ライフサイエンスコーパス: IDDM

1 IDDM can be consistently induced and safely treated in j

2 IDDM is a polygenic and autoimmune disorder in which sub

3 IDDM is a T-cell-mediated autoimmune disease in which th

4 IDDM patients treated with conventional subcutaneous ins

5 IDDM results from a progressive loss of pancreatic beta-

6 IDDM results from the destruction of pancreatic beta-cel

7 IDDM susceptibility was restored in NODJg mu(null) mice

8 IDDM was induced in rats by streptozotocin (STZ) injecti

9 g 22,888 RA, 26,198 AIT, 4,332 MS, and 6,170 IDDM patients compared with the general population.

10 ns from diabetic NOD donors did not abrogate IDDM resistance in NODJg mu(null) mice.

11 cells in NOD mice may result in accelerated IDDM; and 3) irradiated NOD-lpr/lpr mice are resistant t

12 d to IL-4 and/or IL-13 protects mice against IDDM in this model of autoimmunity.

13 gulator of NF-kappaB, should protect against IDDM.

14 53 with impaired neutrophil chemotaxis in an IDDM sample.

15 By multivariate analysis, IDDM was an independent predictor for any late cardiac e

16 udy demonstrates coexistence of RA, AIT, and IDDM at higher than expected rates but reduced comorbidi

17 ment with LTbetaR-Ig prevented insulitis and IDDM, suggesting that LT plays a critical role in the in

18 l destruction, development of insulitis, and IDDM also depend on the cytokine INF-gamma, presumably t

19 between unstable MHC class II molecules and IDDM susceptibility.

20 bjects, autoantibody-negative relatives, and IDDM patients, respectively, against the proinsulin pept

21 n 57 in HLA-DQ alphabeta dimer stability and IDDM susceptibility.

22 proinsulin for healthy control subjects and IDDM patients, respectively, were as follows: 1 microg/m

23 tivated state and rapidly mediate autoimmune IDDM development in the complete absence of CD4 T cell h

24 ontributing to the development of autoimmune IDDM.

25 ectively, these results show that autoimmune IDDM in NOD mice is initiated by MHC class I-dependent T

26 th the GAD65-specific peptides did not block IDDM development in NOD mice deficient in IL-4 expressio

27 HLA-DR antigens are associated with both IDDM and periodontitis.

28 er cross-reacting viruses that fail to cause IDDM could be mapped to point mutations in the CTL epito

29 s susceptible to experimentally induced CIA, IDDM and ATD, and it has an SE in its MHC class II allel

30 tricted beta cell autoreactive T cell clone, IDDM development was retarded by elimination of residual

31 ntrol of the RIP in their beta cells develop IDDM after infection with LCMV and serve as a model for

32 Following LCMV infection, these mice develop IDDM, which depends on Db-restricted anti-self (viral) C

33 DP-BB rats develop IDDM spontaneously.

34 P-BB) x WF backcross animals readily develop IDDM after treatment with polyinosinic:polycytidylic aci

35 prone (DP) BB/Wor rats spontaneously develop IDDM.

36 ed NOD.AI4alphabeta Tg) continued to develop IDDM at a greatly accelerated rate when residual CD4 hel

37 ells but no lymphadenopathy, fail to develop IDDM.

38 e lpr mutation (NOD-lpr/lpr) fail to develop IDDM; 2) transgenic expression of Fas ligand (FasL) on b

39 All five patients developed IDDM lasting longer than 6 months.

40 itive individual at high risk for developing IDDM.

41 nhibits T cell-mediated autoimmune diabetes (IDDM) in nonobese diabetic (NOD) mice.

42 free of T cell-mediated autoimmune diabetes (IDDM), due to non-MHC genes of C57BLKS/J (BKS) origin.

43 ls in regulating insulin-dependent diabetes (IDDM).

44 mice with freshly developed type I diabetes (IDDM).

45 lial psoriasis, asthma, and type-I diabetes (IDDM).

46 mined in 60 individuals with newly diagnosed IDDM (< or = 1 day from diagnosis) in 34 islet cell cyto

47 (PBMC) from individuals with newly diagnosed IDDM or at varying levels of risk for the disease were s

48 Sera from 58% of the newly diagnosed IDDM patients tested were IA-2 autoantibody positive.

49 was significantly higher in newly diagnosed IDDM subjects (14 of 33 [42%]; 3.8+/-4.5 at 10 microg/ml

50 sceptibility to the human autoimmune disease IDDM is strongly associated with those haplotypes of the

51 ter understanding of a more common disorder, IDDM, and has allowed investigators to gain insights int

52 ts a unique opportunity to identify dominant IDDM resistance determinants expressed at the beta cell

53 d, thus providing a promising clue to effect IDDM reversal in humans.

54 impact of diabetes mellitus (DM), especially IDDM, on in-stent restenosis is not known.

55 regeneration and the reversal of established IDDM are exceedingly limited.

56 Five IDDM susceptibility loci map to 2 chromosomal regions, c

57 n is a novel cell-associated risk marker for IDDM.

58 These results support a model for IDDM in which Thl-cell-mediated tissue damage is initial

59 om nonobese diabetic (NOD) mice, a model for IDDM, are more sensitive to various forms of stimulation

60 exert a pathogenic function(s) necessary for IDDM.

61 ody-positive relatives at increased risk for IDDM (6 of 9 [66%]; 3.9+/-3.2) compared with autoantibod

62 in individuals with or at increased risk for IDDM.

63 improved and more cost-effective therapy for IDDM.

64 udies investigating potential treatments for IDDM including islet cell transplantation.

65 secreted IFN-gamma and did not protect from IDDM.

66 in an infectious manner and protection from IDDM.

67 that is not associated with protection from IDDM.

68 II VNTRs that are dominantly protective from IDDM.

69 actions between viral infections and non-HLA IDDM candidate genes, including those that may determine

70 However, IDDM does not occur in NOD mice made MHC class I-deficie

71 However, IDDM was inhibited in mixed chimeras where H2-E was sole

72 rats are used as models of autoimmune human IDDM.

73 etic) mouse is a good animal model for human IDDM.

74 l of the T cell transmigration step in human IDDM.

75 The NOD mouse is a model of human IDDM, which is characterized by a cell-mediated autoimmu

76 ents treated by elective stent implantation, IDDM patients were at higher risk for in-hospital mortal

77 edure) was significantly lower (p=0.0004) in IDDM (60%) compared with non-IDDM (70%) and nondiabetic

78 support the autoantigenic nature of IA-2 in IDDM and suggest the inclusion of cellular immune respon

79 In-hospital mortality was 2% in IDDM, significantly higher (p <0.02) compared with non-I

80 et lesion revascularization (TLR) was 28% in IDDM, significantly higher (p <0.05) compared with non-I

81 ombosis did not differ among groups (0.9% in IDDM vs. 0% in non-IDDM and 0% in nondiabetics, p >0.1).

82 tly important as etiologic dietary agents in IDDM in NOD mice.

83 2), which is a dominant protective allele in IDDM, exhibits the greatest SDS stability among HLA-DQ m

84 rypsin and reactivity with autoantibodies in IDDM sera.

85 in peptide) may serve as key autoantigens in IDDM.

86 that the autoantibodies to IA-2/IA-2 beta in IDDM sera recognize conformational epitopes.

87 for the abnormal behavior of these cells in IDDM are not fully understood.

88 utrophil chemotaxis has been demonstrated in IDDM and in early-onset periodontitis (EOP).

89 itical mediators of beta-cell destruction in IDDM, we conclude that well regulated insulinoma cell li

90 ature insulin protein are rarely detected in IDDM patients.

91 n preventing or delaying the onset of DSP in IDDM patients.

92 and thereby to test the importance of GAD in IDDM, we generated three lines transgenic for murine GAD

93 nding of the prevailing role of HLA genes in IDDM pathogenesis and suggests opportunities to interven

94 of the HLA class II susceptibility genes in IDDM suggests likely molecular mechanisms for several of

95 suggest that: (1) depression of the HCVR in IDDM is associated with hyperglycemia and glycosylation

96 d decarboxylase (GAD) has been implicated in IDDM, there is no direct evidence showing GAD-reactive T

97 ve previously shown that CET is increased in IDDM patients receiving conventional subcutaneous insuli

98 proliferative responses to human insulin in IDDM patients.

