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Diabetes Eye

For the Good of Neural Tissues and Pancreatic Islets

While organs can be transplanted from deceased donors, tissues from the nervous system rapidly lose viability. The mechanisms of neuronal death, and the potential for reversing it, remain poorly defined. Dr. Fatima Abbas, a DRC-funded investigator at the University of Utah, in collaboration with Dr. Frans Vinberg (University of Utah) and Dr. Anne Hanneken (The Scripps Research Institute, La Jolla, CA), published a paper in Nature that questions the irreversibility of neuronal cell death in the retina, an investigation that has implications for visual rehabilitation and for the future of organ transplantation. In the study, the researchers characterized neuronal death and survival and identified conditions for reviving neuronal functioning in postmortem mice and human retinas. This study is a step toward better strategies for preserving the viability and engraftment capability of tissues and cells isolated from organ donors for transplantation, including the pancreas. Given the significant overlap of genes and proteins between pancreatic islet cells and neural tissues, the findings by Abbas and colleagues may have important implications for the improvement of islet cell transplant engraftment and long-term function in type 1diabetics.

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
zhang
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Melanie
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha