ライフサイエンスコーパス: type 1 diabetes

1 autoreactive cells in the NOD mouse model of type 1 diabetes.

2 two models: SS hypertension and STZ-induced type 1 diabetes.

3 es concerning the pathways leading to IA and type 1 diabetes.

4 gression from islet autoimmunity to clinical type 1 diabetes.

5 ng recurrent liver failure episodes and cure type 1 diabetes.

6 pared with AAb(-) relatives of subjects with type 1 diabetes.

7 subjects, including 87 who had progressed to type 1 diabetes.

8 years, another 36 children developed stage 3 type 1 diabetes.

9 o observed in the retina of a mouse model of type 1 diabetes.

10 m IGFs from a cohort of fasted subjects with type 1 diabetes.

11 ones in prediction of DR in adolescents with type 1 diabetes.

12 trategies for prediction and intervention of type 1 diabetes.

13 y for this reason, are not approved to treat type 1 diabetes.

14 nds increased in the islets of patients with type 1 diabetes.

15 known whether this receptor affects BP under type 1 diabetes.

16 l cohort at varying stages of progression to type 1 diabetes.

17 ssibly reflecting its impaired processing in type 1 diabetes.

18 l of metabolites and lipids related to DR in type 1 diabetes.

19 store normal physiology, health, and life in type 1 diabetes.

20 lls (T(CM)) (CD45RO(+)CD62L(+)) in new-onset type 1 diabetes.

21 oglycemia), 2 (dysglycemia), or 3 (clinical) type 1 diabetes.

22 trol subjects and those at various stages of type 1 diabetes.

23 f hyperinsulinemia by comparing GCK-MODY and type 1 diabetes.

24 1c) (P < 0.05), whereas BRS was preserved in type 1 diabetes.

25 d HbA(1c) 2 years after therapy in new-onset type 1 diabetes.

26 r link between MHC class II and the onset of type 1 diabetes.

27 l in countering autoimmune diseases, such as type 1 diabetes.

28 artGuard) in hypoglycaemia-prone adults with type 1 diabetes.

29 used as adjunctive therapy in patients with type 1 diabetes.

30 a clear understanding of the pathogenesis of type 1 diabetes.

31 d be a target for preventing hypertension in type 1 diabetes.

32 cells in pancreatic islets as seen in human type 1 diabetes.

33 eterioration in individuals at high risk for type 1 diabetes.

34 nduced hunger, fasting and poorly controlled type 1 diabetes.

35 an overestimated association between EV and type 1 diabetes.

36 redominates in driving insulin resistance in type 1 diabetes.

37 of treatment in individuals at high risk for type 1 diabetes.

38 guide other disease-modifying approaches for type 1 diabetes.

39 with progression from islet autoimmunity to type 1 diabetes.

40 y improve glycemic outcomes in children with type 1 diabetes.

41 ber predicts moderate DR in adolescents with type 1 diabetes.

42 patients with autoimmune diseases, including type 1 diabetes.

43 n reducing hypoglycemia in older adults with type 1 diabetes.

44 bition for treating autoimmune diseases like type 1 diabetes.

45 the exocrine pancreas in the pathogenesis of type 1 diabetes.

46 ong 203 adults at least 60 years of age with type 1 diabetes.

47 spectrometry method in 648 individuals with type 1 diabetes.

48 beta-agonists might be at increased risk of type 1 diabetes.

49 ve the resolution of a fine-mapping study of type 1 diabetes.

50 s performed on CGM data of 148 subjects with type-1-diabetes.

51 g in mothers of children with presymptomatic type 1 diabetes (3 [1-7]) compared with mothers of child

52 s considered the optimal strategy to control type 1 diabetes, a childhood disease involving autoimmun

53 rial, we randomly assigned participants with type 1 diabetes, a serum urate level of at least 4.5 mg

54 itoring on hypoglycemia in older adults with type 1 diabetes: a randomized clinical trial.

55 iomyopathy (DbCM) is a major complication in type-1 diabetes, accompanied by altered cardiac energeti

56 orst glycemic control among individuals with type 1 diabetes across the lifespan.

57 ts were associated with an increased risk of type 1 diabetes after adjusting for other antiasthmatic

58 1.4- to 3.3-fold in muscle from humans with type 1 diabetes after short-term insulin deprivation.

59 n-inferiority trial in 108 participants with type 1 diabetes, aged 10-21 years and using insulin pump

60 eficiency in T cells with the development of type 1 diabetes and associated autoimmune comorbidities.

61 signed to identify environmental triggers of type 1 diabetes and celiac disease, were followed up at

62 greatest risk factors in the development of type 1 diabetes and celiac disease.

63 prospective cohort study of childhood-onset type 1 diabetes and DCCT/EDIC, we show that the metaboli

64 erular filtration rate (GFR) in persons with type 1 diabetes and early-to-moderate diabetic kidney di

65 rinol on kidney outcomes among patients with type 1 diabetes and early-to-moderate diabetic kidney di

66 effective treatment option for patients with type 1 diabetes and end stage renal disease.

67 which was similar in donors with and without type 1 diabetes and harbored variable effector/memory fr

68 and TCA cycle intermediates in subjects with type 1 diabetes and healthy control subjects followed fo

69 induced in the liver of streptozocin-induced type 1 diabetes and high fat diet-induced type 2 diabete

70 omplex is involved in the mechanisms linking type 1 diabetes and hypertension.

71 t transplantation is an emerging therapy for type 1 diabetes and hypoglycemic unawareness.

72 h before and after the clinical diagnosis of type 1 diabetes and may serve as novel biomarkers to imp

73 elopment of cell encapsulation therapies for type 1 diabetes and other hormone-deficient diseases.

74 lear whether there is an association between type 1 diabetes and school performance in children.

75 ing 153 individuals aged 14 to 24 years with type 1 diabetes and screening hemoglobin A1c (HbA1c) of

76 tively correlated to a higher grade of DR in type 1 diabetes and several triglycerides being negative

77 thy islets and decreased in islets from both type 1 diabetes and type 2 diabetes mouse models.

78 fset acute rises in BP are impaired in early type 1 diabetes, and this impairment could be a target f

79 -retinal and visual pigment is impaired in a type 1 diabetes animal model, which negatively affects v

80 Type 1 diabetes arises from the autoimmune destruction o

81 s that did not show efficacy overall and had type 1 diabetes as the primary end point were analyzed:

82 ted the onset and increased the incidence of type 1 diabetes as well as that of other disorders, incl

83 progression in all people with or at risk of type 1 diabetes; as such, tailored methods relying on pa

84 hed for allo-crossreactive CDR3betas and for Type 1 diabetes-associated autoreactive CDR3betas.

85 nized in the context of several understudied type 1 diabetes-associated HLA molecules.

86 , we report that genetic risk for developing type 1 diabetes autoimmunity is associated with distinct

87 ncludes data from individuals diagnosed with type 1 diabetes before age 20 years who participated in

88 ONThese results indicate that in adults with type 1 diabetes, beta cell responsiveness to hyperglycem

89 loss of insulin production in patients with type 1 diabetes, but interventions that might affect cli

90 Autoimmune beta-cell destruction leads to type 1 diabetes, but the pathophysiological mechanisms r

91 mber 31, 2008, in Finland and diagnosed with type 1 diabetes by 2010 (n = 3,342).

92 T1DM in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study.

93 prevention trial show that the diagnosis of type 1 diabetes can be delayed by treatment with a FcR n

94 s not known.METHODSWe studied 63 adults with type 1 diabetes classified by peak mixed-meal tolerance

95 Among adults aged 60 years or older with type 1 diabetes, continuous glucose monitoring compared

96 Among adolescents and young adults with type 1 diabetes, continuous glucose monitoring compared

97 The primary outcome was presymptomatic type 1 diabetes, defined by 2 or more islet autoantibodi

98 The role of diet in type 1 diabetes development is poorly understood.

99 peutic strategies targeting this pathway, in type 1 diabetes development.

100 or their bioavailability, are reduced during type 1 diabetes development.

101 nd is also implicated in autoimmunity-driven type-1 diabetes, diabetic nephropathy, multiple sclerosi

102 n age was 10.1 (SD 3.9) years at the time of type 1 diabetes diagnosis and 18.0 (4.1) years at follow

103 (DKA) in children and adolescents at time of type 1 diabetes diagnosis in Germany during the first 2

104 logical studies, beta-cells from donors with type 1 diabetes displayed increased Class I transcripts

105 glucose monitoring devices, most people with type 1 diabetes do not achieve their glycemic goals(1).

106 erquartile range {IQR}, 65-71] years; median type 1 diabetes duration, 36 [IQR, 25-48] years; 52% fem

107 Adolescents and young adults with type 1 diabetes exhibit the worst glycemic control among

108 children carrying susceptibility alleles for type 1 diabetes experienced a more rapid decline in insu

109 ildren with a first-degree family history of type 1 diabetes (FDR children) than in children in the g

110 Although the type 1 diabetes field has gained new insights into disea

111 ll-characterized cohort of participants with type 1 diabetes, followed for >23 years.

112 d trial done in people aged 24-75 years with type 1 diabetes for 10 years or longer, HbA(1c) values o

113 and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous

114 Its efficacy for the treatment of type 1 diabetes has not been explored, in part because t

115 Its involvement in murine and human type 1 diabetes has recently been recognized through the

116 e in three adolescents and young adults with type 1 diabetes have at least one early diabetes-related

117 ), sustained albuminuria, longer duration of type 1 diabetes, higher mean pulse rate, higher mean sys

118 people for years following the diagnosis of type 1 diabetes; however, the physiologic significance o

119 transplantation is a promising treatment for type-1 diabetes; however, donor shortage is a concern.

120 f islet autoimmunity (IA) and progression to type 1 diabetes in a prospective high-risk cohort.

121 drugs was associated with the development of type 1 diabetes in childhood in a nationwide, register-b

122 Public health screening for type 1 diabetes in its presymptomatic stages may reduce

123 ested strategies to prevent the diagnosis of type 1 diabetes in people at risk, but the outcomes of p

124 We induced type 1 diabetes in rats by streptozotocin injection and

125 The 3-year cumulative risk for stage 3 type 1 diabetes in the 280 children with presymptomatic

126 rons (IFNs) could provide protection against type 1 diabetes in these patients (Meyer et al., 2016).

127 Anomalies we found in type 1 diabetes included (i) an increase of 'intermediat

128 nd support recent findings that suggest that type 1 diabetes includes abnormalities in the exocrine p

129 0.31%; 95% CI, 0.27-0.35) had presymptomatic type 1 diabetes, including 196 (0.22%) with stage 1, 17

130 tected similarly to TRPV1-knockout mice from type 1 diabetes-induced endothelial dysfunction and impa

131 The risk for autoimmunity and subsequently type 1 diabetes is 10-fold higher in children with a fir

132 Type 1 diabetes is a chronic autoimmune disease that lea

133 Type 1 diabetes is an autoimmune disease characterized b

134 Type 1 diabetes is an autoimmune disease resulting in se

135 Type 1 diabetes is an autoimmune-mediated disease that c

136 n patients with diabetes, and a diagnosis of type 1 diabetes is associated negatively with both recei

137 The autoimmune disease type 1 diabetes is characterized by effector T-cell resp

138 Type 1 diabetes is the prototypical CD4 T cell-mediated

139 The main goal of treatment for type 1 diabetes is to control glycaemia with insulin the

140 n youth with newly diagnosed overt (stage 3) type 1 diabetes is unknown.

141 Previous studies indicate that type-1 diabetes is associated with increased cardiac exp

142 Type 1 diabetes islet cell autoantigen 512 (ICA512/IA-2)

143 insulin resistance consistently occurs with type 1 diabetes, its predominant driver is uncertain.

144 ery and insulin-producing cell therapies for type 1 diabetes management.

145 ion using functional MRI in 80 children with type 1 diabetes (mean +/- SD age 11.5 +/- 1.8 years; 46%

146 he correction of dysglycemia associated with type 1 diabetes mellitus (allogenic islet transplantatio

147 y bowel disease, autoimmune thyroid disease, type 1 diabetes mellitus (T1D), and autoimmune pancreati

148 es how genetic variation in a mouse model of type 1 diabetes mellitus (T1DM) affects long-distance ge

149 alue of HbA(1c) in the care of patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mell

150 to the two main forms of diabetes mellitus - type 1 diabetes mellitus (T1DM) and type 2 diabetes mell

151 The skeleton of type 1 diabetes mellitus (T1DM) has deteriorated mechani

152 Type 1 diabetes mellitus (T1DM) has traditionally been c

153 Patients with type 1 diabetes mellitus (T1DM) have increased thrombosi

154 r partial clinical remission (PCR) phase, of Type 1 diabetes mellitus (T1DM) is a transitory period t

155 Type 1 diabetes mellitus (T1DM) is an autoimmune conditi

156 se transport kinetics among individuals with type 1 diabetes mellitus (T1DM) remains unclear.

