Chronic obstructive pulmonary disease (COPD) is a lung condition that affects more than 75,000 British Columbians. People with COPD have a shortness of breath, chronic cough, and can experience difficulties with the activities of daily life, such as showering, walking, and social activities. Many people with COPD have regular flare-ups, or exacerbations, of their lung condition. These exacerbations result in a severe shortness of breath and overall weakness and fatigue and sometimes lead to long hospital stays. These flare-ups and long hospital stays can cause severe problems with activity tolerance, which then further increases the risk of future flare-ups.
The objective of Dr. Pat Camp's research program is to investigate how physical activity can improve the health outcomes of people who are hospitalized with a COPD flare-up. This research program will include a systematic literature review to summarize the current state of knowledge, validating tools to measure activity in hospitalized COPD patients, and determining if exercise programs for hospitalized patients can improve their quality of life and health outcomes. In addition, Dr. Camp's research program will include projects that incorporate patient input about what activities are important to them, which will indicate the level and type of activity that is necessary in order for these patients to be discharged safely from the hospital.
By developing a thorough understanding of how exercise leads to increased health in COPD patients, this research program aims to improve the quality of life and overall health of patients hospitalized with acute COPD flare-ups. Future work will extend these innovations to other chronic lung disease populations, such as patients with lung transplants or interstitial lung disease.
The purpose of this project is to generate new knowledge that will foster understanding of what constitutes safe nursing care in acute care settings for people who are experiencing problematic substance use and social disadvantage. The target audience will be practicing nurses who provide care to people experiencing substance use, as well as health care administrators, nursing leaders and policy makers. The key research question is: What is culturally safe care from the perspective of patients and nurses in acute care settings and what supports the delivery of culturally safe care?
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Asthma is a serious global health problem, affecting over 300 million people worldwide. The disease is predominantly an inflammatory disorder of the conducting airways, and can be treated or controlled using current therapies. However, un-controlled asthma leads to continual inflammation and damage, resulting in permanent scaring which is termed airway remodeling. Airway remodeling can be defined as changes in the composition, content and organization of cellular and molecular constituents of the conducting airways. One of the structural changes that occurs as a result of airway remodeling is detachment of the cells that line the surface of the airways, called the epithelium. In normal airways, the epithelium forms a barrier against the inhaled external environment which includes aero allergens, viruses and particulate matter, through the formation of apical junction complexes (AJCs). In asthma, part of the abnormal response to inhaled allergens is thought to be due to impaired barrier function caused by damage to the airway epithelium and loss of AJCs. Emerging evidence suggests that AJCs are able to influence other aspects of epithelial function such as release of inflammatory mediators and mechanisms of epithelial repair. Building on earlier work in this area, Dr. Tillie-Louise Hackett’s current research is designed to determine whether AJCs play an important role in normal airway epithelial repair and if the mechanisms involved are altered in asthmatic patients. The results of her research will provide scientists and clinicians with a better understanding of the pathological mechanisms that contribute to multiple respiratory diseases. In addition, Dr. Hackett’s findings will open avenues for the development of new therapeutics to improve the lung health of Canadians living with obstructive lung diseases, such as asthma and Chronic Obstructive Pulmonary Disorder.
Chronic diseases represent an increasing burden for both the patient and healthcare system. Many people also now have more than one chronic disease. For those people with chronic diseases living in rural areas, the risk for hospitalization is more than 60% greater. These patients and their primary care providers face an enormous challenge in meeting their day-today health needs that patients with chronic diseases have.
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Asthma is the most common chronic disease in childhood and continues to increase in prevalence in adults. Every day, lung airways are subjected to challenges that damage their lining, known as the epithelium. The accumulation of damaged epithelium is a common and consistent feature in those with asthma, suggesting that asthmatics are more susceptible to damage, or are less able to repair the epithelium, than people without asthma. While the epithelium normally protects the underlying tissue from noxious particles, epithelial damage may account for airway hyper-reactivity in asthma, and the chronic nature of the disease. Previously supported by an MSFHR Scholar award, Dr. Delbert Dorscheid is researching the role of glycosylated proteins – proteins that have a sugar or sugar chain added to them – in epithelial repair. These proteins appear on the surface of cells that mediate repair, and their formation heralds the start of cell repair. Dorscheid has identified a specific protein that’s linked to the beginning of this process. His goal is to observe any changes in the modification and regulation of this receptor in asthmatic airways and healthy airways, and determine how this may influence injury and repair of the airway. The overall objective is to better understand the differences in asthmatic airways to develop new treatment strategies to improve the quality of life of those who suffer from this disease.
Chronic inflammatory airway diseases include asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF). Together, these conditions contribute to an enormous burden of death and disability worldwide. It’s estimated that 10 to 15% of 13- to 14-year-olds in Canada are asthmatic. COPD affects close to half a million Canadians 35 and older, currently ranking 12th worldwide as a cause of lost quantity and quality of life and projected to rank 5th by the year 2020. CF is the most common, fatal genetic disease affecting Canadian children and adolescents.
There is compelling evidence supporting a hereditary pattern to virtually all of the major inflammatory diseases. For example, more than 1,000 CF-causing gene mutations have been identified. Although some mutations are associated with less severe disease, patients possessing the same mutations often show great variation in disease severity and progression. Significant advances in molecular genetics make it possible to discover the specific genetic variants that determine individual susceptibility to these illnesses.
Dr. Andrew Sandford is investigating the genetic variants that cause susceptibility to asthma and COPD. He is also focused on the role of genetics in CF. He works with a unique group of patient families who have previously been involved in studies to establish the associations between their genetic variations and their disease symptoms. A better understanding of the causes of inflammatory airway diseases will contribute to better prevention and/or intervention measures and more efficient treatment strategies.
Hypertension (high blood pressure) has a direct link to aging and is a major risk factor for atherosclerosis (narrowing and hardening of the arteries over time), stroke, heart attack and chronic renal failure. All known cardiovascular diseases, including hypertension, have in common a disease called endothelial dysfunction. The endothelium is a layer of cells that line the cavities of the heart, as well as the blood and lymph vessels. With endothelial disease, these cells do not function as well. Aging is known to induce and aggravate endothelial dysfunction, suggesting that endothelial dysfunction is unavoidable. One of the hallmarks of endothelial dysfunction is a decrease in the synthesis and availability of nitric oxide, which promotes dilation or relaxation of the blood vessels. Under normal conditions, nitric oxide significantly contributes to resting vasodilator tone and works to maintain a smooth and healthy vascular endothelium.
Dr. Pascal Bernatchez has uncovered a novel molecular approach that increases endothelial function and nitric oxide availability in aged vessels, while young vessels remain unaffected by the intervention. This suggests that there may be a molecular cause for how endothelial dysfunction develops. Bernatchez’s research will contribute to knowledge about how this approach restores endothelial function in an age-specific manner, how it regulates blood pressure and how endothelial dysfunction occurs. The findings may lead to novel therapeutic avenues for the range of cardiovascular diseases characterized by endothelial dysfunction.
Although heart disease is a leading cause of death for men and women, sex/gender differences in the disease have only recently received attention. Evidence suggests there are sex/gender differences relating to prevalence, presentation, diagnosis, treatment and outcomes of heart disease, but little is known about the underlying causes. An emerging area of interest is the fact the magnitude of the sex/gender difference in outcomes following a heart attack (favoring men) is much greater among younger women and men than among older patients. Research in this area suggests that this difference persists even after adjusting conventional risk factors.
A leading investigator in the area of cardiac health outcomes, Dr. Karin Humphries has found in previous research that among women and men with chest pain but no evidence of heart disease, women’s outcomes are worse. Now she is focusing on two primary questions: why these women have worse outcomes than men, and what is the relevance of non-traditional risk factors, such as quality of life and psychosocial factors, in young women and men who present to hospital with a heart attack. The results of these studies will provide new knowledge about sex/gender differences and heart disease. Humphries aims to increase understanding of quality of life differences between young men and women who suffer a heart attack, which may help explain the different outcomes and help with the development of new strategies for diagnosis, treatment and support of women with heart disease.
Atherosclerosis, also known as hardening of the arteries, is a common vascular disease caused by the buildup of a waxy plaque on the inside of blood vessels. This narrowing of blood vessels can cause blood clots, leading to heart attack or stroke. In almost half of all heart transplant patients, an accelerated form of hardening of the arteries, known as Transplant Vascular Disease (TVD), occurs in the transplanted heart. In fact, TVD is a leading cause of death one year after transplantation. The exact mechanisms behind this process remain unclear. Blood vessels are lined with endothelial cells, specific cells that create a barrier between blood and the artery. An important factor in TVD is damage to endothelial cells. This damage increases the size of gaps between cells, allowing fats to accumulate in artery walls. One protein that causes endothelial “”leakiness”” is called Vascular Endothelial Growth Factor (VEGF). VEGF is also important in many other serious diseases, such as cancer and degenerative eye diseases. David Lin is expanding on previous research that showed that VEGF is increased in the muscle cells in arteries of transplanted hearts. He is studying in detail the mechanisms by which VEGF alters the function and structure of endothelial cells. By learning how VEGF works in transplanted hearts, Lin hopes his research will lead to the development of new ways to maintain the health of heart blood vessels following transplantation.
A heart that has become enlarged in response to a pressure overload, such as with high blood pressure, has reduced function compared to a normal heart. This impaired function is particularly apparent during and after interruption of the blood supply, which can occur when a blood clot blocks a diseased coronary artery, or during open heart surgery. This reduced heart function can be very dangerous for the patient. Enlarged hearts use glucose to a greater extent than normal, a situation that appears to contribute to their exaggerated dysfunction. The mechanisms responsible for the accelerated utilization of glucose in enlarged hearts are not yet known. Dr. Minnie Dai was previously funded by MSFHR for her doctoral training. Currently, she is working to determine the mechanisms behind accelerated rates of glucose utilization in enlarged hearts. Using molecular biology techniques, she will selectively and specifically alter the activity of potentially relevant proteins in order to determine their role in causing accelerated glucose utilization. Her studies are unique in that the activity of proteins will be altered at specific times and will be altered only in the heart – ensuring that changes observed are truly related to alterations in these proteins. Many people suffer ill health because of an enlarged heart. By understanding the mechanisms responsible for their accelerated use of glucose, researchers may be able to identify targets for the development of drugs designed to altered glucose use by enlarged hearts, thereby improving their function.