Impact of nutrition and physical education school policies on childhood obesity: Understanding the implementation process and its impact on behavioural and weight outcomes

The prevalence of childhood obesity is rapidly increasing in Canada, increasing fivefold for both boys and girls from 1981-99. As the genetic characteristics of the human population have not changed in the past 30 years, childhood obesity is thought to be caused by behavioural and environmental factors that predispose children to consume more calories than they expend. Obesity is also linked to a number of diseases, including cardiovascular disease, type 2 diabetes, and some cancers. Schools provide an ideal setting to intervene on children’s behaviours. Recently, policy strategies have been proposed to change the school environment to limit access to unhealthy food and to increase opportunities for children to be more physically active. However, these changes are taking place without the scientific evidence necessary to support these strategies. Louise Mâsse is examining the impact of school-based policies on changing nutrition and physical activity behaviours among children. In addition, she is identifying the factors that prevent from implementing healthy school policies and creating healthier environments. The results of her study will provide insightful information for policy-makers to improve the health of BC children

BC Southern Interior Health Services Research Team (BCSIHSR)

The BCSIHSR plans to focus on research to improve the range and quality of services provided to the frail elderly in the Central Okanagan sub-region of Interior Health, where more than 20 per cent of the population is 65 or older. The Team’s research program includes evaluating the costs and quality of services currently provided within Interior Health; developing and implementing an evidence-based decision-making process to reallocate resources among program options; and evaluating outcomes, including quality of care measures. This award funds a program of four workshops to help BCSIHSR develop research capacity, identify research priorities, refine approaches and methods, and prepare funding applications.

Prenatal Alcohol Exposure: Fetal programming, stress responsiveness, and vulnerability to depression and addiction

Women who consume large quantities of alcohol during their pregnancy can deliver babies with Fetal Alcohol Syndrome (FAS) or Alcohol Related Neurodevelopmental Disorder (ARND). Adults with FAS/ARND can exhibit a range of motor, behavioural and neurodevelopmental deficits. They also have higher rates of addiction and depression compared to the normal population. However, the relationship between prenatal exposure to alcohol and these psychiatric conditions is not known. One consequence of prenatal alcohol exposure (PAE) is re-programming of the neural system involved in stress, known as the hypothalamic-pituitary-adrenal (HPA) axis. Activation of the HPA axis during stressful situations is, in the short term, an adaptive response. But prolonged activation or an inability to “shut off” this system can have drastic consequences on brain function and behaviour. HPA dysfunction is implicated in the cause of depression, and activation of this system through stress can influence the initiation and maintenance of, as well as relapse to, drug addiction. Kim Hellemans is exploring how changes in the neural wiring of the HPA through PAE influences behaviours and neuroendocrine function associated with addiction and depression. Early targeting and prevention of psychiatric conditions is a critical goal of health research; the aim of Kim’s research is to determine whether normalizing HPA dysfunction in children with FAS/ARND can prevent their vulnerability to depression and addiction in adulthood.

Molecular Basis of Cancer Cell Invasion

Tumour invasion is the cellular process that initiates the spread of cancer cells from the primary tumour to new sites in a patient’s body (metastasis). Inhibiting this process is important, as solid tumours are much more readily surgically removed if metastasis hasn’t yet occurred. Researchers have identified Dihydromotuporamine C (dhMotC) as a novel tumour invasion inhibitor that may have therapeutic potential. Lianne McHardy is investigating the molecular mechanisms of this compound, focusing specifically on how the protein SNF7 is involved in these mechanisms. SNF7 is normally required for the sorting of intracellular vesicles, which are a basic tool of the cell for organizing metabolism, transport, enzyme storage, as well as being chemical reaction chambers. Lianne will investigate a potential link between the mechanisms controlling vesicle sorting and the invasion abilities of a tumour cell. By pinpointing the mechanisms that allow for metastasis, her studies may aid in the development of dhMotC as a potential drug candidate for metastatic cancers.

Meiotic errors in spermatogenesis: the role of recombination and synapsis in male-infertility and the production of aneuploid sperm

About two per cent of men are infertile due to defects in sperm production. In most cases, the underlying cause is unknown. During sperm production, two similar chromosomes – microscopic bodies that carry heredity DNA – pair up and exchange genetic material in a process called meiotic recombination. Recent studies have shown that recombination rates are significantly reduced in infertile men. Infertile men are also more likely to produce sperm with extra or missing chromosomes (called aneuploid sperm). This aneuploid abnormality is the most frequent cause of miscarriage, and among live births, the most common cause of congenital malformations. Kyle Ferguson is using leading edge technology to determine if and how aberrant recombination causes infertility. He is also investigating the recombination patterns that lead to production of aneuploid sperm. This information will help identify genetic mutations that contribute to male infertility, and may lead to new therapies for the condition.

Mechanistic approaches to androgen-independent prostate cancer

Prostate cancer is the main form of cancer affecting men in the western world. Because cellular mutations within the prostate are regulated in part by androgens (male sex hormones), treatment of prostate cancer usually involves starving the prostate of androgens. While this therapy initially stops cancer progression, over time, the cancer continues to progress. Jennifer Locke is researching why prostate cancer progresses despite the apparent lack of androgens during treatment for the disease. Jennifer is testing the hypothesis that new androgens are produced within the prostate during androgen-deprivation therapy, causing the cancer to reoccur. Using molecular and analytical techniques, she is investigating androgen synthesis pathways. This research could enable identification and evaluation of inhibitors of these pathways, which may lead to new therapeutic options. Her ultimate goal is to improve treatment outcomes and quality of life for prostate cancer patients.

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.

Molecular mechanism of Prp24-mediated U4/U6 formation

Messenger RNA (mRNA) is a single-stranded molecule of ribonucleic acid found in the nucleus of cells that transmits the genetic information needed to produce proteins. This production process involves “splicing” of the mRNA, whereby non-protein coding sections are removed. The splicing process must be precise as errors can result in genetic disease. For example, mutations in BRCA1, which are implicated in some breast cancers, and mutations in SMN2, which cause spinal muscular atrophy, result in defective splicing of their messenger RNA. To minimize mistakes, the cell regulates splicing. However, many of the details of this process are unclear. Dr. Kelly Aukema is studying the molecular mechanisms involved in splicing, using fluorescence resonance energy transfer (FRET) – a cutting-edge technique for measuring interactions between two molecules. She will use FRET to investigate the structural RNA changes of the molecular machinery that carries out splicing. This knowledge should ultimately lead to a better understanding of, and more effective treatments for, splicing-related diseases.

Structural and Functional Studies of Peripheral Components of the Sec Translocase Supercomplex

The delivery of proteins to their correct cellular location is a fundamental aspect of cell biology. For many proteins, reaching a final destination involves crossing membranes, a process known as translocation. Understanding the mechanisms that nature has evolved to translocate proteins across membranes is an important aspect to learning more about the function and dysfunction of this key process. A useful model for studying protein translocation is the evolutionarily-conserved Sec system of Gram negative bacteria (such as E. coli), which exports proteins across and into the inner membrane. The Sec translocase of Gram negative bacteria also serves as the primary conduit for the secretion of virulence factors (toxins and adhesions) in Gram negative bacteria, making it an excellent target for the design of novel antibiotics. David Oliver’s research will expand our understanding of the Sec system and how proteins cross membranes. His work will contribute to improved and possibly novel strategies for protein production for biotechnological and pharmaceutical purposes, as well as to new insights into diseases linked to defects in protein targeting and trafficking.

Optimal use of linked SNP marker data in genetic association studies

Heart disease, diabetes and other complex diseases involve genes that combine with lifestyle and environmental factors to increase disease susceptibility. To find the genetic factors that influence disease outcomes, researchers have begun using haplotypes – sets of closely linked genetic variants inherited together as a unit. However, the use of haplotypes introduces its own complexities, including uncertainty in haplotype measurement, handling of rare haplotypes and the optimal length of haplotypes to examine. By incorporating the genetic relatedness of haplotypes into statistical estimation, Kelly Burkett hopes to address these points to more effectively predict the effects of haplotypes on disease outcomes. The methods will not only enable researchers to identify genetic risk factors but also the connections between genetic and non-genetic factors, such as lifestyle, environmental and occupational risks. The identification of such risk factors is hoped to eventually lead to improved disease treatment and prevention by highlighting new drug targets and lifestyle modifications for those with increased disease susceptibility.