Publications by authors named "Cameron Kos"

Tau protein is implicated in the pathogenesis of Alzheimer's disease (AD) and other tauopathies, but its physiological function is in debate. Mostly explored in the brain, tau is also expressed in the pancreas. We further explored the mechanism of tau's involvement in the regulation of glucose-stimulated insulin secretion (GSIS) in islet β-cells, and established a potential relationship between type 2 diabetes mellitus (T2DM) and AD.

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Aims: To establish pre-clinical proof of concept that sustained subcutaneous delivery of the secretome of human cardiac stem cells (CSCs) can be achieved in vivo to produce significant cardioreparative outcomes in the setting of myocardial infarction.

Methods And Results: Rats were subjected to permanent ligation of left anterior descending coronary artery and randomized to receive subcutaneous implantation of TheraCyte devices containing either culture media as control or 1 × 106 human W8B2+ CSCs, immediately following myocardial ischaemia. At 4 weeks following myocardial infarction, rats treated with W8B2+ CSCs encapsulated within the TheraCyte device showed preserved left ventricular ejection fraction.

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The presentation of islet antigens in the pancreatic LNs (PLNs) of mice is a developmentally regulated process. It has been hypothesized that, during physiological tissue remodeling, a wave of neonatal β-cell apoptosis may initiate diabetes in autoimmune-prone strains of mice. If true, increasing or decreasing physiological β-cell apoptosis in neonatal NOD mice should alter the time-course of antigen presentation in the PLNs.

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Article Synopsis
  • Bcl-xL is a protein that prevents cell death and plays a significant role in the survival of beta-cells, which are crucial for insulin production. The study focused on the effects of removing the Bcl-x gene in these cells.
  • Using various methods, researchers found that beta-cells without Bcl-xL were more susceptible to apoptosis (cell death) induced by low-dose streptozotocin (STZ) and other stressors, although some beta-cells still produced Bcl-xL but didn't offer any survival benefits.
  • The study concludes that while Bcl-xL is not necessary for the initial development of beta-cells, it is critical for their survival under stress, suggesting that
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