We are looking for talented students who are interested in studying the mechanisms of human diseases. As a graduate student in our department, you will enjoy a superb research environment, flexibility in choosing a research area, and excellent opportunities to learn from clinical and basic scientists. Our graduate program places less emphasis on course work and greater emphasis on research, scholarship and independent thinking.
Graduate training in Pathology and Laboratory Medicine provides the foundational skill sets for advanced training and a career in academia (university professor, researchers, teachers), industry (biotechnology companies), and government (research positions in government laboratories). Some of our graduate students continue their training in research through PhD or postdoctoral training to develop into independent scientists. Some students combine their passion for research with clinical training in medicine and some pursue truly unique careers such as medical journalism.
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The following supervisors are presently looking for Graduate Students in their laboratories. Short summaries of their research projects are also provided:
I am recruiting MSc and PhD students in my lab.
The first project is to understand how junctophilin-2, a membrane binding protein, maintains normal function of ryanodine receptor Ca2+ release unit in cardiomyocytes and its implications in ischemic heart disease. Main techniques used to perform this research include: i) qRT-PCR; ii) calcium measurement; iii) protein modifications by ubiquitin; iv) fluorescent microscopy; v) western blot and ChIP; and, vi) cardiomyocyte isolation and culture.
The second project is to investigate the molecular mechanism by which doxorubicin, an effective and widely used anti-cancer drug, causes cardiac injury and heart failure, a fatal condition, and to develop therapeutic approaches to prevent doxorubicin-induced cardiac injury. The study will be focused on modulation of cardiomyocyte autophagic flux and necroptosis in this disease. Main techniques used to perform this research include: i) qRT-PCR; ii) western blot and ChIP; iii) fluorescent microscopy and electron microscopy; iv) animal models (mice); v) echocardiography; and, vi) cardiomyocyte isolation and culture.
In addition, we are currently also studying diabetic cardiomyopathy and multiple-organ injury in sepsis in my lab.
Keywords: myocardial dysfunction, ischemia/reperfusion-injury, cardiomyocyte-cardiac fibroblast interaction
Description of Research Activities: Research in my group focuses on understanding molecular mechanisms involved in myocardial dysfunction/injury related to sepsis, ischemia/reperfusion and diabetic myocardial fibrosis. With a cardiomyocyte-fibroblast co-culture system, we are currently investigating role of cell-cell interactions in the induction of myocardial dysfunction in various pathological conditions. Specifically, 1) we are studying how cardiomyocyte to affect the function of fibroblast to increase collagen production in diabetic condition; 2) we are addressing how fibroblast to decrease cardiomyocyte contractility under septic condition. In this topic, we aim to understand the role of NLRP3 inflammasome activation in fibroblast and its impact on the myocardial function in sepsis.
Keywords: Inflammation, Functional Genetics, Molecular Regulation, Type 2 immunity, Allergic Disease
Research Activities:Dr. Cameron's laboratory is focused on understanding the development and trajectory of inflammatory disease. Her research relies on expertise in the areas of cellular and molecular immunology, functional genetics/genomics and translational science, including patient recruitment and clinical characterization. Dr. Cameron's work on CRTh2, a prostaglandin D 2 (PGD2) receptor expressed by Th2 cells, has shown that single nucleotide polymorphisms (SNPs) in CRTh2 are associated with increased frequency of allergic conditions including asthma due to elevated CRTh2 expression and function. Dr. Cameron is also studying the role of CRTh2 in severe asthma and whether environmental factors such as diet and viral infection may interact with CRTh2 and its variants to modulate disease susceptibility and symptoms. A new area of interest is whether type 2 immunity is influenced by sex hormones and if these pathways differentially influence development of allergic disease in women and men.
Techniques used to perform this research include; i) qRT-PCR ii) flow cytometry, iii) molecular cloning, iv) reporter assays, v) western blot and ChIP, vi) patient recruitment and database management/analysis.