99 Hyperinsulinemia persists in IDDM patients who undergo successful pancreas-kidney tra

100 ne the significance of cow's milk protein in IDDM, 120 NOD mice were maintained, starting from concep

101 ion of the complex CD4(+) T cell response in IDDM.

102 only treatment of mice with STZ resulted in IDDM and mimicked the effects observed following CB4 inf

103 ave a critical and not fully defined role in IDDM in humans and in the NOD mouse.

104 he alphabeta dimer in SDS may play a role in IDDM protection.

105 concept that telomeres might play a role in IDDM.

106 g, disease-promoting, or regulatory steps in IDDM development.

107 I) given as an adjunct to insulin therapy in IDDM, might improve glycaemic control in adolescents; we

108 bit potent APC function remains undefined in IDDM.

109 eta cell-specific Th2 cell clones can induce IDDM.

110 ected with alloxan (50 mg/kg i.v.) to induce IDDM.

111 single-center experience with FK506-induced IDDM in children.

112 be at high risk for developing FK506-induced IDDM.

113 tment was sufficient to prevent LCMV-induced IDDM in rat insulin promoter-LCMV-glycoprotein transgeni

114 LCMV and serve as a model for virus-induced IDDM.

115 We induced IDDM in 11 juvenile cynomolgus monkeys after a single (1

116 MHC class II molecules to additively inhibit IDDM in NOD mice.

117 e intervention protocols designed to inhibit IDDM by introduction of putatively protective MHC molecu

118 macrophages/dendritic cells (DC)) to inhibit IDDM.

119 egulatory process was induced that inhibited IDDM.

120 Only patients with labile IDDM (e.g., hypoglycemic unawareness, insulin reactions,

121 ternative for nonuremic patients with labile IDDM.

122 proportional hazards model shows that longer IDDM duration, hypertension, poor glycemic control, heig

123 ment of insulin-dependent diabetes mellitus (IDDM) and after immunotherapy are unclear.

124 ticular insulin-dependent diabetes mellitus (IDDM) and autoimmune thyroid disease (ATD), share geneti

125 nset of insulin-dependent diabetes mellitus (IDDM) and may be critical to the pathogenic process.

126 le with insulin-dependent diabetes mellitus (IDDM) and renal failure to maintain a more normal lifest

127 ns with insulin-dependent diabetes mellitus (IDDM) and those with islet autoantibodies at increased r

128 oimmune insulin-dependent diabetes mellitus (IDDM) because nonobese diabetic (NOD) mice and humans wi

129 ance to insulin-dependent diabetes mellitus (IDDM) but the immunologic mechanisms involved are not un

130 Insulin-dependent diabetes mellitus (IDDM) can lead to ventilatory depression and decreased s

131 ment of insulin-dependent diabetes mellitus (IDDM) caused by virus-induced pancreatic cell damage.

132 S), and insulin-dependent diabetes mellitus (IDDM) during 1990-1999.

133 ts with insulin-dependent diabetes mellitus (IDDM) had higher risk of cardiac death for any MPS resul

134 sulin-dependent or Type 1 diabetes mellitus (IDDM) has been associated with an increased severity of

135 ype 1 (insulin-dependent) diabetes mellitus (IDDM) has been studied extensively and the disorder has

136 oimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions,

137 ype 1 (insulin-dependent) diabetes mellitus (IDDM) has shown that the disease is caused by a combinat

138 agnosed insulin-dependent diabetes mellitus (IDDM) have autoantibodies to insulin, and the majority o

139 ence of insulin-dependent diabetes mellitus (IDDM) in adults, but the incidence of IDDM in pediatric

140 sustain insulin-dependent diabetes mellitus (IDDM) in humans and in non-obese diabetic (NOD) mice.

141 on from insulin-dependent diabetes mellitus (IDDM) in NOD mice.

142 type I insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice.

143 prevent insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice.

144 revents insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice.

145 such as insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic mice (NOD).

146 oimmune insulin-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restric

147 o cause insulin-dependent diabetes mellitus (IDDM) in transgenic mice whose pancreatic beta cells exp

148 ype 1 (insulin-dependent) diabetes mellitus (IDDM) is 1.

