ライフサイエンスコーパス: type 1 diabetes

1 Childhood-onset type 1 diabetes.

2 the skin of pigs with experimentally induced type 1 diabetes.

3 egies to limit or prevent the development of type 1 diabetes.

4 on with a strong agonist insulin mimetope in type 1 diabetes.

5 eting cellular calcium homeostasis to combat type 1 diabetes.

6 imize the effect of immune interventions for type 1 diabetes.

7 antibody-positive relatives of patients with type 1 diabetes.

8 TCRs from the iNKT repertoire of people with type 1 diabetes.

9 n with high or low genetic susceptibility to type 1 diabetes.

10 nt in children at increased genetic risk for type 1 diabetes.

11 changed the routine management of autoimmune type 1 diabetes.

12 inflammation, leading to beta cell death in type 1 diabetes.

13 tion with insulin treatment in patients with type 1 diabetes.

14 oimmune comorbidity, such as thyroiditis and type 1 diabetes.

15 major effector cell population in autoimmune type 1 diabetes.

16 s maintain normoglycemia in a mouse model of type 1 diabetes.

17 his isotype, from spontaneous development of type 1 diabetes.

18 ologic approaches to glycemic management for type 1 diabetes.

19 ong-term goal of limiting the progression of type 1 diabetes.

20 es (START) trial of ATG therapy in new-onset type 1 diabetes.

21 eas tissues, which holds great potential for type 1 diabetes.

22 on with a strong agonist insulin mimetope in type 1 diabetes.

23 MH of rats with streptozotocin (STZ)-induced type 1 diabetes.

24 his hypothesis using the NOD murine model of type 1 diabetes.

25 th cardiovascular events in individuals with type 1 diabetes.

26 clinically approved JAK1/JAK2 inhibitors for type 1 diabetes.

27 g recurrent life-threatening hypoglycemia in type 1 diabetes.

28 effective and convenient self-management of type 1 diabetes.

29 nsition to young adulthood for patients with type 1 diabetes.

30 re the physical response to blood glucose in type 1 diabetes.

31 lin in patients with inadequately controlled type 1 diabetes.

32 slet-infiltrating T cells from patients with type 1 diabetes.

33 mproved by initiation of CSII in adults with type 1 diabetes.

34 nic mechanisms underlying the development of type 1 diabetes.

35 ement, and follow-up of AKI in children with type 1 diabetes.

36 rapies aiming to restore immune tolerance in type 1 diabetes.

37 ates for determining susceptibility to human type 1 diabetes.

38 control in adolescents and young adults with type 1 diabetes.

39 ms underlying pancreatic beta-cell demise in type 1 diabetes.

40 cell metabolism in the progression of human type 1 diabetes.

41 be explored as a cytoprotective strategy in type 1 diabetes.

42 e neuropathic abnormalities in patients with type 1 diabetes.

43 1 diabetes and at least 1 family member with type 1 diabetes.

44 was more similar to type 2 diabetes than to type 1 diabetes.

45 rol in patients with inadequately controlled type 1 diabetes.

46 children, adolescents, and young adults with type 1 diabetes.

47 for antigen specific immunotherapy (ASI) of type 1 diabetes.

48 tylated in OVE26 mice, a transgenic model of type 1 diabetes.

49 During follow-up, 1999 children developed type 1 diabetes.

50 children, adolescents, and young adults with type 1 diabetes.

51 A total of 11,245 youths with type 1 diabetes (0 to 19 years of age) and 2846 with typ

52 ted Kingdom, case-control study of childhood type 1 diabetes (1993-1994) in order to examine 4 exposu

53 An analysis of children whose parent had type 1 diabetes (210 events) yielded an adjusted HR of 0

54 In a mouse model of streptozotocin-induced type 1 diabetes, (52)Mn(2+) uptake in the pancreas was d

55 hite non-Hispanic; 57.6% with a sibling with type 1 diabetes), 550 completed the trial including 389

56 Among patients with type 1 diabetes, absolute changes during the study perio

57 In most patients with type 1 diabetes, adequate glycemic control is not achiev

58 ritis (adjusted OR = 1.7; 95% CI = 1.5-1.9), type 1 diabetes (adjusted OR = 1.6; 95% CI = 1.3-2.0), a

59 ults highlight the difficulty of identifying type 1 diabetes after age 30 years because of the increa

