diabetic subjects by independent, masked examiners.

129 ment of glycated insulin in plasma of type 2 diabetic subjects by specific RIA gave circulating level

130 en in the adipose tissue of obese and type 2 diabetic subjects can be recapitulated ex vivo by TNF-al

131 cetylases (HDACs) class IIa in the brains of diabetic subjects compared with control subjects, and th

132 levels were significantly elevated in type 1 diabetic subjects compared with in control subjects (P <

133 levels were significantly elevated in type 1 diabetic subjects compared with in control subjects in t

134 and muscle lipid content in obese and type 2 diabetic subjects compared with lean healthy volunteers.

135 ion and PI3K activity are impaired 40-50% in diabetic subjects compared with lean or obese subjects.

136 ce of coronary artery calcification (CAC) in diabetic subjects compared with nondiabetic subjects and

137 ose tissue of obese normoglycemic and type 2 diabetic subjects compared with that of nonobese normogl

138 as decreased in type 2 diabetic and in obese diabetic subjects compared with those in equally obese i

139 in individual amyloid-containing islets from diabetic subjects, compared with control subjects, but a

140 IL-2R signaling in CD4(+) T-cells of type 1 diabetic subjects contributes to decreased persistence o

141 gen specificities in the periphery of type 1 diabetic subjects could be a reliable reporter for progr

142 rised healthy controls (C) (n = 10), healthy diabetic subjects (DC) (n = 12), and diabetic subjects w

143 n FA of the left ALIC with hemoglobin A1c in diabetic subjects (DC+DD; P=.016).

144 ells (Tregs) has been demonstrated in type 1 diabetic subjects despite the role of these IL-2-depende

145 KCNJ11 gene for mutations in 77 U.K. type 1 diabetic subjects diagnosed under the age of 2 years.

146 essment of gluconeogenesis in nondiabetic or diabetic subjects during a traditional (i.e., 2-3 h) hyp

147 o 90% of control levels, and NTX exposure of diabetic subjects elevated the labeling index by up to e

148 C. albicans predominated; however, diabetic subjects, especially those with high levels of

149 The diabetic subjects exhibited markedly reduced awakening f

150 17; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increasing ins

151 though NRF-1 expression is decreased only in diabetic subjects, expression of both PPAR gamma coactiv

152 In type 2 diabetic subjects, extrapancreatic KATP channel activati

153 Type 2 diabetic subjects failing glyburide therapy were randomi

154 diagnosed (<or=3 years), drug-naive, type 2 diabetic subjects (fasting plasma glucose <or=10 mmol/l)

155 ells were captured from three East-Asian non-diabetic subjects for scRNA-seq.

156 imulated PI/C-peptide ratio decreased in the diabetic subjects from 4.4 +/- 1.5% before to 1.8 +/- 0.

157 rt summarizes the results for the first 2368 diabetic subjects from 767 families enrolled in FIND-Eye

158 Non-diabetic subjects from Bogalusa Heart Study, a longitudi

159 etic retinopathy in an independent cohort of diabetic subjects from the Wisconsin Epidemiologic Study

160 al thickness increased over 12 months in the diabetic subjects, from 217 +/- 22 mum to 222 +/- 20 mum

161 cycling in the control subjects, but in the diabetic subjects, glycogen cycling contributed to 25% o

162 e statistically significantly higher in both diabetic subject groups compared with normal control sub

163 no differences in the one- versus two-kidney diabetic subject groups, respectively, in glomerular bas

164 In the one- versus two-kidney diabetic subject groups, respectively, serum creatinine

165 Obese and type 2 diabetic subjects had attenuated exercise-stimulated AMP

166 ach fiber type, muscle from obese and type 2 diabetic subjects had greater lipid content (P < 0.01).

