Our Research Members

Dr. Cafazzo leads the development of technologies as a way to keep people out of hospital by allowing for self-care at home for those with chronic conditions such as diabetes, asthma, end-stage renal disease and congestive heart failure.

These strategies are aimed at helping people before their conditions become acute and medical intervention is required. The emphasis here is improving patient self-efficacy.

One such solution is bant. Designed for adolescents with Type I diabities, bant simplifies diabetes management by connecting to a glucometer via Bluetooth. It also connects teens in a secure community of peers and helps them self-manage by rewarding positive behaviour every time they use their glucometer.

Main interests are mechanisms of neural synchrony and entrainment (epilepsy), hypoglycemic seizures, and neurodegenerative processes.
A) We have several projects on cellular mechanisms and local system dynamics of epilepsy, particularly the biophysics of the transition to seizure, and the role of electrotonic coupling via gap junctions. Molecular biological and cellular electrophysiological techniques are being used to measure the upregulation of gap junctions in several in vitro and in vivo seizure models.
B) Hypoglycemic seizures are a major problem in juveniles with diabetes. We are studying the pathophysiology of hypoglycaemic seizures in juvenile animals both in vitro and in vivo, noting that the most severe seizures seem to be associated with mainly subcortical seizure-like EEG activity, which could also be related to the ‘dead in bed’ or sudden unexplained death sometimes noted with juvenile hypoglycemic events. Also we are examining the pathophysiology of neuronal injury which is enhanced by glucose reperfusion. Glucose reperfusion is also associated with a significant upregulation of gap junctional expression, the significance of which remains to be elucidated. However is is known that provision of nutrients to neurons requires intact astrocytic gap junctional communication.

Current research interests in type 1 diabetes mellitus include the physiology of renal hyperfiltration in diabetic nephropathy, cardiorenal interactions and endothelial function, the effect of pharmaceutical agents on the urinary proteome, and functional gene polymorphisms in humans.

The overall theme of my research program is to enhance and support translation of Canadian diabetes and cardiovascular guidelines on nutrition therapy to reduce the risks of these diseases in all Canadians. I test the broadscale application of our recommended dietary patterns by designing digital adherence tools, while also challenging policy themes meant to support public adherence and exploring improvements to methodologies used in study designs to improve efficiency and the application of sex and gender-based analyses. A main research focus is on developing and testing strategies and tools using mobile health (mHealth) technologies to increase uptake of recognized dietary patterns to mitigate diabetes and CVD risk with implementation in clinical practice to show the impact of improving health service delivery. Pragmatic randomized controlled trials (RCTs) are used to explore the effect of collaboratively designed translational tools and changes to health service delivery, with adaptive design built-in based on user feedback to optimize delivery of effective and ready-to-use tools and strategies for broader implementation.

I am currently leading a CIHR-funded pragmatic trial of our Portfolio Diet Program (PortfolioDiet.app with integrated text messages and behaviour change curriculum) in 1,100 secondary and high-risk primary prevention adults (50% diabetes) in primary care. The primary outcome at 1-year is proportion achieving a ≥8% reduction in LDL-C or non-HDL-C (lower limit of efficacy of drugs as add-on therapy) and major adverse cardiovascular event at 7-year. Another project underway is an assessment of the Portfolio Diet Program for knowledge translation and mobilization in high-risk communities in the Peel region for the prevention and management of diabetes. My particular interest in mHealth and exploring drivers of adherence and sustainable behaviour change will optimize impact and application across communities with an inclusive lens to guide future policy to improve the diabetes and cardiovascular health of all Canadians.

Research in my lab focuses on the relationship between diet, gut microbiota and health. We have been focusing on the establishment of the intestinal barrier and the role played by the gut microbiota in its regulation, at the transcriptional and post-transcriptional gene expression level. Building on recent findings linking gut microbiota, intestinal barrier and the metabolic syndrome, we are now expanding our research to understand how the establishment of the gut microbiota in early life may be linked to developing this condition in later life.