60 T cells from subjects with type 1 diabetes also exhibited lower intracellular ATP l

61 rinsic mitochondrial dysfunction observed in type 1 diabetes alters mitochondrial ATP and IFNgamma pr

62 We followed up 36 258 patients with type 1 diabetes and 179 980 controls between Jan 1, 2001

63 749 (2%) individuals with type 1 diabetes and 2882 (2%) controls were diagnosed wi

64 5052 white [69.9%]), 64.9% of patients with type 1 diabetes and 42.2% of patients with type 2 diabet

65 1), 37.0% were black (n = 54), and 18.5% had type 1 diabetes and a mean (SD) hemoglobin A1C level of

66 iNKT repertoire of people with recent onset type 1 diabetes and age- and gender-matched healthy cont

67 0 infants with HLA-defined predisposition to type 1 diabetes and at least 1 family member with type 1

68 Among patients with type 1 diabetes and at least 1 risk factor for hypoglyce

69 owledge, the independent association between type 1 diabetes and atrial fibrillation has not been stu

70 in a region harboring a previously reported type 1 diabetes and autoimmune disorder locus.

71 while members of the B species were found in type 1 diabetes and cardiomyopathy.

72 ibility complex protein associated with both type 1 diabetes and celiac disease.

73 fatal outcomes were similar in patients with type 1 diabetes and controls, whereas patients with type

74 Children aged 18 years or younger with type 1 diabetes and DKA and with complete medical record

75 In patients with both type 1 diabetes and end-stage renal disease, SPK recipie

76 we recruited adults (aged >/=18 years) with type 1 diabetes and HbA1c below 7.5% from Addenbrooke's

77 living conditions for 4 weeks in adults with type 1 diabetes and HbA1c below 7.5% is safe and well to

78 ory CD4(+) T cell subsets from patients with type 1 diabetes and healthy donors, that patients have s

79 e 1, 2016 that included 161 individuals with type 1 diabetes and hemoglobin A1c (HbA1c) of at least 7

80 encing diabetic kidney disease in those with type 1 diabetes and highlight some key pathways that may

81 during hypoglycemia between 1) patients with type 1 diabetes and IAH, 2) patients with type 1 diabete

82 increased lactate oxidation in patients with type 1 diabetes and IAH.

83 of hypoglycemia (NAH), and 10 patients with type 1 diabetes and impaired awareness (IAH) to test whe

84 r of transcription (STAT) 1 pathway in human type 1 diabetes and in mouse models, especially in beta-

85 of subsequent hypoglycemia in patients with type 1 diabetes and NAH, but does not in patients with I

86 in 11 healthy participants, 10 patients with type 1 diabetes and normal awareness of hypoglycemia (NA

87 a randomized crossover trial, patients with type 1 diabetes and normal awareness of hypoglycemia (NA

88 th type 1 diabetes and IAH, 2) patients with type 1 diabetes and normal awareness of hypoglycemia, an

89 of NT-ES-beta-cells for cell replacement for type 1 diabetes and provide proof of principle for thera

90 t transplantation is an effective therapy in type 1 diabetes and recalcitrant hypoglycemia.

91 larly difficult for both the individual with type 1 diabetes and the health-care provider.

92 istent hypertension in three mouse models of type 1 diabetes and two models of type 2 diabetes by ade

93 After excluding patients with type 1 diabetes and ungradable fundus images, 361 partic

94 Cases of post-polio syndrome, type 1 diabetes, and chronic cardiomyopathy were investi

95 Pregnant women with type 1 diabetes are a high-risk population who are recom

96 ycaemic control in adults with long-standing type 1 diabetes as suggested by current guidelines, but

97 We genetically defined type 1 diabetes as the additional cases of diabetes that

98 cy as it occurs in the pathological state of type-1 diabetes as well as during islet transplantation.

99 ion factor 19 (TCF19) has been reported as a type 1 diabetes-associated locus involved in maintenance

100 ntima-media thickness (cIMT), in adults with type 1 diabetes at increased risk for cardiovascular dis

101 8,676 children at increased genetic risk of type 1 diabetes at six sites in the U.S. and Europe.

