Psychological stress has been frequently implicated in disease development and progression, but the determinants of this relationship remain unclear. A recent finding has demonstrated that chronic and perceived stress affects health by influencing the rate of cellular aging. The literature also shows that social support buffers against stress. Jillian Satin is exploring the relationship among stress, social support and cellular aging in women who have been diagnosed with breast cancer. While chronological age is usually used as a predictor of age-related disease, cellular aging may be a more accurate predictor of onset and a potential route of disease prevention. Jillian’s research is examining whether social support modulates the relationship between objective stressful life events and cellular aging. Since social support has been shown to decrease perceived stress, Jillian’s hypothesis is that social support decreases the accelerated rate of cellular aging. If this hypothesis is correct, it would suggest that social support interventions should be made available to those at risk and should be integrated into the health care that women with cancer receive. Although this study focuses on breast cancer, the findings could prompt further exploration into treatment of cancer and age-related diseases.
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Who has Epilepsy in British Columbia?
According to national surveys, an estimated 30 per cent of Canadian children between six and 18 years of age suffer from chronic conditions and/or disabilities, including seizure disorders. However, these surveys do not allow for provincial analysis, due to small sample sizes, and there is limited comparability between surveys because of differences in target groups, methodologies and conceptual frameworks. Currently, there are no comprehensive prevalence data on children with special health care needs in BC, such as children with epileptic seizures, who account for half the visits to specialists because of neurological disease. Veronica Schiariti is researching the influences of neighbourhood income, population density, health care availability and community resources on the treatment prevalence of epilepsy in BC children under the age of 19. She is examining both diagnosis and treatment patterns of pediatric patients with epilepsy. Veronica hopes that her research will contribute to improved treatment for epileptic children by identifying disparities in health service delivery, informing health care policy decisions, and enabling long-term tracking and study of health and development outcomes at the individual level and in the broader population.
Genetic Variation in Apoptotic Genes and Susceptibility to Non-Hodgkin Lymphoma
Non-Hodgkin’s Lymphoma (NHL) is a cancer of lymphocytes – a type of white blood cell that moves throughout the body as part of its role in immune defense. As a complex disease with both environmental and genetic factors contributing to its development, NHL is incurable and the fourth highest cause of cancer deaths in Canada. Johanna Schinas aims to identify the genetic factors contributing to NHL susceptibility. She is focusing on the role of apoptosis which is a natural process of cell death triggered by genes and carried out by the immune system. When an immune cell originally meant for destruction escapes apoptosis, it becomes an ideal environment for further changes that can cause progression to malignant cancer. By searching for DNA variants in apoptosis genes that are associated with the development of lymphoma, she hopes to identify markers of genetic susceptibility to lymphoma. This will lead to not only a better understanding of the molecular basis of this cancer, but also assist in the design of effective surveillance programs for at-risk individuals.
Optimizing the Role Nurses Play in Preventing Pediatric Deaths: An Application of Situational Awareness
Up to 23,000 preventable deaths are estimated to occur each year in Canadian hospitals. Nurses who provide care at the bedside are well positioned to promote patient safety, because a critical component of their role is to notice and gauge potential risks. Although research suggests that nurses’ workload, training and experience influence patient mortality, little is known about the actual processes that nurses use to prevent or reduce error. Kim Shearer is applying the model of “Situational Awareness” (SA) to study pediatric nurses performing resuscitation of children in hospital. SA – defined as knowing what is going on in your environment – has been proposed as the primary basis for decision-making and performance in complex, dynamic systems, helping researchers understand how threats within the environment are gauged and safety is facilitated. Kim’s study will identify factors that promote or impede nurses’ ability to gauge the work environment and make decisions, generating the basic knowledge needed to create computer simulations for teaching and testing SA in pediatric resuscitation. Findings of this research will help to prevent or minimize error and enable development of novel health education interventions to improve SA and hence the safety of children in dynamic and complex acute care environments.
Quantitative Single Cell Proteomics for Stem Cell Analysis in Microfluidic Devices
Stem cells are defined by their unique capabilities to either replicate (self-renew) or differentiate into more specialized cell types such as nerve cells (neurons), immune cells and skin cells. If health researchers could controllably direct stem cells to differentiate into particular cell types, stem cells could potentially be used as clinical therapeutics for a diverse range of diseases, including neurodegenerative diseases, autoimmune disorders, heart and liver disease, and cancer. Presently, the control of stem cell differentiation is hampered because researchers lack the necessary knowledge and tools for studying the molecular pathways that guide stem cell differentiation into specific cell types. Anupam Singhal’s research seeks to harness recent advances in micron-sized fluid-handling devices and nanotechnology in order to quantitatively study stem cells at the single cell level. In particular, he will propose a general platform for performing rapid and high-throughput quantification of multiple proteins in single stem cells. This strategy should help to identify proteins (e.g. transcription factors for gene expression, secreted proteins) that influence the stem cell fate decision. This information will then be used to construct model molecular pathways that guide stem cell differentiation, a critical milestone that must be reached before stem cells will find widespread clinical applications.