Dr. Connelly is a clinician scientist and staff physician at St Michael’s Hospital where his clinical responsibilities involve echocardiography and cardiac MRI. His basic science laboratory is involved in exploring mechanisms of diabetic complications, principally diastolic heart failure and developing novel therapeutic strategies to treat this. Dr. Connelly also collaborates closely with the Sunnybrook Health Sciences Centre in elucidating the role of real time cardiac metabolism in the pathogenesis of post MI remodeling, and developing novel MR techniques to enable non-invasive tissue characterization.

The research interests of the laboratory are in the study of patients at risk for Type 2 Diabetes or at risk for the complications of diabetes and identifying serum biomarkers that will predict patient outcomes. The most recent focus has been on the adipokine adiponectin and on the enzyme paraoxonase-1 (PON1). Adiponectin is an insulin-sensitizing protein produced by adipocytes.PON1 is an anti-inflammatory component of high density lipoproteins. We have studied these factors in four patient groups:
1) The Sandy Lake Oji-Cree
2) Women at risk for post-gestational diabetes
3) Patients with renal failure on dialysis; and
4) Renal transplant recipients

Type-1 diabetes (T1D) is an autoimmune disease characterized by loss of self-tolerance, T cell-mediated immune attack of pancreatic β-islets and β-cell dysfunction. Allogeneic β-islet transplantation can restore β-islet cell function but despite the use of immunosuppressive drugs, the risk of allo- and autoimmune-mediated b-cell loss remains high. A true ‘cure’ for T1D requires approaches that restore β-islet function and also prevent immune-mediated pathology without immunosuppressive drugs. Our lab focuses on harnessing lymphocyte populations that have immunoregulatory or tissue repair properties in cell-based therapies for transplantation and autoimmunity. Ongoing studies are focused on delineating cross-talk between immune cells and β-islet cells, and assessing whether adoptive transfer of populations of lymphocytes can enhance β-islet cell transplantation approaches by regulating aberrant immune responses or supporting β-islet cells directly.

Developing optical technologies to assess tissue viability in the diabetic lower extremity. The aim is to develop novel devices in the prevention, diagnosis and management of Diabetic Foot Ulcers (DFU’s). The research laboratory is a combination of physics, engineering and clinical translation with the aim to have a direct impact on the lives of patients.

Research in the Cummins lab relates to the study of nuclear hormone receptors that are important in the control of glucose and lipid metabolism. Our lab is interested in all areas of nuclear receptor biology including the identification of new ligands; the study of signaling pathways upstream and downstream of receptor activation; the characterization of novel co-regulatory proteins; and the influence of nuclear receptor modulation on whole animal physiology. Our studies primarily investigate the importance of the glucocorticoid receptor (GR), the liver X receptor  (LXRα and LXRβ) and the peroxisome proliferator activated receptor (PPARα, PPARδ and PPARγ) signaling pathways in the context of diabetes and dyslipidemia.

The goal of Dr. Cybulsky’s research program is to elucidate novel cellular and molecular mechanisms regulating intimal macrophage burden at early stages of atherosclerosis. The vision is to use this information to develop new therapies to inhibit the progression of early atherosclerotic lesions to advanced plaques. Individuals with known risk factors for atherosclerosis would benefit from such therapies because complications arising from advanced plaques cause myocardial infarction and stroke, and therapies that inhibit disease progression would alleviate the morbidity and mortality associated with atherosclerosis. Our research program to reduce intimal macrophages in early atherosclerotic lesions and inhibit lesion progression focuses on several aspects of myeloid cell biology including macrophage exit from atherosclerotic lesions, inhibition of monocyte recruitment, macrophage proliferation and survival in early lesions and understanding how systemic risk factors influence macrophage gene expression triggered by pro-inflammatory stimuli. Previous research has focused on hypercholesterolemia, a key risk factor for atherosclerosis; however, future studies will also include hyperglycemia and advanced glycation endproducts, which are found in patients with diabetes. The burden of diabetes, particularly adult onset or type II diabetes, is increasing, as is its contribution to atherosclerosis-related conditions.