167 Type 2 diabetic subjects had higher (P < 0.05) concentrations o

168 Type 1 diabetic subjects had higher MVo(2) and lower myocardial

169 Purified plasmin(ogen) from diabetic subjects had impaired fibrinolytic activity com

170 The diabetic subjects had lower FMD than did the control sub

171 type, skeletal muscle from obese and type 2 diabetic subjects had lower oxidative enzyme activity th

172 Type 2 diabetic subjects had reduced basal PGC-1 gene expressio

173 Diabetic subjects had significantly (P<0.001) higher PI

174 RESULTS- Obese and type 2 diabetic subjects had significantly elevated TLR4 gene e

175 Diabetic subjects had significantly lower mean fractiona

176 Individuals with GRS >/=8 (19% of diabetic subjects) had almost a 2-fold increase in CHD r

177 ion of ceramides within tissues in obese and diabetic subjects has been well described.

178 teomic and peptidomic analyses of urine from diabetic subjects have been published in the quest for a

179 We examined whether obese type 2 diabetic subjects have impaired exercise stimulation of

180 C-purified plasma pool from four male type 2 diabetic subjects (HbA(1c) 8.1 +/- 0.2%, plasma glucose

181 emia in 10 nondiabetic subjects and 7 type 1 diabetic subjects (HbA1c 6.5 +/- 0.2%) using 13C nuclear

182 In type 1 diabetic subjects, higher HbA(1c) was associated with lo

183 seen after 18 months in type 1 versus type 2 diabetic subjects in autonomic symptoms (cardiovascular

184 A study of 155 diabetic subjects in China showed that chromium reduced

185 The study of diabetic subjects in China was the only one to report th

186 hyperglycemia on glucose turnover in type 2 diabetic subjects in good control (GC) (n = 14, age 51.7

187 T cells infiltrate the exocrine pancreas of diabetic subjects in high numbers and not only endocrine

188 Controls were other diabetic subjects in the cohort.

189 oncentrations; the combined data from the 38 diabetic subjects in the other studies did not.

190 ly related to mortality, more strongly so in diabetic subjects, in the study population.

191 This association was stronger among diabetic subjects, in whom the risk of death in a compar

192 Seventy-seven diabetic subjects, including 13 with mild or no retinopa

193 ions of pulmonary infection risk, such as in diabetic subjects, increased SGLT1 activity may prevent

194 Ten nondiabetic and 10 diabetic subjects ingested (2)H(2)O the evening before s

195 f B cell compartment were observed in type 1 diabetic subjects, irrespective of PTPN22 genotype, reve

196 n isoprostane production and NO synthesis in diabetic subjects is consistent with the hypothesis that

197 g hypoglycemia in intensively treated type 2 diabetic subjects is largely unknown.

198 metabolic inflexibility to glucose in type 2 diabetic subjects is mostly related to defective glucose

199 et MMP-9 mRNA levels are decreased in type 2 diabetic subjects, islet MMP-9 activity may also be decr

200 ificant vasodilation in the obese and type 2 diabetic subjects (leg vascular resistance = mean arteri

201 oid deposits in the pancreas of most type II diabetic subjects, likely reflecting compromised secreto

202 nalysis, skeletal muscle in obese and type 2 diabetic subjects mani-fests disturbances of oxidative e

203 Type 2 diabetic subjects manifest both disordered insulin actio

204 hat in recently diagnosed, drug-naive type 2 diabetic subjects, markers of inflammation and fibrinoly

205 s in the increasingly stressed beta cells of diabetic subjects may be a consequence of general defect

206 Our findings suggest that obese type 2 diabetic subjects may need to exercise at higher intensi

207 CETP activity was higher in diabetic subjects (mean 84 arbitrary units [AU]) than in

208 tion of the first-phase insulin secretion in diabetic subjects might explain the reversal of type 2 d

209 Autoantibody-positive diabetic subjects (n = 1,384) and population-based contr

210 nse to a working-memory task (WMT) in type 1 diabetic subjects (n = 16) with that in age-matched nond

211 sizes and subclasses differed between type 1 diabetic subjects (n = 194, age 30-55 years) and age- an

212 ime of cesarean section from the GDM and non-diabetic subjects (n = 6 for each group), and the platel

213 ied in 134 patients (age 60.2 +/- 9.7 years; diabetic subjects, n = 43).

