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2,348 results for “type 1 diabetes”
Effect of Advanced Hybrid Closed Loop System, MiniMed 780G in Newly Diagnosed Children and Adolescents With Type 1 Diabetes on Glycemic Control and Patient Reported Outcomes Compared to Standard Insul
ClinicalTrials.gov study NCT06919029. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
The Effect of Uric Acid Lowering in Type 1 Diabetes
ClinicalTrials.gov study NCT02344602. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Impact of COVID-19 lockdown on glycemic control in adults with type 1 diabetes mellitus: information and standardized questions regarding follow-up during lockdown
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Supplement to: Hippocampal neurochemical profile and glucose transport kinetics in patients with type 1 diabetes
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Data analysis on the healthcare personnel engaged in type 2 diabetes treatments and their communication activities as part of Co-exploration Activity 1
<p>This analysis compared the findings from two health-service guidelines and the feedback from the health professionals who participated in Co-design Activity 1 to delineate patient journeys through type 2 diabetes treatments. The patent journeys described the healthcare personnel (health professionals and auxiliary staff) engaged in the treatments, communication activities, and the relevant health contents they commonly deliver to diabetic patients.</p>
Type 1 diabetes adolescent transition study
<p><b>Objectives:</b> Adolescents with type 1 diabetes experience dramatic excursions in blood sugars as they transition to adult care. Trials on single interventions have struggled to demonstrate lasting improvements in clinical outcomes. Thus, the purpose of this study was to evaluate the effect of a multi-component intervention on glycemic control, clinic attendance, and diabetes distress amongst adolescents with type 1 diabetes transitioning to adult health services.</p> <p><b>Design:</b> Prospective controlled quasi-experimental study.</p> <p><b>Setting:</b> Adolescents with type 1 diabetes from an urban academic pediatric hospital (control group) and a community regional hospital (intervention group) were recruited and followed for 1 year after their last pediatric diabetes visit.</p> <p><b>Participants: </b>101 adolescents with type 1 diabetes transitioning to adult care, including 68 from the control group and 33 from the intervention group.</p> <p><b>Interventions:</b> The intervention group had access to (1) a diabetes nurse transition coordinator, (2) joint pediatric-adult diabetes clinic visits, and (3) pediatric and adult clinics being in the same building. Those in the control group were referred to an adult diabetes provider at their last pediatric diabetes visit without any formal transition program or additional supports.</p> <p><b>Primary and secondary outcome measures: </b>The primary outcome was longitudinal change in A1C. The secondary outcomes were number of A1C tests obtained, number of adult diabetes visits attended, time gap between pediatric and adult visits, and diabetes distress.</p> <p><b>Results:</b> There was a difference in A1C trajectory between the control and intervention groups (base model p=0.004, adjusted model p=0.003). A1C continued to rise in the control group after the transition to adult care, whereas A1C decreased in the intervention group. However, there were no statistically significant differences in the secondary outcomes between the two groups.</p> <p><b>Conclusion:</b> A multi-component intervention can mitigate the glycemic excursions experienced by adolescents with type 1 diabetes transitioning to adult care.</p>
Data from: Childhood adiposity and type 1 diabetes: a Mendelian randomization study
BACKGROUND: The incidence of type 1 diabetes (T1D) is increasing globally. One hypothesis is that increasing childhood obesity rates may explain part of this increase, but, as T1D is rare, intervention studies are challenging to perform. The aim of this study was to assess this hypothesis with a Mendelian randomization approach that uses genetic variants as instrumental variables to test for causal associations. METHODS AND FINDINGS: We created a genetic instrument of 23 single nucleotide polymorphisms (SNPs) associated with childhood adiposity in children aged 2-10 years. Summary-level association results for these 23 SNPs with childhood-onset (<17 years) T1D were extracted from a meta-analysis of genome-wide association study with 5,913 T1D cases and 8,828 reference samples. Using inverse-variance weighted Mendelian randomization analysis, we found support for an effect of childhood adiposity on T1D risk (odds ratio 1.32, 95% CI 1.06-1.64 per standard deviation score in body mass index [SDS-BMI]). A sensitivity analysis provided evidence of horizontal pleiotropy bias (p = 0.04) diluting the estimates towards the null. We therefore applied Egger regression and multivariable Mendelian randomization methods to control for this type of bias and found evidence in support of a role of childhood adiposity in T1D (odds ratio in Egger regression, 2.76, 95% CI 1.40-5.44). Limitations of our study include that underlying genes and their mechanisms for most of the genetic variants included in the score are not known. Mendelian randomization requires large sample sizes, and power was limited to provide precise estimates. This research has been conducted using data from the Early Growth Genetics (EGG) Consortium, the Genetic Investigation of Anthropometric Traits (GIANT) Consortium, the Tobacco and Genetics (TAG) Consortium, and the Social Science Genetic Association Consortium (SSGAC), as well as meta-analysis results from a T1D genome-wide association study. CONCLUSIONS: This study provides genetic support for a link between childhood adiposity and T1D risk. Together with evidence from observational studies, our findings further emphasize the importance of measures to reduce the global epidemic of childhood obesity and encourage mechanistic studies.