157 Type 1 diabetes mellitus (T1DM) substantially increases

158 the long-term prognosis of young people with type 1 diabetes mellitus (T1DM).

159 immunotherapy at best delays progression of type 1 diabetes mellitus and points to opportunities to

160 risk of death and cardiovascular outcomes in type 1 diabetes mellitus have been sparsely studied.

161 d to be associated with an increased risk of type 1 diabetes mellitus in childhood, but the reasons a

162 Type 1 diabetes mellitus is believed to result from dest

163 3.9%; univariate P = 0.038), while those for type 1 diabetes mellitus remained statistically stable (

164 Type 1 diabetes mellitus results from autoimmune destruc

165 Patients with type 1 diabetes mellitus were followed up until death or

166 , waist-hip ratio, diastolic blood pressure, type 1 diabetes mellitus, and insulin use.

167 In contrast to type 1 diabetes mellitus, the dominant immune cell type

168 a cross-sectional study of individuals with type 1 diabetes mellitus, those who were designated to b

169 n essential component in the pathogenesis of type 1 diabetes mellitus.

170 higher risk of complications than those with type 1 diabetes mellitus.

171 plex lowers BP in diabetic animals; that (b) type 1 diabetes modulates the levels of MD2 expression i

172 The effect of type 1 diabetes on the developing brain is a topic of pr

173 cells from healthy donors and patients with type 1 diabetes or Sezary syndrome.

174 Interestingly, type 1 diabetes pancreata displayed significant reductio

175 eas Analysis Program (HPAP) to procure human type 1 diabetes pancreata for an extensive array of tiss

176 ith multiple AAb and those who progressed to type 1 diabetes, particularly postdiagnosis.

177 of amyloid in intraportal islet implants of type 1 diabetes patients has been proposed as cause in t

178 a promising treatment option for intractable type 1 diabetes patients.

179 sodes associated with fatal complications in type-1 diabetes patients.

180 Patients with type 1 diabetes, prediabetes, and gestational diabetes w

181 outside the HLA DR-DQ region in the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study i

182 (IA), with potential as vaccine targets for type 1 diabetes prevention.

183 In type 1 diabetes, proinsulin-specific CD8(+) T cells, esc

184 Forty type 1 diabetes recipients of intraportal islet cell gra

185 ted insulin delivery systems for people with type 1 diabetes rely on an accurate subcutaneous glucose

186 tic islet transplantation (Tx) as a cure for type 1 diabetes remains limited.

187 lycemia on neurodevelopment in children with type 1 diabetes remains unclear.

188 nceptual advance about four decades ago that type 1 diabetes represents an autoimmune disease, hope a

189 While the vast majority of type 1 diabetes research efforts have focused on endocri

190 n of T-cell epitopes is a critical aspect of type 1 diabetes research.

191 stem cell transplantation and with new onset type 1 diabetes, respectively.

192 K-MODY but was 29% and 22% less effective in type 1 diabetes, respectively.

193 Type 1 diabetes results from the autoimmune-mediated des

194 l connections, such as autoimmune disorders (type 1 diabetes, rheumatoid arthritis, and multiple scle

195 ng point for further investigations on how a type 1 diabetes risk factor impacts the young immune sys

196 uman milk feeding are associated with higher type 1 diabetes risk.

197 the battle to stave off the complications of type 1 diabetes, showing dramatic declines in the develo

198 NOD mice develop spontaneous autoimmune type 1 diabetes similar to that seen in humans.

199 Type 1 diabetes studies consistently generate data showi

200 GFBPs were unchanged in individuals with pre-type 1 diabetes, suggesting that total IGF levels may re

201 toid arthritis (RA) (n = 194, HD n = 64), 2) type 1 diabetes (T1D) (n = 200, HD n = 200), 3) systemic

202 Patients with type 1 diabetes (T1D) (n = 41) and healthy age-, sex-, a

203 Children at increased genetic risk for type 1 diabetes (T1D) after environmental exposures may

204 diabetes, the existence of brain changes in type 1 diabetes (T1D) and both their neuroanatomical and

205 observed in individuals with newly-diagnosed type 1 diabetes (T1D) and declines over the first year a

206 nal hypoxia, in adolescents with and without type 1 diabetes (T1D) and relate the ratio to albuminuri

207 cts (POEs), have been hypothesised to affect type 1 diabetes (T1D) and rheumatoid arthritis (RA).