149 Insulin-dependent diabetes mellitus (IDDM) is a risk factor for periodontitis.

150 Type I diabetes mellitus (IDDM) is a T cell-dependent autoimmune disease resulting

151 Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease resulting from apoptotic

152 Insulin-dependent diabetes mellitus (IDDM) is characterized by the T cell-mediated destructio

153 lity to insulin-dependent diabetes mellitus (IDDM) is the insulin-linked polymorphic region (ILPR, al

154 Insulin-dependent diabetes mellitus (IDDM) is the second most prevalent chronic illness of ch

155 hin the insulin-dependent diabetes mellitus (IDDM) locus IDDM4 on chromosome 11q13.

156 oimmune insulin-dependent diabetes mellitus (IDDM) occurs spontaneously in mice-bearing transgenes en

157 develop insulin-dependent diabetes mellitus (IDDM) only after LCMV infection.

158 induces insulin-dependent diabetes mellitus (IDDM) resembling the final step of disease progression i

159 ers and insulin-dependent diabetes mellitus (IDDM) susceptibility.

160 trol in insulin-dependent diabetes mellitus (IDDM) to prevent complications may be difficult to achie

161 abetes (insulin-dependent diabetes mellitus (IDDM)) in vivo without affecting systemic viral clearanc

162 rved in insulin-dependent diabetes mellitus (IDDM), although the cellular mechanism(s) of dysfunction

163 esis of insulin-dependent diabetes mellitus (IDDM), an LTbeta receptor-immunoglobulin fusion protein

164 IBD and insulin-dependent diabetes mellitus (IDDM), as a control disease, were identified by age 26 y

165 tation in insulin-treated diabetes mellitus (IDDM), non-IDDM patients, and nondiabetic patients.

166 trolled insulin-dependent diabetes mellitus (IDDM), we used 13C-NMR spectroscopy to monitor the peak

167 d treat insulin-dependent diabetes mellitus (IDDM).

168 ment of insulin-dependent diabetes mellitus (IDDM).

169 ment of insulin-dependent diabetes mellitus (IDDM).

170 se from insulin-dependent diabetes mellitus (IDDM).

171 oimmune insulin-dependent diabetes mellitus (IDDM).

172 lity to insulin-dependent diabetes mellitus (IDDM).

173 ts with insulin-dependent diabetes mellitus (IDDM).

174 rapy of insulin-dependent diabetes mellitus (IDDM).

175 eads to insulin-dependent diabetes mellitus (IDDM).

176 rity of insulin-dependent diabetes mellitus (IDDM).

177 tage of insulin-dependent diabetes mellitus (IDDM).

178 Human diabetes mellitus (IDDM; type I diabetes) is a T cell-mediated disease that

179 abetes (insulin-dependent diabetes mellitus [IDDM]) in the past year.

180 abetes (insulin-dependent diabetes mellitus, IDDM) is a disease controlled by the major histocompatib

181 abetes (insulin-dependent diabetes mellitus, IDDM)-associated HLA-DR4 molecule.

182 In both mouse models, IDDM resulted in depression of the hypercapnic ventilato

183 marrow chimera analyses that Idd13 modulates IDDM development at the level of non-hematopoietically d

184 , rat inflammatory arthritis, rat and murine IDDM, histamine sensitization, immunity to exogenous ant

185 ural outcome was found to be similar for non-IDDM compared with nondiabetic patients.

186 nsulin-treated diabetes mellitus (IDDM), non-IDDM patients, and nondiabetic patients.

187 fer among groups (0.9% in IDDM vs. 0% in non-IDDM and 0% in nondiabetics, p >0.1).

188 ificantly higher (p <0.02) compared with non-IDDM (0%) and nondiabetics (0.3%).

189 ificantly higher (p <0.05) compared with non-IDDM (17.6%) and nondiabetics (16.3%).

190 r (p=0.0004) in IDDM (60%) compared with non-IDDM (70%) and nondiabetic patients (76%).

191 NOR IDDM resistance was previously found to be largely contr

192 sulin levels in 14 euglycemic normolipidemic IDDM PKT patients with near-normal kidney function (crea

193 phenotype, and parallels the acceleration of IDDM we had seen in young adult NOD mice.

194 europathy affects the exercising capacity of IDDM patients, and whether regular, intense training has

195 either the duration nor the complications of IDDM (i.e., nephropathy and hypertension) had an effect

196 cM) intervals both contribute components of IDDM resistance.