102 trol Among Adolescents and Young Adults With Type 1 Diabetes (BE IN CONTROL) study was an investigato

103 We screened 4407 adolescents with type 1 diabetes between the ages of 10 and 16 years of a

104 tation is a promising clinical treatment for type 1 diabetes, but success is limited by extensive bet

105 ove metabolic control in young patients with type 1 diabetes, but the association with short-term dia

106 fferent autoimmune diseases, including human type 1 diabetes, but their relationship to changes in th

107 ement and improve glycaemia in patients with type 1 diabetes, but whether it has cardiovascular benef

108 Failure to diagnose late-onset type 1 diabetes can have serious consequences because th

109 variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross

110 The pathogenesis of human type 1 diabetes, characterized by immune-mediated damage

111 cally investigated pleiotropy between PD and type 1 diabetes, Crohn disease, ulcerative colitis, rheu

112 Among adolescents and young adults with type 1 diabetes, daily financial incentives improved glu

113 Type 1 diabetes development in the NOD mouse model is wi

114 31-60 years, the clinical characteristics of type 1 diabetes differed from those of type 2 diabetes:

115 The majority of individuals with type 1 diabetes do not meet recommended glycemic targets

116 The inability to manage type 1 diabetes effectively during these years is associ

117 eutics used to treat other diseases to treat type 1 diabetes, especially when there is evidence for o

118 ent cohorts, that T cells from patients with type 1 diabetes exhibited mitochondrial inner-membrane h

119 In patients who have had type 1 diabetes for 5 years, current recommendations reg

120 al, we recruited women aged 18-40 years with type 1 diabetes for a minimum of 12 months who were rece

121 most promising alternatives to allograft in type 1 diabetes for addressing organ shortage.

122 te persons aged 8 years or older who had had type 1 diabetes for at least 2 years and had an HbA1c le

123 In this cross-sectional analysis, we used a type 1 diabetes genetic risk score based on 29 common va

124 non-HLA gene polymorphisms identified by the Type 1 Diabetes Genetics Consortium (T1DGC).

125 Patients with type 1 diabetes had roughly 40% greater reduction in car

126 ies have shown is beneficial for adults with type 1 diabetes, has not been well-evaluated in those wi

127 Individuals with celiac disease or type 1 diabetes have been reported to have high titers o

128 18-75 years and had inadequately controlled type 1 diabetes (HbA1c between >/=7.7% and </=11.0% [>/=

129 ts (aged 14-20) with suboptimally controlled type 1 diabetes (hemoglobin A1c [HbA1c] >8.0%) were recr

130 omics data set discerning the development of type 1 diabetes in a non-obese diabetic mouse model.

131 termine whether oral insulin delays onset of type 1 diabetes in autoantibody-positive relatives of pa

132 iation between early exposure to animals and type 1 diabetes in childhood is not clear.

133 f life is associated with the development of type 1 diabetes in childhood.

134 ciation between exposure to dogs and risk of type 1 diabetes in childhood.

135 ard ratio [HR], 1.00; 95% CI, 0.86-1.16) and type 1 diabetes in childhood.

136 between fGAD65 and tGAD65 autoantibodies for type 1 diabetes in relation to HLA-DQ.

137 betes to provide valuable insights for human type 1 diabetes in terms of pancreatic histopathology, i

138 randomised controlled trial, 75 adults with type 1 diabetes in the CGM group of the DIAMOND trial we

139 Type 1 diabetes in the nonobese diabetic mouse stems fro

140 ctive case-control study of individuals with type 1 diabetes in the Swedish National Diabetes Registr

141 rall unadjusted estimated incidence rates of type 1 diabetes increased by 1.4% annually (from 19.5 ca

142 e risk of atrial fibrillation in people with type 1 diabetes increased with renal complications and p

143 k of atrial fibrillation in individuals with type 1 diabetes increased with worsening glycaemic contr

144 Among young patients with type 1 diabetes, insulin pump therapy, compared with ins

145 Type 1 diabetes is a challenging condition to manage for

146 Type 1 diabetes is a T cell-mediated autoimmune disease

147 Type 1 diabetes is associated with an increased risk of

148 Use of CGM during pregnancy in patients with type 1 diabetes is associated with improved neonatal out

149 Type 1 diabetes is characterized by the loss of insulin

150 plantation of pancreatic islets for treating type 1 diabetes is restricted to patients with critical

151 Type 1 diabetes is typically considered a disease of chi

152 associated with incident CVD in people with type 1 diabetes is unknown.

153 Genetic susceptibility to young-onset type 1 diabetes is well defined and does not predispose

154 Hypoglycemia, common in patients with type 1 diabetes, is a major barrier to achieving good gl

155 notransplantation is a promising therapy for type 1 diabetes, its clinical application has been hampe

156 rhesus factor), while incorporating previous type 1 diabetes knowledge.