Impact of chronic psychological stress on platelet membrane fatty acid composition in type 1 diabetes mellitus
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Type 1 Diabetes and Youth Sports in Sweden: A Field Experiment on Discrimination
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Detection of insulin in insulin-deficient islets of patients with type 1 diabetes_original microscopy images
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Figure 1 from: Mohammad JA, Almulathanon AAY, Fathi FH (2021) Assessment of the effects of metformin and glibenclamide on the concentration of selected trace elements in type 2 diabetic patients. Pharmacia 68(4): 845-849. https://doi.org/10.3897/pharmacia.68.e72080
Figure 1 Effects of metformin versus glibenclamide on serum concentrations of A) Cu, B) Zn, and C) Mg in type 2 diabetic patients.* indicates statistically significant differences compared to the control group (**p < 0.01; ***p < 0.001; ****p < 0.0001); # indicates statistically significant differences compared to the newly diagnosed group (#p < 0.05; ###p < 0.001); $ indicates statistically significant differences between the metformin and glibenclamide treated groups, as determined by the Kruskal-Wallis test followed by a Dunn's multiple comparisons post-hoc test.
Human adipose-derived mesenchymal stem cells prevent type 1 diabetes induced by immune checkpoint blockade
<p class="MsoNormal"><span><strong>Aims/hypothesis</strong></span></p> <p class="MsoNormal"><span> Immunomodulators blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) or programmed death-ligand 1 (PD-L1) have improved the treatment of a broad spectrum of cancers. These immune checkpoint inhibitors (ICIs) reactivate the immune system against tumour cells but can also trigger autoimmune side effects, including type 1 diabetes. Mesenchymal stem cell (MSC) therapy is the most prevalent cell therapy, with tissue-regenerating, anti-fibrosis and immunomodulatory functions provided by the secretome of the cells. Here, we examined whether systemic MSC treatment could prevent the development of type 1 diabetes in a NOD mouse model.</span></p> <p class="MsoNormal"><span><strong>Methods</strong> </span></p> <p class="MsoNormal"><span>The purified PD-L1 monoclonal antibody was administered to induce diabetes in male NOD mice which normally do not develop diabetes. Human adipose-derived MSCs were administered by tail vein injections. T cells, macrophages and monocyte-derived macrophages expressing C-X-C motif chemokine ligand 9 (CXCL9) in pancreatic sections of NOD mice and a cancer patient who developed diabetes following the ICI treatments were analysed by immunofluorescence. Tissue localisation of the injected MSCs, plasma exosome levels and plasma cytokine profiles were also investigated.</span></p> <p class="MsoNormal"><span><strong>Results</strong> </span></p> <p class="MsoNormal"><span>PD-1/PD-L1 blockade induced diabetes in 16 of 25 (64%) NOD mice which received anti-PD-L1 mAb without hMSCs [MSC(−)], whereas MSC administration decreased the incidence to four of 21 (19%) NOD mice which received anti-PD-L1 mAb and hMSCs [MSC(+)]. The PD-1/PD-L1 blockade significantly increased the area of CD3-positive T cells (6.2-fold) and Macrophage-2 (Mac-2) antigen (2.5-fold)- and CXCL9 (40.3-fold)-positive macrophages in the islets. MSCs significantly reduced T cell (45%) and CXCL9-positive macrophage (67%) accumulation in the islets and the occurrence of diabetes. The insulin content (1.9-fold) and islet beta cell area (2.7-fold) were also improved by MSCs. T cells and CXCL9-positive macrophages infiltrated into the intricate gaps between the beta cells in the islets by PD-1/PD-L1 blockade. Such immune cell infiltration was largely prevented by MSCs. The most striking difference was observed in the CXCL9-positive macrophages, which normally did not reside in the beta cell region in the islets but abundantly accumulated in this area after PD-1/PD-L1 blockade and were prevented by MSCs. The CXCL9-positive macrophages were also observed in the islets of a cancer patient who developed diabetes following the administration of ICIs but little was observed in a control patient. Mechanistically, the injected MSCs accumulated in the lung but not in the pancreas and strongly increased plasma exosome levels and changed plasma cytokine profiles.