Research Location: University of British Columbia

Transforming community-based primary health care delivery through comprehensive performance measurement and reporting

This award is co-funded by Health Research BC, through CIHR’s Community-Based Primary Health Care (CBPHC) Innovation Teams Grant. 

 

Most Canadians enter the health care system through a visit to a doctor, nurse practitioner or healthcare team based in their communities for the treatment and management of a wide variety of acute and chronic health problems. CBPHC covers a range of services across the continuum of care: primary prevention (including public health) and primary care services; health promotion and disease prevention; chronic disease diagnosis, treatment and management; rehabilitation support; home care and end-of-life care.

 

Although Canada is spending an increasing share of its revenue on healthcare, it is falling behind other industrialized nations in obtaining value for its investment. While Canada has made substantial financial investments in renewing CBPHC over the last decade, no information system exists to routinely capture whether renewal efforts improve CBPHC performance or quality of care in Canada.

 

Dr. Sabrina Wong, a professor in the School of Nursing and Centre for Health Services and Policy Research at the University of British Columbia (UBC) co-led a multi-provincial research program to improve the science and reporting of performance measurement of the primary health care system in Canada.

 

Working with co-PIs, Drs. William Hogg and Sharon Johnston of the Bruyère Institute in Ottawa and Fred Burge at Dalhousie University, the team conducted four studies over the five-year research program using data collected and analyzed from three study regions in British Columbia, Ontario and Nova Scotia with similar socio-demographic characteristics. The aim of their work was to learn how comprehensive performance measurement and reporting could support improvements and innovation in the delivery of primary care services to Canadians, especially populations vulnerable by multiple poor determinants of health.

 

By measuring and reporting on how regions within the health system performs, Wong’s research — the first of its kind in British Columbia and Nova Scotia — provides a foundation to transform the organization and delivery of the Canadian CBPHC system, leading to an enhanced patient experience, improved health outcomes and reduced costs.

End of Award Update – February 2022

Most exciting outputs

The TRANSFORMATION study set out to improve the science of performance measurement in primary health care in Canada. As the project comes to a close, it has demonstrated success in identifying performance measures of significance to patients, clinicians, and policy makers; advancing methods for the collection of patient reported experience and outcome measures; developing health segmentation methods and inter-provincially comparable indicators of primary care performance using health administrative data. Findings have been shared through conference presentations, journal publications, and engagement of policy makers and health region administrators.

 

Impact so far

The study has advanced the use of mixed methods in this area of research. Knowledge translation and the training of graduate and post-graduate students in primary health care research methods has resulted in spin-off projects. The Public Health Agency of Canada has recently funded a project to address vaccine hesitancy through primary care practices using a patient outreach and survey system piloted as part of the Transformation project. In Nova Scotia, the study has informed development of annual surveys of patient health experience required for institutional accreditation.

 

In BC, work completed by TRANSFORMATION on the patient reported experiences and outcomes survey was used to inform the office of Patient Centred Measurement in their work on development of a population-based primary care experiences survey (originally slated to roll out in 2021). This work was also used by Doctors of BC in their development and implementation of a practice-based patient experiences survey. Work completed on using administrative data to formulate population segments informed the work of the BC Ministry of Health in how different segments of the population use primary care services. The work of TRANSFORMATION has also been used by scholars and research students, providing opportunities to publish, present results, and connect with other leading primary health care researchers across Canada.

 

Potential future influence

Learnings from this project are being used to inform development of the patient reported indicator surveys for the Organisation for Economic Co-operation and Development. Knowledge, methods, partnerships and software developed through this project is already increasing the capacity for performance measurement, including by developing supporting infrastructure for a primary care learning health system in Canada.

 

Next steps

Our next stage of work is moving the science, theory, and discoveries from this work, into practice. This work is in progress, including the further development of automated systems to collect data from patients in a timely manner and provide practices with data for near real time QI efforts. In addition, there is interest in integrating data from electronic medical records to support quality improvement and performance measurement in primary health care. Future work will be needed to refine methods for using these measures to influence behaviour – both at the level of primary care patients and practices and at the health policy level.

 

Useful Links

Effects of Adult Aging on Neural Control and Muscle Fatigue

Individuals 65 years of age and older constitute the fastest growing age group in Canada. With natural adult aging, the neuromuscular system (the muscles of the body and the nerves that supply them) undergo degenerative changes that are characterized by reductions in strength and power due to decreased muscle size. This age-related muscle weakness and overall decline in muscle function is referred to as sarcopenia. Sarcopenia not only interferes with tasks as lifting and carrying groceries, navigating stairs, and performing smooth complex movements, it is highly linked to physical disabilities and risk of falls. Sarcopenia is caused by a decrease in the number and function of motor units (MU), which consists of a single nerve branch and all of the muscle fibres it supplies. During the aging process, some of the MUs die off, while other MUs change structurally to compensate. As a result, there are fewer MUs present, but each one supports more muscle fibers. This MU remodeling process is a compensatory mechanism that acts to maintain muscle strength until a critical threshold is reached and strength decreases at an accelerated rate, usually by the eighth decade of life.

To understand the underlying biological mechanisms of MU remodeling, Dr. Brian Dalton is using a technique called single-unit microneurography. This research tool uses tiny electrodes inserted through the skin and into a peripheral nerve to stimulate and record signals from individual MUs. Using this technique, he will measure the integrity of functioning MUs in aged adult volunteers to determine if MU remodeling impairs neuromuscular function and muscle performance in the older adult. This work will help build a more comprehensive understanding of the neuromuscular system, specifically the process of sarcopenia and how it impacts natural adult human aging. The information gained from this study will aid in the design of functional training programs to improve and maintain muscle function — and quality of life — in older adults.

Serotonergic mechanisms underlying sex differences in stress neuroendocrine function

Depressive disorders are a leading global cause of disability. Although the incidence of depressive disorders is two-fold higher in women compared to men, the neurobiological basis for this disparity is unknown. Depressive disorders are often characterized by elevated blood levels of the glucocorticoid steroid hormone, cortisol. In both humans and rodents, females secrete greater levels of glucocorticoids than males in response to stress, which may at least partially explain the increased rates of affective disorders in women.

Dr. Nirupa Goel's research aims to elucidate the mechanisms behind the gender differences in stress responses. Previous studies suggest that deficits in serotonin neurotransmission may be a central cause for the increase in glucocorticoid secretion in depression. Most of these findings, however, come from research using male subjects. A critical first step for Dr. Goel is to identify how serotonin contributes to the gender difference in stress responses. The results of her preliminary studies indicate that blocking the serotonin 1A receptor reduces the glucocorticoid response to stress and that this effect is larger in male than in female rats. In brain tissue from the same animals, there were marked gender differences in stress-induced neuronal activation of the serotonin-producing dorsal raphe nucleus and of forebrain regions that regulate glucocorticoid release.

Based on the strength of her initial findings, Dr. Goel will further examine how stress, gender and serotonin intersect in the brain. To do this, she will measure biochemical markers of serotonin function in male and female rats under basal conditions and in response to repeated stress exposure. She will use serotonin receptor blockers to determine which receptors are involved in the gender differences in stress adaptation. Overall, these studies will elucidate the mechanisms by which serotonin mediates sex differences in stress responses. The findings have realistic clinical implications for discovering individual and sex-based differences in the development and potential treatments of affective disorders.

Pathophysiological contributions of T-type calcium channel variation towards thalamocortical network hyperexcitability and absence epilepsy

More than 50 million people worldwide suffer from epilepsy. Approximately 90 percent of those treated with current drugs experience significant side effects, and around 30 percent do not respond to current medical treatments at all. Therefore, significantly better treatments are required to improve the quality of life for epilepsy sufferers in Canada and worldwide. To achieve this, a far greater understanding of how the brain works both normally and during seizures is necessary.

Epilepsy is a difficult disorder to study in humans; however, in the 1980s, a strain of rats that naturally suffer from a type of seizure very similar to the human condition and involving the same brain regions was identified. These rats are extremely useful in helping us understand the causes of epilepsy in humans and test new drugs being developed to treat epilepsy. Two years ago, Dr. Stuart Cain’s research characterized a newly discovered genetic mutation in the epileptic rat strain responsible for a large portion of seizures. Epileptic seizures can be caused by changes in the way certain brain nerve cell proteins, known as "calcium channels," conduct electricity — the mutation characterized by Dr. Cain alters the way in which a specific type of calcium channel conducts electrical signaling. This was significant as these particular calcium channels are able to generate patterns of electrical pulses, known as “firing patterns,” predicted to contribute to epileptic seizures.

Dr. Cain’s research project aims to determine how the calcium channel mutation alters communication between nerve cells and affects different firing patterns. His laboratory is the only site in North America currently studying the epileptic rat strain. Understanding what causes the firing properties of epileptic nerves to change during seizures should allow the design of new drug treatments with the ability to block these changes directly, and to also reduce side effects compared to many of the broad-target drugs currently used clinically.

