Research shows that a growing number of Canadian adolescents are becoming less active, threatening their physical and mental health by increasing their risk of being overweight. While there has been substantial research on physical activity, the primary factors that influence levels of activity have not been identified. Catherine Sabiston’s past research has focused on ways adolescents and young adults deal with feelings and emotions related to their body. In this research, she has found initial links between body image and physical activity. She is now looking at whether body image (perceptions and attitudes about one’s body and physical appearance) and actual body characteristics related to shape and weight contribute to decreasing physical activity levels among adolescents. Catherine is also interested in how these factors affect boys and girls differently. Her goal is to come up with realistic recommendations that will lead Canadian adolescents toward increased activity levels and eventually healthier lifestyles.
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Anoxia and the regulation of intracellular ion concentrations in hippocampal neurons
Neurons (nerve cells) need a regular supply of oxygen and nutrients to survive. When neurons are deprived of these essential factors for more than a few minutes, such as during a stroke or cardiac arrest, they undergo changes that lead to cell death. Intracellular concentrations of ions (e.g. sodium ions, calcium ions and protons) show dramatic changes during and following periods of anoxia or ischemia (oxygen deprivation). These changes play an important role in determining subsequent neuronal damage or death. Claire Sheldon is characterizing these anoxia-evoked changes in sodium ions, calcium ions and protons in hippocampal neurons and hopes to identify the mechanisms which contribute to their production. Her research focuses on the role(s) of intracellular pH regulating mechanisms to the changes observed, with particular emphasis on the Na+/H+ exchanger, an acid-extruding mechanism present in hippocampal neurons. Claire hopes her research will lead to new strategies to prevent or limit neuron death and the debilitating effects that stroke or cardiac arrest have on the central nervous system.
Characterization of a YAC mouse model of Huntington disease for use in therapeutic trials
Huntington disease (HD) is an inherited, neurodegenerative disease characterized by loss of motor control and cognitive decline, eventually leading to death. Elizabeth Slow is studying atrophy and cell loss in the striatum, the most affected region of the brain, and the motor dysfunction associated with HD. A group of proteins called caspases split other proteins, including huntingtin, the protein produced by the HD gene. In collaboration with researchers at Harvard, the University of California and the Buck Institute in California, Elizabeth is investigating whether this process triggers inappropriate cell suicide in the neurons affected by HD, thus causing the disease. If so, the results will determine whether caspase inhibitors are an effective treatment option for people with Huntington disease, which currently has no treatments to prevent or delay the condition.
Model Membrane studies of Amphotericin B's mechanism of action (towards less toxic AmB formulations and new tools for drug/membrane studies)
Amphotericin B (AmB) is an antifungal antibiotic used to treat infections in patients with depressed immune systems, such as cancer patients, organ donor recipients, diabetics and people with AIDS. Fungal infections are thought to account for up to 30 per cent of deaths among these patients. Although effective, use of AmB is limited because it can also cause kidney toxicity. AmB is known to interact with parts of the cell membrane, forming pores that allow leakage and ultimately cause cell death, but this process is poorly understood. Robin Stoodley is researching how the drug interacts with the body at the cellular and molecular levels, with the goal of finding ways to reformulate AmB to reduce its toxicity and improve effectiveness. The techniques Robin develops for this research may also be used to study chemotherapy and other drugs, leading to the development of better drug therapies.
Pathogenesis of confined placental mosaicism (CMP) during pregnancy
The frequency of chromosomal abnormalities in reproduction is significant — 15 to 20 per cent of all pregnancies end in spontaneous abortion, and half of these miscarriages are associated with chromosomal abnormalities. In 1983, two UBC professors discovered a condition now known as confined placental mosaicism (CPM), where a chromosomal abnormality is present in the placenta but not the fetus. CPM allows a pregnancy that would otherwise spontaneously abort to continue to term, and is present in at least two per cent of pregnancies. In his earlier research, Paul Yong confirmed that some types of CPM increase the risk for poor fetal outcomes such as low birth weight or complications such as pre-eclampsia. Now he is studying how chromosomal abnormalities cause alterations in placental structure and function. The hope is to identify potential therapeutic interventions in pregnancies affected by chromosome abnormalities in the placenta.
