Graduate Student Opportunities
New MSc and PhD Program Opportunities
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.
To contact the potential supervisors below please click here.
The following supervisors are presently looking for Graduate Students in their laboratories. Short summaries of their research projects are also provided:
Dr. Tianqing Peng
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.
Dr. Tao Rui
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.
Drs. Anthony Jevnikar and ZhuXu Zhang
We were the first to describe RIPK3-mediated necroptosis in organ ischemia injury and transplant rejection. We have found that inhibition of caspase function enhanced necrotic death and inhibition of RlPK1/3 function results in decreased necrotic death and danger molecule release. Most recently we have demonstrated that mitochondria critically participate in necroptosis as well as apoptosis. We are now studying the molecular path of necroptosis to try to identify new mechanisms for cell death. We aim to develop novel strategies to prevent cell death and transplant rejection.
Our second project is studying the role of NK cells in immune tolerance. We were the first to reveal that NK cells can kill epithelial and endothelial cells, and contribute substantially to heart and kidney ischemic injury and chronic graft rejection. We are now studying the regulatory roles of diverse receptor and ligand interactions on NK cell functions.
Dr. Lisa Cameron
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.
Dr. Samuel Asfaha
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.
Dr. Fred Dick
Dr. Christopher Howlett
Keywords: mouse models of cancer, inflammation, cancer therapeutics, cancer dormancy
Description of Research Activities: Our research is interested in understanding molecular, cellular, and histological events in animal models of human cancer. We have a number of animal models in use or under development that are intended as tools to understand how normal, pre-malignant cells bearing cancer causing mutations proliferate, transdifferentiate, and interact with the immune system. Similarly, we are interested in studying processes that facilitate cancer progression and its response to molecularly targeted therapy. Students engaged in these projects will gain experience with a variety of cell culture and genetically modified mouse models of cancer. The incorporation of this work with the latest cancer genomic analyses and therapeutic approaches will provide a diverse and dynamic training opportunity.
Dr Weiping Min
Keywords: cancer, transplantation, siRNA, miRNA
Summary of research: MinLab is currently recruiting graduate (PhD or MSc) students to carry on exciting work that we are doing using immune modulation for cancer therapy, transplant rejection and autoimmunity. My laboratory has been the first in the world to define a bi-directional feedback loop between T regulatory cells (Treg) and tolerogenic dendritic cells (DCs). This finding sheds new light on how the immune system can be artificially "tricked" into permanently accepting foreign organs in transplantation without having to use systemic immune uppression. Additionally, my laboratory was the first to develop the technique of RNA interference for modification of immune responses. We are currently setting us systems to use this novel approach in pre-clinical and clinical situations.
Current projects in my laboratory include: 1) Therapeutic manipulation of immune responses in cancer-bearing hosts. 2) RNAi-based vaccine for cancer and autoimmune diseases. 3) Nanoparticle-based tissue (cell)-targeted delivery of siRNA. 4) Mechanisms of immunomodulation between tolerogenic DC and Treg cells. 5) The roles of microRNA in immune manipulation and immunotherapy. You may get more information from http://publish.uwo.ca/~mweiping/.
Dr. Joan Knoll
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
Dr. Michael Strong
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.