Synthetic lethal interactions with cancer CIN genes: investigating potential therapeutic targets

Genetic instability is a hallmark of cancer cells. One type of genomic instability seen in >80 percent of solid tumours is called Chromosome Instability (CIN). Cancer cells can contain mutations in CIN genes, and these genes make the cells more genetically susceptible to mutation than normal cells. Cells with CIN have large aberrations in chromosome structure and/or number, including the gain or loss of chromosomes and chromosomal breaks and fusions. This creates a vulnerability that can potentially be exploited therapeutically to selectively kill these cells. However, because of their nature, mutated CIN genes are difficult to identify directly.

Dr. Melanie Bailey is using RNA interference (RNAi) technology to specifically identify CIN genes of interest. She will be collaborating with Dr. Jason Moffat's laboratory at the University of Toronto to search for genes that pair with known CIN genes and are mutated in spontaneous and rare hereditary cancers. She will also be collaborating with Dr. Phil Hieter's lab at the University of British Columbia (UBC) to test a network of gene pairs previously identified by computer analysis of a public genetic database (BIOGRID) in a human cell line using RNAi.

By combining these approaches, Dr. Bailey expects to identify novel gene pairs that will be further studied using various cell biology and biochemical methods. She hopes that her research will help to better understand how CIN works and that it will provide insight into finding novel ways of killing CIN-mutated cells. Finally, Dr. Bailey will identify inhibitors of the CIN genes through collaboration with Dr. Michel Roberge, whose lab at UBC regularly screens chemical compounds for their inhibitory potential. These inhibitors may represent a viable cancer therapy for the future, as they would be specific for killing CIN-mutated cells.

ATP-sensitive potassium channels: electrical signaling of cellular metabolism

Many types of rare inherited genetic disorders profoundly affect children and their families. While disorders like Anderson syndrome, Bartter's syndrome, and DEND (Diabetes with Epilepsy and Neuromuscular Defects) affect different organ systems and manifest with different symptoms, these diseases are all caused by genetic mutations in the KIR family of proteins. Mutations in KIR proteins can also be involved in less severe symptoms, including cardiac arrhythmias and vascular defects. The KIR proteins are a family of ion channels known as inwardly rectifying potassium channels. These ion channel proteins form pores in cell membranes, which can be switched on or off, by opening or closing “gates” in the ion-conducting pore. When the gates are open, charged ions can pass across the membrane, generating electrical currents and influencing the membrane voltage. These KIR proteins regulate a diverse set of processes, from beating of the heart to hormone release from the pancreas, and can be influenced by a number of cellular processes and molecules.

Dr. Harley Kurata’s work is focused on the KATP channel, which is a member of the KIR family and is regulated by the “fuel” (ATP) that drives all cells. The KATP channel can sense the metabolic state of cells and serves as a critical trigger for insulin release from pancreatic beta-cells. KATP channel mutations are now recognized as an important cause of genetically inherited insulin disorders, ranging from diabetes (too little insulin released) to hyperinsulinism (too much insulin). Dr. Kurata's team hopes that by identifying the specific mutations involved in KATP, therapeutic approaches to both diseases can be developed. KATP channels are also present in the heart, and although their role in cardiovascular function remains enigmatic and controversial, further investigation of this unique set of proteins has the potential to impact other diseases.

Investigating the structure and function of the PIKK family of protein kinase

Many major chronic diseases, including cancer, Type 2 diabetes, and neurodegenerative disorders, are caused by perturbations in the internal communication network of the cells within the body. Signaling molecules, which are an important part of the intracellular communication network, coordinate different processes by relaying signals to switch on or off the proper sets of cellular machineries at the appropriate time. By understanding how these signaling molecules work, scientists hope to understand the molecular basis of different diseases and how to treat and prevent these diseases.

One important group of signaling molecules are the PIKK kinases. PIKK kinases are responsible for regulating cell growth and initiating responses to DNA damage, processes that are often disrupted or exploited in cancer formation and progression. Although recent research has identified the different proteins and protein complexes that PIKK kinases receive signals from or transmit signals to, exactly how these communication events occur at the molecular level remains poorly defined.

Dr. Calvin Yip's research program aims to understand the role of PIKK kinases in cancer progression. He is characterizing the three-dimensional structural and biochemical details of these molecules using an advanced imaging technique known as single-particle electron microscopy. Dr. Yip has obtained the first information on the 3D shape of a signaling complex formed by TOR, a member of the PIKK kinase family. With this foundation, he will use an interdisciplinary approach to combine cutting-edge electron microscopy technology and other biochemical and molecular biology methods to further determine how the TOR signaling complex receives and integrates information and how it sends signals to its targets.

Dr. Yip hopes that by focusing on how TOR and other PIKK signaling molecules carry out their biological activities, he will gain a deeper understanding of the fundamental processes of cell growth regulation. This will help pave the way for the development of new therapeutic approaches against cancer.