Phenotypic Rescue of Neuronal Structure and Function in a Rett Syndrome Mouse Model
Rett syndrome is a debilitating neurodevelopmental disorder that affects between one in 10,000 to one in 15,000 females. Symptoms that appear in early childhood include severe mental disabilities, impaired speech and movement, and seizures. Individuals with Rett syndrome show abnormalities in the size and structure of certain neurons in the brain. At present, there is very little treatment available for this disease. In most patients, Rett syndrome is caused by mutations in a single gene called MECP2. David Stuss’ research is part of a collaborative effort that is investigating methods for introducing a functional form of this gene into the brain at the appropriate developmental stage. This is expected to allow neurons to follow their normal course of growth and maturation. The methods being developed use engineered lentivirus vectors that are capable of delivering genetic material into differentiated, non-dividing cells like neurons. These viral vectors can also introduce genes for fluorescent proteins into targeted cells at the same time, allowing detailed microscopic visualization of the effects of treatment on neuronal structure. If the rescue of neuronal structure and brain development following therapeutic gene transfer can be demonstrated, this research will be an important first step in creating a therapeutic strategy for treating the devastating effects of Rett syndrome in children.
Mechanisms of calcium waves and their contribution to vasomotion in the cerebral circulation
Calcium that is released from one part of a smooth muscle cell can sometimes travel along the length of the same cell in a wave-like manner. This phenomenon is known as a calcium wave. Under certain conditions, a calcium wave can synchronize with other calcium waves from neighbouring cells to cause rhythmic contractions of blood vessels, known as vasomotion. Why vasomotion occurs is not completely understood, but it may be important in controlling blood flow in small diameter blood vessels, such as the cerebral arteries in the brain. Cerebral arteries regulate the flow of blood to working areas of the brain, but this flow is compromised during conditions such as stroke, hypertension or diabetes. There is evidence that the frequency of vasomotion is affected in these conditions. Harley Syyong is studying vasomotion and its underlying mechanisms. Using both molecular and ultrastructural methods, he is exploring the contribution of calcium waves to vasomotion. This research will explore how calcium waves are generated, their role in vasomotion and how the physical structure of the cell supports their propagation. This project is laying the groundwork for future studies to examine how the underlying mechanisms of vasomotion are affected during pathological conditions such as stroke, hypertension and diabetes. Ultimately, this may lead to new drug therapies for treatment of these conditions.
Identification of Mycobacterium tuberculosis virulence factors by pathogen effector protein screening in yeast (PEPSY)
Tuberculosis is a devastating disease that infects one-third of the world’s population, leading to eight million new cases and three million deaths per year. The prevalence of this disease is largely due to the ability of Mycobacterium tuberculosis (the bacteria that causes tuberculosis) to evade destruction by the immune system. Normally, when bacteria invade the body, the human response system triggers specialized cells called macrophages to engulf and destroy bacteria. In the case of tuberculosis, M. tuberculosis succeeds not only in escaping annihilation, but is able to enter and live inside the very cells that are programmed to destroy it. Using yeast as a model organism, Emily Thi is studying and identifying the components of the arsenal that Mycobacterium tuberculosis uses to successfully infect and survive within human macrophages. Her research on M. tuberculosis proteins that disrupt normal macrophage function may lead to the identification of novel targets for drug and vaccine development, which could result in new strategies to combat this challenging disease.
The Role of CREB in Long-term Memory in Caenorhabditis elegans
Currently 30 million Americans suffer from some form of clinically recognized memory disorder. During the last 25 years, basic neurobiological research has begun to identify the underlying molecular mechanisms for memory formation. One of the key players discovered to be involved in the formation of protein synthesis dependent long-term memory (LTM) is the transcription factor cAMP response element binding protein (CREB). CREB has been shown to be a necessary protein for the formation of LTM in diverse species including sea hares, fruit flies, mice and humans. Tiffany Timbers is exploring whether CREB is also essential for the long-term habituation observed in Caenorhabditis elegans (a tiny nematode), which can become “used to” repeated stimulation such as tapping on the Petri dish where it lives. Tiffany will determine whether CREB activity (resulting in the transcription of cAMP responsive genes) occurs in the neurons that generate the plasticity responsible for LTM. By investigating the involvement of CREB in the biological pathway underlying the memory of habituation in C. elegans, this research could contribute to the development of new gene targets, drug screens and preclinical data to suggest drug classes capable of helping those affected by memory cognition defects.
The Cell Biology of the NIMA-Related Kinase Defective in Polycystic Kidney Disease
Polycystic kidney disease (PKD) affects one in 800 people worldwide and is the major reason for dialysis treatment and kidney transplantation. One of the most common genetic diseases in the world, PKD has many forms, ranging from aberrant cell proliferation in the kidney to defects in other organ systems, such as the liver and pancreas. This abnormal growth within kidneys and other organs eventually leads to organ failure. The age of onset and disease severity for PKD are highly variable and are affected by additional genetic mutations. Mouse models of the disease have been used to identify many of the genes involved in the polycystic pathology and to determine links between gene and disease. Many of these genes encode proteins that localize to the cilia, a hair-like cell projection that senses the extracellular environment of the cell. The loss of a cilium results in the inability of a cell to response to external cues controlling normal growth. It has been shown that the failure of a kidney cell to build cilia results in PKD. Nek8 is an enzyme which, when mutated, causes PKD in mice. Melissa Trapp’s work has shown that Nek8 is also found within the cilia. This research project is focused on the role of Nek8 within cells, particularly how mutated Nek8 can alter the cilium and cause defects in cell growth. By manipulating the protein levels in Nek8 within cultured kidney cells and introducing mutant forms of Nek8, she is examining the effects on ciliary assembly and cell proliferation. This research will contribute to the body of knowledge accumulating about Nek8 and the cause of PKD. It could also contribute to our understanding of other cystic kidney diseases.