My lab conducts research on several areas related to cardio-respiratory physiology and pathophysiology. For example, we are studying: 1) how the heart initially adapts to hypertension before the development of contractile dysfunction and heart failure; 2) skeletal and cardiomyocyte cell signalling during normal and hypoxic conditions; 3) proteomic alterations that occur in limb muscles during exercise; 4) key post-translational modifications of myofilament proteins that arise during the development of whole muscle dysfunction as a result of fatigue or ischemia; and, 5) dyastolic dysfunction in various physiological and pathological states, such as aging, sex differences, and models of heart failure.Learn More
Keyword: Healthy aging
To date, my research program has focused on strategies used to execute safe movement during adapted locomotor tasks (steering, obstacle circumvention, obstacle stepping) and the role of vision in these tasks. I am also interested in exploring the impact of cognitive or brain function on locomotor control. Given the commonness of dual tasking in our daily living, I hope to map patterns of cognitive-locomotor interference for multiple adapted locomotor (e.g. obstacle circumvention) and cognitive activities (e.g. visuo-spatial cognitive tasks) and ascertain optimal training strategies for dual-task performance.Learn More
The primary goals of my research program are 1) to understand where posture is controlled 2) to understand what sensory information contributes to successful movement and equilibrium.
By investigating these two key questions I believe we will have a better understanding of how sensory decline contributes to a loss of mobility as we age. My research program involves two key areas of study:
1) To perform direct recordings from sensory afferents and motor efferents in awake human subjects to investigate sensory contributions to movement, balance control, and reflex responses.
2) To elicit balance perturbations to test the function of these reflex loops, and sensory contributions to the maintenance of equilibrium and postural control.
More than 4 million Canadians have arthritis and the number of people living with arthritis continues to increase year after year. Osteoarthritis involves multiple tissues and often includes cartilage damage, bone sclerosis and synovial inflammation. A pressing need remains for joint localized therapies and interventions that could slow or ideally stop this debilitating disease.
In our research, we use genetic and surgical models of spontaneous osteoarthritis (with old age) and post-traumatic osteoarthritis (following injury). We follow the progression of disease in a joint in order to better understand how proteins such as TRPV4, integrin alpha1beta1 and cilia influence chondrocyte signal transduction and thus the development of osteoarthritis.
My lab focuses on two main axes of research:
1) Unfolded Protein Response and Human Diseases: We study proteins that play key roles in animal stress responses, specifically the Unfolded Protein Response (UPR), which has been linked to animal development, cell differentiation, as well as a variety of human diseases such as Alzheimer’s, diabetes, cancer and viral infection.
2) Molecular Mechanisms of Aging: We are working to establish planarians as a new aging model to test the hypothesis that longevity requires multiplex resistance to stress. We hope to identify genes or alleles that confer such multiplex stress resistance and/or promote longevity.
While animal models have lead to huge advancements in our understanding of neurobiology, there is controversy over whether overexpression/silencing of gene expression is representative of diverse disease states. Indeed, the lack of availability of primary human neurons has made evaluating the pathological consequences of genomic mutations arduous. The use of human induced pluripotent stem cell (hiPSC) technology overcomes these limitations by providing a source of human neurons from both normal and disease genetic backgrounds. We currently focus on stem cell based models of Parkinson's Disease (PD) to study how mitochondrial stress mechanisms impact on neuronal function in human disease.Learn More
My research program adopts a broad and integrative approach to the study of chronic musculoskeletal pain, incorporating both basic and clinical sciences. A major arm to my research program is investigating the underlying pathophysiologic mechanisms using both animal and human models. My research also aims to advance reliable diagnostic criteria (imaging, biomarkers) and physical assessment techniques (quantitative sensory testing, electromyography) that enable effective and reliable treatment and management strategies. By emphasizing transdisciplinary and multi-institutional collaborations, my research program will continue to inform future clinical and experimental initiatives in the field of chronic musculoskeletal pain.Learn More
Currently, there are several major areas of research focus including the study of basic fatty acid metabolism, understanding the association between plasma fatty acids and health outcomes, omega-3 fatty acids in the prevention of breast cancer, and examining determinants of health in the Guelph Family Health Study. In addition, related projects include the study of fats in brain health (concussion, Alzheimer's Disease), fatty liver disease, fatty acid metabolism, bone development and nutrigenomics.Learn More
Skeletal muscle is a remarkable tissue which regulates many metabolic processes, generates heat and is the basic motor of locomotion allowing us to meaningfully interact with our environment. When a muscle is activated at various lengths it produces a given predictable amount of force. However, when that muscle is actively lengthened or shortened those predictions go out the window. We actually know very little regarding dynamic muscle contraction. My research program focuses on muscle contractile properties and gaining a deeper understanding of how muscle works. I use altered states to tease out some of these fine muscle details such as muscle fatigue, aging, and training.Learn More
The primary aim of my research is to better understand the mechanisms that control, and functional consequences of, sympathetic outflow at rest and during stress in humans with and without cardiovascular disease. To uncover these mechanisms, my laboratory employs direct intra-neural recordings of postganglionic sympathetic traffic, studying both multi- and single-fibre preparations. Additionally, we are also interested in understanding the mechanisms responsible for the large inter-individual variability in blood pressure responses to stress, as well as testing novel interventions to reduce resting blood pressure, a major modifiable risk factor for cardiovascular disease.Learn More