197 Genetic control of IDDM in both species is complex, including both major hi

198 roduction are conserved during the course of IDDM.

199 essful islet transplantation and the cure of IDDM.

200 erefore, the neutrophil chemotaxis defect of IDDM appears to be independent of these HLA-DR-associate

201 aR-Ig treatment prevented the development of IDDM by diabetogenic T cells in an adoptive transfer mod

202 cells is responsible for the development of IDDM.

203 bute to the understanding of the etiology of IDDM and may lead to the development of better strategie

204 Exacerbation of IDDM correlated with an increased frequency of IFN-gamma

205 have delayed onset and reduced incidence of IDDM after adoptive transfer of diabetogenic NOD spleen

206 the insulin B chain reduced the incidence of IDDM by 50% in this model.

207 litus (IDDM) in adults, but the incidence of IDDM in pediatric renal transplant recipients treated wi

208 g diets resulted in comparable incidences of IDDM in NOD mice, demonstrating that neither cow's milk

209 n the nonobese diabetic (NOD) mouse model of IDDM is thought to be a T-cell-mediated process due to a

210 blood glucose levels in two mouse models of IDDM: (1) streptozotocin-induced diabetes in C57BL/6J mi

211 4Ralpha genes were examined for the onset of IDDM.

212 ologous peptides and a delay in the onset of IDDM.

213 her our understanding of the pathogenesis of IDDM and to further the development of novel modes to pr

214 nity to this molecule in the pathogenesis of IDDM in humans remains unclear.

215 d lysis of beta cells in the pathogenesis of IDDM in nonobese diabetic (NOD) mice includes: 1) Fas-de

216 The pathogenesis of IDDM involves the transmigration of autoimmune T cells i

217 to clarify their role in the pathogenesis of IDDM.

218 y be a critical event in the pathogenesis of IDDM.

219 WBCs that play a role in the pathogenesis of IDDM.

220 rther define its role in the pathogenesis of IDDM.

221 primary role of CB4 in the precipitation of IDDM is to damage tissue, causing release and presentati

222 ells and had no effect on the progression of IDDM.

223 n has distinct effects on the progression of IDDM.

224 uired for the development and progression of IDDM.

225 Analysis of the reactivity of IDDM sera with the different regions of the intracellula

226 ta cell mass, and alleviates the severity of IDDM in acutely diabetic NOD mice.

227 activation by NAC attenuated the severity of IDDM.

228 iolar vasodilation during the early stage of IDDM, changes that likely contribute to the etiology of

229 eated at early or late preclinical stages of IDDM.

230 NKT cells between individuals, our study of IDDM patients and healthy controls, including discordant

231 elected MT1-MMP inhibitors in the therapy of IDDM in humans.

232 Investigation of the treatment of IDDM is hindered by the lack of a reproducible and easil

233 significantly affected by 5 or more years of IDDM.

234 ecture and is affected by 5 or more years of IDDM.

235 ropathy (DSP) in a cohort of childhood-onset IDDM patients.

236 prevented progression of insulitis and overt IDDM in NOD mice exhibiting extensive beta cell autoimmu

237 nsulitis and subsequent development of overt IDDM.

238 iabetic (NOD) mice and in turn prevent overt IDDM at different preclinical stages of disease developm

239 effectively suppresses progression to overt IDDM, requires the production of IL-4, and is dependent

240 lowing the viral insult clearly precipitates IDDM.

241 LCMV viral ("self") protein did not prevent IDDM, because no such regulatory cells were induced.

242 ing GAD65-IgGFc and IL-4, however, prevented IDDM.

243 cell function for the purpose of preventing IDDM even at a late stage of disease development.

244 ell responses to a Th2 phenotype, preventing IDDM.

245 B chain by a variety of strategies prevents IDDM in NOD mice.

246 ween polymorphic DNA markers and 15 putative IDDM susceptibility loci, designated IDDM1-IDDM15.

247 F1 female recipients of NOD marrow remained IDDM free; in contrast, all of the NOD recipients became

248 le or no support was found for most reported IDDM loci (lods were less than 1), despite larger sample

249 n insulin levels, LpL, and CET that resemble IDDM patients treated with conventional subcutaneous ins

250 r (WF x DP-BB)F1 animals develop spontaneous IDDM.

