School of Nursing Research Laboratory
Our lab fosters interdisciplinary research at the forefront of science by bringing together faculty, postdoctoral scholars and students in nursing in a highly collaborative and progressive research environment.
Founded in 1997 by Janet Pierce, Ph.D., as the first independent nursing laboratory, our lab provides facilities and structure to enable faculty to conduct research and teaching using various models. Our lab supports research to bridge each stage of nursing innovation, from basic science to translational research.
Our goal is to conduct research to help advance the science of nurse researchers working to improve patient care and treatments. Our investigators have successfully translated research discoveries into interventions that improve patient care, including for patients who suffer from deadly forms of heart failure.
Explore some of our publications to learn how we advance interdisciplinary research, promote student growth and cultivate innovative research methods and processes.
Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome in which the patient has a normal or near normal left ventricular ejection fraction. This type of heart disease has a high rate of morbidity and mortality, and patients with HFpEF are often misdiagnosed because they describe symptoms such as dyspnea on exertion that are non-specific. Thus, health care providers have difficulty distinguishing HFpEF from heart failure with reduced ejection fraction (HFrEF) on a clinical basis alone. The optimal treatment for patients with HFpEF should be related to the underlying biologic mechanisms of the syndrome; however, there is an incomplete understanding of the pathophysiology of HFpEF. Researchers propose that one mechanism for the development of HFpEF is reduced myocardial bioenergetics.
Heart failure (HF), the leading cause of morbidity and mortality in the US, affects 6.6 million adults with an estimated additional 3 million people by 2030. More than 50% of HF patients have heart failure with preserved left ventricular ejection fraction (HFpEF). These patients have impaired cardiac muscle relaxation and diastolic filling, which investigators have associated with cellular energetic impairment. Patients with HFpEF experience symptoms of: (1) fatigue; (2) shortness of breath; and (3) swelling (edema) of the lower extremities. However, current HF guidelines offer no effective treatment to address these underlying pathophysiologic mechanisms. Thus, we propose a biobehavioral symptom science study using ubiquinol and D-ribose (therapeutic interventions) to target mitochondrial bioenergetics to reduce the complex symptoms experienced by patients with HFpEF.
Morbid obesity remains the most common cause of high output failure. The prevalence of obesity is growing when two-thirds of American adults already are overweight or obese. Obesity is the risk factor for heart disease and eventually leads to heart failure. High output heart failure is common in obese patients and is characterized by high cardiac output, decreased systemic vascular resistance and increased oxygen consumption. It often occurs in patients with chronic severe anemia, hyperthyroidism, pregnancy, arterial-venous fistulas and liver disease. However, the pathogenesis of obesity-related high output heart failure is not fully understood. The clinical management of obesity-related high output heart failure follows conventional heart failure regimens due to lack of specific clinical recommendations. This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.
Patients with heart failure with preserved ejection fraction (HFpEF) experience fatigue due to impaired myocardial bioenergetics. Cardiomyocyte function depends on the delivery of adenosine triphosphate (ATP), yet there is no convenient bedside method to measure ATP. The purpose of this study was to develop a point-of-contact measurement of ATP that can be used in a clinical setting.
Diastolic heart failure, or heart failure with preserved ejection fraction, is a leading cause of morbidity and mortality. There are no current therapies effective in improving outcomes for these patients. The aim of this article is to review the literature and examine the role of coenzyme Q10 in heart failure with preserved ejection fraction related to mitochondrial synthesis of adenosine triphosphate and reactive oxygen species production. The study results reflect that myocardial energetics alters in diastolic heart failure and that there is defective energy metabolism and increased oxidative stress. Studies are emerging to evaluate coenzyme Q10 , particularly ubiquinol, as a supplemental treatment for heart-failure patients. In diastolic heart-failure patients, clinicians are beginning to use supplemental therapies to improve patient outcomes, and one promising complementary treatment to improve left ventricular diastolic function is ubiquinol. Additional studies are needed using large-scale randomized models to confirm if ubiquinol would be beneficial. Since ubiquinol is an antioxidant and is required for adenosine triphosphate production, clinicians and health scientists should be aware of the potential role of this supplement in the treatment of diastolic heart failure.
Heart failure with preserved ejection fraction (HFpEF) is a significant cardiovascular condition for more than 50% of patients with heart failure. Currently, there is no effective treatment to decrease morbidity and mortality rates associated with HFpEF because of its pathophysiological heterogeneity. Recent evidence shows that deficiency in myocardial bioenergetics is one of the key pathophysiological factors contributing to diastolic dysfunction in HFpEF. Another known mechanism for HFpEF is an overproduction of free radicals, specifically reactive oxygen species. To reduce free radical formation, antioxidants are often used. This article is a summative review of the recent relevant literature that addresses cardiac bioenergetics, deficiency in myocardial bioenergetics, and increased reactive oxygen species associated with HFpEF and the promising potential use of antioxidants in managing this condition.
The symptom of fatigue is prevalent among patients with chronic diseases and conditions such as congestive heart failure and cancer. It has a significant debilitating impact on patients’ physical health, quality of life, and well-being. Early detection and appropriate assessment of fatigue is essential for diagnosing, treating, and monitoring disease progression. However, it is often challenging to manage the symptom of fatigue without first investigating the underlying biological mechanisms. In this narrative review, we conceptualize the symptom of fatigue and its relationship with mitochondrial bioenergetics using the National Institute of Health Symptom Science Model (NIH-SSM). In particular, we discuss mental and physical measures to assess fatigue, the importance of adenosine triphosphate (ATP) in cellular and organ functions, and how impaired ATP production contributes to fatigue. Specific methods to measure ATP are described. Recommendations are provided concerning how to integrate biological mechanisms with the symptom of fatigue for future research and clinical practice to help alleviate symptoms and improve patients’ quality of life.
One of the most important organelles in the body is the mitochondria. It is crucial for generating energy and producing free radicals. Mitochondrial health is essential to the prevention and treatment of diseases. However, cellular or molecular mechanisms such as mitochondrial dysfunction are not adequately addressed in the current essentials of the American Association of Colleges of Nursing (AACN) for all nursing programs. Thus, mitochondrial function content should be incorporated into all nursing curricula that are practice-based. In this article, we will review the anatomy and physiology of the mitochondria (i.e., coenzyme Q10), and the need to include mitochondrial health as a concept in nursing. We will present various diseases/conditions that are affected by mitochondrial dysfunction such as coronary artery disease, diabetes, and aging. In the future, with the expanding advances in the biological sciences, nurses need to learn more about cellular function particularly the mitochondria. Consequently, there should be a new emphasis on mitochondrial health by nurses in education and practice.