157 own how frequently genetic susceptibility to type 1 diabetes leads to a diagnosis of diabetes after a

158 sent 10-11% of patients with newly diagnosed type 1 diabetes <18 years of age, tGADA analysis should

159 issue to boost Tr1 cells may be important in type 1 diabetes management.

160 of available distal technologies to improve type 1 diabetes management.

161 We conclude that preventing HAAF in type 1 diabetes may require the recruitment of both anti

162 abolic imbalance in chronic diseases such as type-1 diabetes may lead to detectable perturbations in

163 Of 2018 participants, 1746 had type 1 diabetes (mean age, 17.9 years [SD, 4.1]; 1327 no

164 Among 5453 youths with type 1 diabetes (median age at initial diagnosis, 11 yea

165 393 patients with DG (37.7% male; 9.9% with type 1 diabetes; median age, 58.2 years [range 20-76]; m

166 ellitus, to compare DR rates for youths with type 1 diabetes mellitus (T1DM) and those with T2DM, and

167 Individuals with type 1 diabetes mellitus (T1DM) have a high risk of card

168 Type 1 diabetes mellitus (T1DM) results from an autoimmu

169 ensive glycemic control improves outcomes in type 1 diabetes mellitus (T1DM), iatrogenic hypoglycemia

170 es in pancreatic elasticity in children with type 1 diabetes mellitus (T1DM).

171 ices were tested in each of 12 patients with type 1 diabetes mellitus in a clinical set-up for 12h.

172 Type 1 diabetes mellitus is a chronic autoimmune disease

173 -mediated beta-cell dysfunction and death in type 1 diabetes mellitus, although the mechanisms are in

174 s for an improved treatment of patients with type 1 diabetes mellitus.

175 promising target for beta-cell protection in type 1 diabetes mellitus.

176 n and glucose homeostasis in both type 2 and type 1 diabetes mouse models.

177 Patients with type 1 diabetes (n = 49) were included-11 with severe po

178 could help to distinguish LADA (n = 50) from type 1 diabetes (n = 50) and type 2 diabetes (n = 50).

179 hildren and adolescents with newly diagnosed type 1 diabetes (n = 654) and healthy control subjects (

180 Adults aged 40 years and older with type 1 diabetes of at least 5 years' duration and at lea

181 We recently reported that insulitis in type 1 diabetes of mice and humans is preceded by intrai

182 not been extensively studied in persons with type 1 diabetes or type 2 diabetes.

183 antibody-positive relatives of patients with type 1 diabetes, oral insulin at a dose of 7.5 mg/d, com

184 did not delay or prevent the development of type 1 diabetes over 2.7 years.

185 replacement to be applied as a treatment for type 1 diabetes, oxygen and nutrient delivery to beta ce

186 In human type 1 diabetes pancreatic islets, fasting conditions re

187 Numerous aspects of human type 1 diabetes pathogenesis are recapitulated in the LE

188 ex vivo human cell assays, using PBMCs from type 1 diabetes patients, had significant improvements i

189 porter is also a major self-antigen found in type 1 diabetes patients.

190 f blood glucose concentration in people with type 1 diabetes predisposes to hypoglycaemia.

191 ent analysis, LADA patients overlapping with type 1 diabetes progressed faster to insulin therapy tha

192 Among adolescents with type 1 diabetes, rapid increases in albumin excretion du

193 nd type 2 diabetic rats but not in rats with type 1 diabetes receiving insulin supplementation that d

194 for infants with genetic susceptibility for type 1 diabetes reduced the cumulative incidence of diab

195 ion reduced the cytotoxicity of human-origin type 1 diabetes-relevant autoreactive CD8(+) T cells.

196 nse to establish durable immune tolerance in type 1 diabetes remains a substantial challenge.

197 Type 1 diabetes requires intensive self-management to av

198 Type 1 diabetes requires major lifestyle changes and car

199 o investigate the frequency and phenotype of type 1 diabetes resulting from high genetic susceptibili

200 Type 1 diabetes results from chronic autoimmune destruct

201 INTERPRETATION: Genetic susceptibility to type 1 diabetes results in non-obesity-related, insulin-

202 posed children) also was not associated with type 1 diabetes risk.