Development of a direct computer interface using descending motor potentials recorded from the spinal cord
A variety of devices are available for individuals with motor impairments, such as electrical stimulation systems for locomotion. But people with severe disabilities are often unable to control these devices effectively. Dr. Jaimie Borisoff, who has published research papers on neural regeneration in the journals Experimental Neurology and Molecular and Cellular Neuroscience, is researching assistive technologies to enhance quality of life for people with severe disabilities. Jaimie is investigating whether motor control information can be recorded directly from the spinal cord, since much of the intentional and logistical processing has already been performed in the brain before the signal pathway terminates at the spinal lesion. If so, this information could be used to create a control system that uses signals from the spinal cord.
Gap Junctional Hemichannels in Astrocytes: Regulation in Normal and Injured CNS
Gap junctions are connections between cells that allow free passage of ions and small molecules. Because ions can flow through them, gap junctions permit changes in membrane potential to pass from cell to cell in most body organs, including the brain. Gap junctions are key elements in cellular communication that are essential for normal embryonic development and function in adult organs. Combining his engineering background with more recent training in biochemical research, Dr. Francisco Cayabyab is using a number of research methods to investigate deficient levels of gap junctions and examine their regulation and function. He hopes this research will contribute to the development of new therapeutic strategies targeting gap junction proteins for certain neurological disorders, including stroke, epilepsy and schizophrenia.
Molecular mechanisms of SP12-mediated virulence in Salmonella Typhimurim
Salmonella enterica serovar Typhimurium is a bacterium that causes gastroenteritis, a type of food poisoning characterized by abdominal pain, fever, vomiting, and diarrhoea. Most Salmonella infections arise from oral ingestion of tainted food or water and are a significant cause of disease and death in animals and humans worldwide. Dr. Brian Coombes is studying the molecular mechanisms by which Salmonella use virulence factors to modify their host environment. Once injected into mammalian host cells, these virulence factors rearrange and reprogram the cells so that Salmonella can replicate and evade the body’s immune system. Learning more about how bacteria use specific virulence factors to manipulate their environment during infection may lead to the design of new therapeutic strategies to treat or block the disease process.
Mechanisms of pathogenic E. coli – host cell interactions
Escherichia coli (E. coli) bacteria cause numerous diseases including meningitis, urinary tract infections and diarrhea. Worldwide, enteropathogenic E. coli (EPEC) is one of the leading causes of diarrhea in children and is an endemic health threat in the developing world, causing the death of several hundred thousand people each year. Isolated outbreaks of enterohaemorrhagic E. coli (EHEC) also occur in developed countries, often transmitted in contaminated hamburgers and water supplies, and can cause diarrhea and fatal kidney disease. After binding to the cells that line the intestine, E. coli injects several proteins that lead to diarrhea and disease. Dr. Philip Hardwidge aims to identify these proteins and determine their structure and function. He is also examining how intestinal cells respond to E. coli at the level of gene expression, using an advanced technique to analyze several thousand genes at a time. This research could guide the design of future vaccines and antibiotics to prevent and treat E. coli.
Molecular mechanism linking Hox transcription factors to leukemia
Leukemia affects one to two per cent of the population in the industrialized world. The disease occurs when the genes that control the normal process of blood cell formation function abnormally, and bone marrow produces malignant white blood cells as a result. These cancerous cells accumulate, interfere with the body’s production of healthy blood cells, and make the body unable to protect itself against infections. A family of genes called Hox genes are present in elevated levels in patients with some forms of leukemia, and are known to play a crucial role in the disease. Dr. Koichi Hirose is investigating the molecular function of these genes to explain how they transform normal blood cell development into leukemia. His research could help in the development of new therapies for treating Hox-related leukemia.