214 In type 2 diabetic subjects, NN2211, in comparison with placebo, i

215 ssion was dramatically more likely in type 1 diabetic subjects not treated with ACE inhibitor/angiote

216 ealthy (OH) (>50 years), and 19 older type 2 diabetic subjects (OD).

217 In non-diabetic subjects of AA (n = 20,209) and European ancest

218 including healthy and non-insulin-dependent diabetic subjects of either gender, with teeth in the an

219 hort of 160 extensively characterized type 2 diabetic subjects on two occasions 12 months apart.

220 Total ISR largely increased in diabetic subjects only when glucose was administered ora

221 ow-density lipoprotein cholesterol uptake in diabetic subjects only.

222 caloric deprivation and weight loss in obese diabetic subjects over 16 weeks in the context of a doub

223 Reclining uncovered in 47% of diabetic subjects (P = 0.016 compared with controls) an

224 ation of small amounts of fructose to type 2 diabetic subjects partially corrected the regulation of

225 AND A total of 11 intensively treated type 1 diabetic subjects participated in stepped hyperinsulinem

226 For type 1a diabetic subjects, PLN iNKT cell clones from three sampl

227 nd September 2011 prospectively included 376 diabetic subjects previously exposed to benfluorex who w

228 monstrated in the peripheral blood of type 1 diabetic subjects receiving human fetal pancreatic tissu

229 Lipid-lowering treatment among type 1 diabetic subjects, recommended to prevent cardiovascular

230 In type 1 diabetic subjects, reduced fractional anisotropy correla

231 human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic.

232 s sustain functional beta-cell mass in human diabetic subjects remains unclear.

233 and 50 T1D subjects revealed that 16% of the diabetic subjects showed anti-gastric ATPase autoantibod

234 endent vasodilation seen in obese and type 2 diabetic subjects, suggesting an important contribution

235 in 12 healthy lean, 12 obese, and 12 type 2 diabetic subjects taking metformin 850 mg b.i.d. versus

236 In control and type 2 diabetic subjects, TGD/nonoxidative glucose disposal cor

237 6-H611 haplotype were present in more type 2 diabetic subjects than control subjects (one-tailed P =

238 min)) was almost threefold higher in type 2 diabetic subjects than in control subjects (14.2 +/- 1.7

239 .M.)) was approximately 50% higher in type 2 diabetic subjects than in control subjects (29.4 +/- 3.0

240 pe was significantly more frequent in type 2 diabetic subjects than in control subjects (60 vs. 54%,

241 Pro12Ala variant was significantly lower in diabetic subjects than in nondiabetic subjects (0.15 vs.

242 luconeogenesis was three times higher in the diabetic subjects than in the control subjects (0.59 +/-

243 as approximately 35% lower (P < 0.02) in the diabetic subjects than in the nondiabetic subjects.

244 ctions were markedly lower (P < 0.01) in the diabetic subjects than in the nondiabetic subjects.

245 to hypoglycemia were reduced during sleep in diabetic subjects (the final awake versus asleep values

246 In obese type 2 diabetic subjects, the appearance rate of 9,12,12-[(2)H]

247 nce (P = 0.34) in SI between meals in type 1 diabetic subjects, the diurnal pattern of SI taken acros

248 ide (GIP) did not differ between control and diabetic subjects, the incretin effect was lower in the

249 In a population of 12,367 non-diabetic subjects, the variable body mass index (BMI) wa

250 Among diabetic subjects, the variant was associated with great

251 Within both type I and type II diabetic subjects, there was neither a significant relat

252 diabetic subjects and three groups of type 1 diabetic subjects (those studied during euglycemia, hype

253 level of brain activation required by type 1 diabetic subjects to attain the same level of cognitive

254 conducted in 37 diabetic patients and 36 non-diabetic subjects to determine their morphological (tota

255 avitreal bevacizumab (IVB) administration in diabetic subjects undergoing pars plana vitrectomy (PPV)

256 We tested 12 normal and 17 diabetic subjects using bilateral infrared pupillometry.

257 r limb of internal capsule (ALIC) in MDD and diabetic subjects using diffusion tensor imaging tractog

258 tudy immune responses in young, elderly, and diabetic subjects vaccinated with the seasonal influenza

259 s 9%, whereas CMRglu was 21% lower in type 1 diabetic subjects versus control subjects.