203 ernative to insulin monotherapy for treating type 1 diabetes since deletion or inhibition of GcgRs co

204 seen in the Study of Thymoglobulin to arrest Type 1 Diabetes (START) trial of ATG therapy in new-onse

205 cells were present at higher frequencies in type 1 diabetes subjects compared with those in healthy

206 th 12 months postislet transplantation in 10 type 1 diabetes subjects referred with severe hypoglycem

207 uce hypoglycemia and glycemic variability in type 1 diabetes subjects with severe hypoglycemia.

208 ions are suspected environmental triggers of type 1 diabetes (T1D) and macrophage antiviral responses

209 pecimens from six subjects with recent-onset type 1 diabetes (T1D) and six nondiabetic matched contro

210 We investigate subgroups of individuals with type 1 diabetes (T1D) defined by autoantibody positivity

211 B lymphocytes play a key role in type 1 diabetes (T1D) development by serving as a subset

212 Type 1 diabetes (T1D) has a strong genetic component.

213 ose (hyper- or hypoglycemia) associated with type 1 diabetes (T1D) has been linked to cognitive defic

214 and cause selective beta cell destruction in type 1 diabetes (T1D) has focused on peptides originatin

215 Events defining the progression to human type 1 diabetes (T1D) have remained elusive owing to the

216 selective S1PR1 agonist, CYM-5442, prevented type 1 diabetes (T1D) in the mouse Rip-LCMV T1D model.

217 A logical cure for type 1 diabetes (T1D) involves replacing the lost insuli

218 Type 1 diabetes (T1D) is a chronic autoimmune disease th

219 Type 1 diabetes (T1D) is an autoimmune disease leading t

220 Type 1 diabetes (T1D) is an autoimmune disease that resu

221 Type 1 diabetes (T1D) is characterized by the autoimmune

222 The incidence of type 1 diabetes (T1D) is increasing globally.

223 Although type 1 diabetes (T1D) is primarily perceived as a T cell

224 Autoimmune type 1 diabetes (T1D) is thought to be caused by a defec

225 Type 1 diabetes (T1D) manifests when the insulin-produci

226 -risk children prospectively followed up for type 1 diabetes (T1D) or CD.

227 Poor glycemic control in Type 1 Diabetes (T1D) patients is strongly associated wi

228 7 (encoded by Tnfrsf9) deficiency suppressed type 1 diabetes (T1D) progression in NOD mice.

229 Type 1 diabetes (T1D) results from T cell-mediated destr

230 Type 1 diabetes (T1D) results from the autoimmune destru

231 autoantibodies and continue to contribute to type 1 diabetes (T1D) risk among autoantibody-positive c

232 Although over 40 type 1 diabetes (T1D) risk loci have been mapped in huma

233 eactive T cells found in peripheral blood of type 1 diabetes (T1D) subjects is unclear, partly becaus

234 Insulin replacement is the cornerstone of type 1 diabetes (T1D) treatment; however, glycemic contr

235 rgan-specific autoimmune diseases, including type 1 diabetes (T1D), are intracellular membrane protei

236 more prevalent in type 2 diabetes (T2D) than type 1 diabetes (T1D), but the mortality risk is higher

237 lar metabolomic perturbations to humans with type 1 diabetes (T1D), we analyzed serum metabolomic pro

238 Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg(+) TRMs formed

239 ncy, and in mouse models of pancreatitis and type 1 diabetes (T1D).

240 are ultimate goals for the complete cure of type 1 diabetes (T1D).

241 MDA5, correlate with the risk of developing type 1 diabetes (T1D).

242 higher blood pressure (BP) in patients with type 1 diabetes (T1D).

243 believed to contribute to beta-cell death in type 1 diabetes (T1D).

244 esents a central objective for prevention of type 1 diabetes (T1D).

245 se effect of insulin therapy for people with type 1 diabetes (T1D).

246 ment of autoimmunity in children at risk for type 1 diabetes (T1D).

247 tolerance in autoimmune diseases, including type 1 diabetes (T1D).

248 s associated with a high risk for developing type 1 diabetes (T1D).

249 e populations isolated from 81 subjects with type 1 diabetes (T1D).

250 ransgenic mice or AD transgenic animals with type 1 diabetes (T1D).

251 reactive T cell responses ultimately causing type 1 diabetes (T1D).

252 ty are early features in the pathogenesis of type 1 diabetes (T1D).

253 naive nonobese diabetic (NOD) mice [model of type 1 diabetes (T1D)] by transfer of CD4(+) T cells.