208 The pathogenesis of Type 1 diabetes (T1D) arises from the destruction of ins

209 ic analyses have significantly refined human type 1 diabetes (T1D) associated loci.

210 High-affinity islet autoantibodies predict type 1 diabetes (T1D) but do not cause beta cell destruc

211 elivery of pancreatic islets for a potential type 1 diabetes (T1D) cell replacement therapy.

212 iation study (GWAS) for HbA(1c) in a Finnish type 1 diabetes (T1D) cohort, FinnDiane.

213 ain HLA class II genes increase the risk for type 1 diabetes (T1D) development while others provide p

214 ical characteristics.METHODSIndividuals with type 1 diabetes (T1D) for 50 or more years underwent eva

215 une dysregulatory syndromes diagnosed, where type 1 diabetes (T1D) forms part of the autoimmune manif

216 The vast majority of type 1 diabetes (T1D) genetic association signals lie in

217 Maternal type 1 diabetes (T1D) has been linked to preterm birth a

218 Type 1 diabetes (T1D) imposes a significant health burde

219 Antigen (Ag)-specific tolerization prevents type 1 diabetes (T1D) in non-obese diabetic (NOD) mice b

220 Therapeutic approaches to combat type 1 diabetes (T1D) include donor pancreas transplanta

221 Type 1 diabetes (T1D) is a significant problem in Indian

222 Type 1 diabetes (T1D) is a T cell-mediated autoimmune di

223 Type 1 diabetes (T1D) is an autoimmune disease of insuli

224 Type 1 Diabetes (T1D) is an autoimmune disease that is a

225 y islet transplantation for the treatment of type 1 diabetes (T1D) is currently limited by donor tiss

226 Although the etiology of type 1 diabetes (T1D) is not well understood, it is beli

227 The rising prevalence of type 1 diabetes (T1D) over the past decades has been lin

228 tion by autoreactive T cells is essential in type 1 diabetes (T1D) pathogenesis.

229 euronal components play an important role in type 1 diabetes (T1D) pathogenesis.

230 ned IA-2var AAb in first-degree relatives of type 1 diabetes (T1D) probands from the TrialNet Pathway

231 CD137 modulates type 1 diabetes (T1D) progression in NOD mice.

232 People with type 1 diabetes (T1D) require exogenous administration o

233 Type 1 diabetes (T1D) results from the progressive destr

234 Although most patients with type 1 diabetes (T1D) retain some functional insulin-pro

235 Optimal immune-based therapies for type 1 diabetes (T1D) should restore self-tolerance with

236 ng CD137) is a candidate gene for the Idd9.3 type 1 diabetes (T1D) susceptibility locus in the nonobe

237 pool of beta cell-specific CD8(+) T cells in type 1 diabetes (T1D) sustains an autoreactive potential

238 ontrol group composed of 30 individuals with type 1 diabetes (T1D) were evaluated in a national refer

239 pregenual anterior cingulate cortex (ACC) in type 1 diabetes (T1D) without depression affects emotion

240 The etiopathogenesis of type 1 diabetes (T1D), a common autoimmune disorder, is

241 -DQA1 and -DQB1 are strongly associated with type 1 diabetes (T1D), and DQ8.1 and DQ2.5 are major ris

242 zation in thymocytes of NOD mice, a model of type 1 diabetes (T1D), and the diabetes-resistant C57BL/

243 lar helper T (T(FH)) cells are implicated in type 1 diabetes (T1D), and their development has been li

244 extraintestinal autoimmune diseases such as type 1 diabetes (T1D), but a direct causal link between

245 ethylation may be involved in development of type 1 diabetes (T1D), but previous epigenome-wide assoc

246 In type 1 diabetes (T1D), DEs are predominated by one clono

247 phoprotein 2 (SKAP2) gene is associated with type 1 diabetes (T1D), suggesting SKAP2 as a causal cand

248 icted with diabetes worldwide, about 5% have type 1 diabetes (T1D), while the remaining ~95% of diabe

249 to achieve in children and adolescents with type 1 diabetes (T1D), yet the influence of dysglycemia

250 Type 1 diabetes (T1D)-an autoimmune disease that destroy

251 isease progression in the NOD mouse model of type 1 diabetes (T1D).