Keywords: general gastroenterology, inflammatory bowel diseases, colorectal cancer
Description of Research Activities: Our research focuses on identifying the cellular origin of colorectal cancer by characterizing the intestinal and colonic stem cells of the gut. We are focused on understanding the fundamental processes regulating normal and mutated intestinal/colonic stem cells and aim to define the role of these stem cells in tissue regeneration and carcinogenesis. We utilize a range of approaches from transgenic mouse models to in vitro “mini-guts” to elucidate the key pathways important in cancer and tissue repair.
Keywords: human/medical genetics, molecular cytogenetics, cancer genetics, genomics
Description of Research Activities: My research is translational in nature with a goal of moving genetic research findings into the clinical laboratory setting. My laboratory’s research activities include: (1) phenotype/genotype correlations in inherited diseases with chromosome abnormalities, and examining chromosome structure at the submicroscopic level; (2) identifying genome copy number changes and their relationship to inherited diseases such as leukemia and acquired diseases such as leukemia and breast cancer; and, (3) developing novel cytogenomic and genomic technology to improve disease diagnosis
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which motor neurons progressively degenerate, giving rise to paralysis with death within 3 to 5 years of onset. There is only one approved pharmacotherapy with limited efficacy and no cure. Our research program has been pivotal in determining that up to 50% of affected individuals will have a frontotemporal degeneration resulting in a range of neuropsychological deficits. We have shown that this process is associated with the intraneuronal and glial deposition of tau protein that is pathologically phosphorylated at the Thr175 residue. Increasingly, the motor neuron degeneration of ALS is being shown to be associated with alterations in RNA biology. Our research program focuses on both of these processes. In the former, having demonstrated that pThr175-tau gives rise to pathological cellular inclusions in vitro and that the consequence of this is phosphorylation of Thr231-tau, we are examining the extent to which this pathway is active in not only ALS but also in Chronic Traumatic Encephalopathy (CTE). We have developed a novel rat model of pThr715-tau expression and in 2016 we will be focusing expressing mutated TDP-43 concurrently in this model. Behaviour testing and imaging modalities in collaboration with Drs Bartha and Schmidt allow us to track behaviour and any abnormalities in the brain post injection. In our studies of altered RNA metabolism, we are focusing on characterizing novel regulators of RNA stability in ALS, including how novel RNA binding proteins and microRNAs alter the stoichiometry of the neurofilament expression in a manner consistent with that known to occur in ALS. We have discovered a new protein involved in RNA stabilization (Rho Guanine Nucleotide Exchange Factor; RGNEF) and continue to work on defining the interaction of this protein with NEFL mRNA, other RNAs and RNA binding proteins like TDP-43 and FUS/TLS. We are also interested in the effect of microRNA expression in ALS, as most microRNA are downregulated in this disease. A handful are upregulated however and, interestingly, some of these impact NEFL mRNA expression in a manner conducive to decreasing NEFL mRNA stability. The ultimate goal of our research is to dissect the mechanisms behind neuronal death in ALS, and to identify potential targets that may serve as intervention points for the disease.
We are the first to reveal that NK cells can kill epithelial cell and heart endothelial cell and contribute substantially to heart and kidney ischemic injury and chronic heart graft rejection. We are now studying NK cells-mediated allograft vasculopathy and whether the NK cell and necroptosis axis plays a critical role in prolonged inflammation in transplantation.
Our 2nd project is necroptosis in regulation of cell death and allograft rejection. We have found that inhibition of caspase function enhanced necrotic death and inhibition of RlPK1/3 function results in decreased necroptotic death and danger molecule HMGB1 release. We are now studying the molecular path of necroptosis and try to identify new mechanisms for necroptotic cell death. We aim to develop novel strategies to prevent cell death and transplant rejection.
Keywords: virus evolution, bioinformatics, phylogenetics, molecular evolution, phylodynamics, machine learning
Summary of research: My research focus is designing and implementing new computational methods to reconstruct the spread and adaptation of viruses from their genetic sequence variation. Viruses evolve so rapidly that a single infection can become genetically unique within weeks or months of transmission. We can use this evolutionary proliferation to characterize how a virus population has adapted to that patient’s immune system; to detect “hotspots” of virus transmission in an epidemic in real time; and to reconstruct the historical spread of a virus in human populations. To accomplish this, we use a blend of techniques from mathematical modeling, phylogenetics, pattern recognition, open-source software development and high performance computing.