260 azone treatment on insulin sensitivity in 26 diabetic subjects was assessed by hyperinsulinemic-eugly

261 Statin use among hypertensive and diabetic subjects was associated with lower aldosterone

262 Natural Ad-36 infection in nondiabetic and diabetic subjects was associated with significantly lowe

263 Muscle from type 2 diabetic subjects was characterized by a 60% decrease in

264 expression in CD4(+)CD25(+) Tregs of type 1 diabetic subjects was diminished in the presence of IL-2

265 Visual field improvement/deterioration in diabetic subjects was evaluated using significance limit

266 late molecular-physiological phenotypes of a diabetic subject, we generated induced pluripotent stem

267 try with an analysis tailored for monitoring diabetic subjects, we were able to demonstrate progressi

268 Results in control subjects and type 2 diabetic subjects were compared at baseline.

269 Twenty-four diabetic subjects were randomized to either a standard d

270 As a proof of concept, nondiabetic and diabetic subjects were screened for the presence of Ad-3

271 incidence rates for nondiabetic subjects and diabetic subjects were similar: 3.1 deaths per 100 perso

272 al in type 2 diabetes, 14 nondiabetic and 12 diabetic subjects were studied.

273 nt responses in antibody-positive and type 1 diabetic subjects were to ppIAPP(9-17).

274 ntidiabetic therapy on this defect in type 2 diabetic subjects who failed glyburide treatment by the

275 Fifty diabetic subjects who have different stages of NPDR and

276 Even when diabetic subjects, who have greater risk, were excluded,

277 In conclusion, there are asymptomatic type 1 diabetic subjects whose diabetes was diagnosed by the 2-

278 focal laser scanning corneal microscopy from diabetic subjects whose levels of neuropathy were measur

279 changes were examined using the sf-mfERG in diabetic subjects with and without diabetic retinopathy.

280 nocyte activity and sCAMs with AT therapy in diabetic subjects with and without macrovasculopathy.

281 Group B (n = 94) contained diabetic subjects with classic symptoms of gastroparesis

282 The oligoclonally expanded T cells from diabetic subjects with DR4, a susceptibility allele for

283 c subjects without retinopathy (NoR), and 16 diabetic subjects with early NPDR was examined.

284 r cause of death and disability in obese and diabetic subjects with insulin resistance.

285 lar abnormalities and inflammation in type 1 diabetic subjects with microvascular complications.

286 S) training on hepatic fat content in type 2 diabetic subjects with NAFLD.

287 zymatic activity between normal controls and diabetic subjects with neuropathy and chronic wounds.

288 red with subjects without pancreatic cancer, diabetic subjects with pancreatic cancer were more likel

289 The annual incidence rate for diabetic subjects with renal failure, peripheral vascula

290 y was to test if the proportion of new-onset diabetic subjects with the HLA-DR3/4-DQB1*0302 genotype

291 was higher in grossly obese (BMI >40 kg/m2) diabetic subjects with the variant.

292 , which forms MG-derived AGE, is elevated in diabetic subjects with vascular disease.

293 healthy diabetic subjects (DC) (n = 12), and diabetic subjects with very early diabetic microangiopat

294 act GLP-1, total GIP, and glucagon in type 2 diabetic subjects, with no additional glucose lowering w

295 ion and biomarkers of inflammation in type 1 diabetic subjects without macrovascular disease with tha

296 The comparison of control and diabetic subjects without NPDR/mild NPDR was statistical

297 ctivity, and CET were measured in 195 type 1 diabetic subjects without renal failure and 194 nondiabe

298 One eye of each of 26 normal subjects, 16 diabetic subjects without retinopathy (NoR), and 16 diab

299 Group C (n = 94) contained diabetic subjects without symptoms of gastroparesis.

300 ons in healthy lean and obese but not type 2 diabetic subjects, without affecting glucagon or energy