</span></p> <p class="MsoNormal"><span><strong>Conclusions/interpretation</strong></span></p> <p class="MsoNormal"><span> Our results suggest that MSCs can prevent the incidence of diabetes associated with immune checkpoint cancer therapy and may be worth further consideration for new adjuvant cell therapy.</span></p> <p class="MsoNormal"><span><strong>Data availability</strong> </span></p> <p class="MsoNormal"><span>All datasets were deposited to DOI https://doi.org/10.5061/dryad.xwdbrv1fh.</span></p>
Physical activity interventions and nutrition-based interventions for children and adolescents with type 1 diabetes mellitus
<p>1. Baseline characteristics of participants</p> <p>2. Description of studies</p> <p>3. Data extraction_Excel</p>
Figure 1 from: Almulathanon AAY, Mohammad JA, Allwash TA (2021) Evaluation the effects of insulin on oxidant/antioxidant status in type 1 diabetic patients. Pharmacia 68(3): 699-704. https://doi.org/10.3897/pharmacia.68.e70495
Figure 1 Effects of insulin on serum levels of A)MDA, B)CAT, C)GSH, vitamins C and E. The data are viewed as mean ± SD. (***p < 0.001; ****p < 0.0001) denotes statistically significant differences versus the control group; (##p < 0.01; ###p < 0.001) denotes statistically significant differences between insulin-treated and newly diagnosed patients, using the Kruskal-Wallis test followed by a Dunn's multiple comparison test.
Methylation haplotypes of the insulin gene promoter in children and adolescents with type 1 diabetes: could a dimensionality reduction approach predict the disease?
<p>The aim of the present study was to identify insulin gene promoter (IGP) methyl-haplotypes among children and adolescents with T1D and suggest a predictive model for the discrimination of cases and controls according to methyl-haplotypes. Fourty individuals (20 T1D) participated. IGP-region from peripheral whole blood DNA of 40 participants (20 T1D) was sequenced by next generation sequencing, sequences were read using FASTQ files, and methylation status was calculated by python-based pipeline for targeted deep bisulfite sequenced amplicons (ampliMethProfiler). Methylation profile at 10 CpG sites proximal to transcription start site of the IGP was recorded and coded as 0 for unmethylation or 1 for methylation. A single read could result in “1111111111” methyl-haplotype (all methylated), “000000000” methyl-haplotype (all unmethylated) or any other combination.</p>
Minimum dataset and R-script for analysis of inflammatory proteins associated with risk of Coronary Artery Disease in type 1 diabetes patients
<p>Data for CAD manuscript</p>
Clinical Trial on Ladarixin Adjunctive Therapy to Improve Glycemic Control in Type 1 Diabetes.
ClinicalTrials.gov study NCT05368402. IPD Sharing: NO. Countries: 1. Publications: 0.
A Learning Algorithm for MDI Individuals With Type 1 Diabetes to Adjust Recommendations for High Fat Meals and Exercise Management
ClinicalTrials.gov study NCT05041621. IPD Sharing: YES. Countries: 1. Publications: 0.
Impact of Metformin on Peripheral Arterial Calcification in Type 1 Diabetes
ClinicalTrials.gov study NCT04583462. IPD Sharing: YES. Countries: 1. Publications: 0.
Continuous Ketone Monitoring in People With Type 1 Diabetes Using SGLT2 Inhibitors
ClinicalTrials.gov study NCT06753994. IPD Sharing: YES. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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