252 rventions and Complications (EDIC) cohort of type 1 diabetes (T1D).

253 ets is closely related to the development of type 1 diabetes (T1D).

254 relation to retinopathy in individuals with type 1 diabetes (T1D).

255 in the peripheral blood of individuals with type 1 diabetes (T1D).

256 or beta cell replacement in the treatment of type 1 diabetes (T1D).

257 hanism of Nrf2-mediated myocardial damage in type 1 diabetes (T1D).

258 imuli demonstrate alterations in established type 1 diabetes (T1D).

259 en islet-reactive T and B lymphocytes drives type 1 diabetes (T1D).

260 whether obesity can act as an accelerator of type 1 diabetes (T1D).

261 in the residual islets of organ donors with type 1 diabetes (T1D).

262 ave revealed 59 genomic loci associated with type 1 diabetes (T1D).

263 cell (CTL)-mediated beta-cell destruction in type 1 diabetes (T1D).

264 development of islet autoantibodies (IA) and type 1 diabetes (T1D).

265 utoantigens is a characteristic of childhood type 1 diabetes (T1D).

266 sed as an alternative treatment strategy for type 1 diabetes (T1D).

267 entially causal associations with autoimmune type 1 diabetes (T1D).

268 herapeutic interventions in the treatment of type 1 diabetes (T1D).

269 fate of beta-cells and hence progression of type 1 diabetes (T1D).

270 and nitration free adducts in patients with type 1 diabetes (T1DM) during onset of microalbuminuria

271 cal mouse models of experimental PH, HF, and type 1 diabetes that are associated with altered glucose

272 n resistance is an underappreciated facet of type 1 diabetes that occurs with remarkable consistency

273 In type 1 diabetes, the appearance of islet autoantibodies

274 r predicting change in beta-cell function in type 1 diabetes, the finding that abatacept blunts this

275 n this 16-week trial involving children with type 1 diabetes, the glucose level was in the target ran

276 In a model of type 1 diabetes, the induction of podVEGFC overexpressio

277 Type 1 diabetes therapies that afford tighter glycemic c

278 address the enduring challenges of emerging type 1 diabetes therapies.

279 ture potentially causal DR associations with type 1 diabetes, this list of residuals is expected to i

280 e patients with well-controlled recent-onset type 1 diabetes, those with type 2 diabetes show early b

281 e, 6 to 21 years) with newly diagnosed overt type 1 diabetes to receive subcutaneous golimumab or pla

282 ratio, children 6 to 13 years of age who had type 1 diabetes to receive treatment with the use of eit

283 Seven people with type 1 diabetes undergoing automated insulin delivery us

284 al deaths per year per 100 000 patients with type 1 diabetes undergoing treatment.

285 transcriptomes from donors with and without type 1 diabetes using both bulk-sorted and single beta-c

286 ic function and cardiac vascular function in type 1 diabetes using new and sensitive methods.

287 tive impact of HbA(1c) and kidney disease in type 1 diabetes varies according to diabetes duration.

288 Progression to clinical type 1 diabetes varies among children who develop beta-c

289 etes in the 280 children with presymptomatic type 1 diabetes was 24.9% ([95% CI, 18.5%-30.7%]; 54 cas

290 Type 1 diabetes was associated negatively with receiving

291 appraisal of the T-cell epitopes targeted in type 1 diabetes was completed over a decade ago, providi

292 dress the role of PD-1 in the GC reaction in type 1 diabetes, we used tetramers to phenotype insulin-

293 tudy participants with HLA susceptibility to type 1 diabetes were collected.

294 f antiasthmatic drugs and the development of type 1 diabetes were investigated using time-dependent a

295 ultiple islet autoantibodies (presymptomatic type 1 diabetes) were invited to participate in a progra

296 tibody) involving relatives of patients with type 1 diabetes who did not have diabetes but were at hi

297 o access and study patients (Medalists) with type 1 diabetes who have been insulin dependent for 50 y

298 roaches to prevent the loss of beta cells in type 1 diabetes will emerge into clinical practice.

299 rom 26 control subjects and 62 patients with type 1 diabetes with (n = 17) and without (n = 45) DSPN

300 lines derived from matched individuals with type 1 diabetes with and without retinopathy.