251 Three monkeys with spontaneous IDDM (two Macaca fascicularis and one Ceropithecus aethi

252 additional control macaques with spontaneous IDDM received the immunosuppressive protocol without isl

253 the ability of PDL cells from long-standing IDDM patients to form mineralized tissue and to determin

254 tic (DM) corneas including both type 1 (T1DM/IDDM) and type 2 (T2DM/NIDDM) diabetes.

255 These data indicate that IDDM and likely other autoimmune diseases are caused by

256 using RIP LCMV perforin-deficient mice, that IDDM does not occur in the absence of perforin.

257 In this study, we show that IDDM development is greatly accelerated in a stock of NO

258 ll lines and PBL, the protein encoded by the IDDM-protective allele HLA-DQA1*0102/DQB1*0602 was the m

259 ibody-negative first-degree relatives of the IDDM subjects, and in 28 autoantibody-negative control s

260 Structural studies of the IDDM-susceptible allele, HLA-DQA1*0301/DQB1*0302, have c

261 of this Th2 cytokine does not represent the IDDM protective immunoregulatory process mediated by H2-

262 er (Lt) mouse strain, closely related to the IDDM-prone nonobese diabetic (NOD)/Lt strain, demonstrat

263 in monocytic IL-1 beta secretion within the IDDM patients.

264 Thirty-three IDDM sera that immunoprecipitated full-length IA-2 were

265 To initially test whether they contribute to IDDM as APC, NOD B lymphocytes were transferred into NOD

266 Hence, B lymphocytes appear to contribute to IDDM in NOD mice as APC with a preferential ability to p

267 ly normal allelic variants may contribute to IDDM in NOD mice, the search for Idd genes in humans sho

268 nt in prediabetic NOD mice and contribute to IDDM.

269 may initiate a sequence of events leading to IDDM.

270 es 4 and 13 that show significant linkage to IDDM expression and insulitis.

271 ance, not seen in animals not predisposed to IDDM.

272 These results suggest that a true IDDM susceptibility locus (designated IDDM12) is located

273 266, 509-528, and 524-543), to our "in vitro IDDM" (ivIDDM) model.

274 can improve HbA1c values in adolescents with IDDM without overt toxic effects, but they raise questio

275 maintaining glycemic control in adults with IDDM.

276 iabetes in adolescents and young adults with IDDM.

277 ay in which the HLA-DQ genes associated with IDDM bias the immunologic repertoire toward autoimmune s

278 beta cell apoptosis has been associated with IDDM onset in both animal models and newly diagnosed dia

279 -DR53 (p < or = 0.001) were associated with IDDM.

280 capacity to secrete IL-4 is correlated with IDDM.

281 nonobese diabetic (NOD) mice and humans with IDDM are both reported to express severe deficiencies in

282 ased methodology to test whether humans with IDDM have associated NKT cell defects.

283 times more common in infants of mothers with IDDM than in infants born to nondiabetic mothers.

284 2-23.06) and 4.27 (1.24-14.46), but not with IDDM.

285 53 patients with IDDM (26 male, 27 female) with a median age of 16.1 year

286 A convenience sample of patients with IDDM and complications not seeking transplants were enro

287 Patients with IDDM and renal dysfunction who received either SPK or KT

288 Diabetic women and patients with IDDM appear to have greater risk of cardiac death than o

289 transplantation for nonuremic patients with IDDM has been controversial because of the less favorabl

290 hortened TRF length of WBCs of patients with IDDM likely reflects a marked reduction in the TRF lengt

291 PDL cells were isolated from 4 patients with IDDM treated with insulin for at least 5 years and from

292 e, the TRF length from WBCs of patients with IDDM was significantly shorter than that of nondiabetic

293 om 234 white men comprising 54 patients with IDDM, 74 patients with NIDDM, and 106 control subjects.

294 ngth of telomeres of WBCs from patients with IDDM, we tested the concept that telomeres might play a

295 on the TRF length of WBCs from patients with IDDM.

296 he mealtime treatment of 1,008 patients with IDDM.

297 with insulin therapy in young patients with IDDM.

298 ength and retain their ability to react with IDDM sera.

299 Among those with IDDM, adjusted AIT rates were higher than expected for b

300 om 8 diabetic donors (aged 43-66 years, with IDDM for 2-17 years) and 12 eyes from 6 normal donors (a