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 o hypoglycemia in intensively treated type 1 diabetic subjects.

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

4 s therapeutic agents for asthma in obese and diabetic subjects.

5 on and accelerated cardiovascular disease in diabetic subjects.

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

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

8 gulatory response seen in tightly controlled diabetic subjects.

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

10 adipose tissue from diabetic compared to non-diabetic subjects.

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

12 tic retinopathy screening examinations among diabetic subjects.

13 f glycogenolysis in both the nondiabetic and diabetic subjects.

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

15 issue explants obtained from nondiabetic and diabetic subjects.

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

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

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

19 ere also approximately twofold higher in the diabetic subjects.

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

21 contribute to cognitive deficits observed in diabetic subjects.

22 as reassessed after 4 years in 124 available diabetic subjects.

23 e macular edema and improve visual acuity 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 selection criterion for bariatric surgery in diabetic subjects.

33 p between particle size and calcification in diabetic subjects.

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

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

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

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

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

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

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

41 myocardial infarction is abnormally high in diabetic subjects.

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

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

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

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

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

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

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

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

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

51 d with MN-siCas-3 and infused into recipient diabetic subjects.

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

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

54 ce of the metabolic abnormalities present in diabetic subjects.

55 elate with midperipheral retinal ischemia in diabetic subjects.

56 NGF for the prevention of cardiomyopathy in diabetic subjects.

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

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

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

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

61 .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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 justed mean: 2.03 ng/ml +/- 0.90 SD) vs. non-diabetic subjects (adjusted mean: 1.79 ng/ml +/- 0.89 SD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP

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

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

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

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

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

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

109 Since diabetic subjects are characterized by a prothrombotic a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 The diabetic subjects exhibited markedly reduced awakening f

148 17; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increasing ins

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

150 In type 2 diabetic subjects, extrapancreatic KATP channel activati

151 Type 2 diabetic subjects failing glyburide therapy were randomi

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

153 In non-diabetic subjects, FKBPL was positively correlated with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Diabetic subjects had significantly lower mean fractiona

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

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

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

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

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

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

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

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

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

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

183 mplicit time and diabetes duration in type 2 diabetic subjects in four out of five rings (p < 0.001).

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

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

186 Controls were other diabetic subjects in the cohort.

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

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

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

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

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

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

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

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

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

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

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

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

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

200 Type 2 diabetic subjects manifest both disordered insulin actio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 nish with weight loss in nondiabetic but not diabetic subjects, possibly representing sustained infla

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

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

226 In type 1 diabetic subjects, reduced fractional anisotropy correla

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

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

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

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

231 rbidly obese nondiabetic subjects but not in diabetic subjects, suggesting continued inflammation.

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

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

234 6-H611 haplotype were present in more type 2 diabetic subjects than control subjects (one-tailed P =

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

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

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

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

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

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

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

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

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

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

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

246 Among diabetic subjects, the variant was associated with great

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

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

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

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

251 Twenty eyes of 20 diabetic subjects type 2 without retinopathy and 20 eyes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

269 and the delay in P1-implicit time in type 2 diabetic subjects were statistically significant in most

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

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

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

273 Fifty diabetic subjects who have different stages of NPDR and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 53 adults, consisting of 234 T2D and 119 non-diabetic subjects with/without CVD, matched for age, BMI

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

293 Forty controls, 36 diabetic subjects without clinical retinopathy (NoDR), 3

294 We aimed to assess early retinal changes in diabetic subjects without clinical retinopathy using mul

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