254 Zinc (Zn(2+)) is involved in both type 1 diabetes (T1DM) and type 2 diabetes (T2DM).

255 There is yet no cure for type 1 diabetes (T1DM) so far.

256 People with type 1 diabetes tend to be at least as inactive as the g

257 GADA had a higher diagnostic sensitivity for type 1 diabetes than both fGADA and RSRGADA.

258 (tGAD65) autoantibodies may better delineate type 1 diabetes than full-length GAD65 (fGAD65) autoanti

259 pulation with high genetic susceptibility to type 1 diabetes than in the half of the population with

260 Also similar to human type 1 diabetes, the canonical canine disorder appears t

261 impaired awareness of hypoglycemia (IAH) in type 1 diabetes, the capacity to transport lactate into

262 ucagon activity is blocked in the setting of type 1 diabetes, the plasma ghrelin level rises, prevent

263 r initial diabetes diagnosis for youths with type 1 diabetes; the American Diabetes Association recom

264 m cells (NT-ESs) derived from a patient with type 1 diabetes to differentiate into beta-cells and pro

265 mine the effectiveness of CGM in adults with type 1 diabetes treated with insulin injections.

266 Type 1 diabetes treated with insulin pump therapy or wit

267 Among patients with inadequately controlled type 1 diabetes treated with multiple daily insulin inje

268 continuous glucose monitoring in adults with type 1 diabetes treated with multiple daily insulin inje

269 The proportions of type 1 diabetes, types 2 diabetes, and other types of di

270 investigated MHC-II-mediated protection from type 1 diabetes using a previously reported NOD mouse li

271 aily injections (MDI) to CSII in adults with type 1 diabetes using CGM.

272 ous insulin infusion; CSII) in patients with type 1 diabetes using continuous glucose monitoring (CGM

273 should be offered to all pregnant women with type 1 diabetes using intensive insulin therapy.

274 ried along a C-peptide-driven continuum from type 1 diabetes via LADA to type 2 diabetes.

275 relative annual increase in the incidence of type 1 diabetes was 1.8% (P<0.001) and that of type 2 di

276 %) were girls; mean (SD) age at diagnosis of type 1 diabetes was 5.1 (2.6) years.

277 , this bias in the clonal iNKT repertoire in type 1 diabetes was associated with increased GM-CSF, IL

278 Type 1 diabetes was identified using diagnosis codes fro

279 ived measures of dog exposure with childhood type 1 diabetes was identified.

280 the risk of atrial fibrillation in men with type 1 diabetes was slightly raised, whereas for female

281 In recipients with type 1 diabetes, we aimed to determine whether long-term

282 nic DO11.10 x RIPmOVA (DORmO) mouse model of type 1 diabetes, we asked whether autoimmune insulitis w

283 purified serum antibodies from patients with type 1 diabetes, we detected human ZnT8A bound to live I

284 These genetically defined cases of type 1 diabetes were distributed across all ages of diag

285 ceptibility genotypes for celiac disease and type 1 diabetes were followed up for up to 20 years for

286 characteristics of the group diagnosed with type 1 diabetes when aged 30 years or younger.

287 characteristics of the group diagnosed with type 1 diabetes when aged 31-60 years were similar to th

288 was poor at reversing glycemia in a model of type 1 diabetes, whereas 1F11 induced early and prolonge

289 etinoid metabolism in the eye is impaired in type 1 diabetes, which leads to deficient generation of

290 nt and repertoire generation are abnormal in type 1 diabetes, which suggest that short CDR3s increase

291 on exercise management for individuals with type 1 diabetes who exercise regularly, including glucos

292 er than 9.7% (<83 mmol/mol) or in women with type 1 diabetes who had HbA1c lower than 8.8% (<73 mmol/

293 of atrial fibrillation was noted in men with type 1 diabetes who had HbA1c lower than 9.7% (<83 mmol/

294 Among adults with type 1 diabetes who used multiple daily insulin injectio

295 n glycaemia and hypoglycaemia in adults with type 1 diabetes who were living at home and participatin

296 Among patients with type 1 diabetes who were receiving insulin, the proporti

297 ide, we randomly assigned 1402 patients with type 1 diabetes who were receiving treatment with any in

298 United States that included 158 adults with type 1 diabetes who were using multiple daily insulin in

299 atic islets of three young organ donors with type 1 diabetes with a short disease duration with high-

300 Patients with type 1 diabetes younger than 20 years and diabetes durat