Education and Career Development
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The awardees are listed below, including a short description of their research and their assigned mentors:
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| Wang L. (Steve) Cheung, MD, PhD - Assistant Professor, Department of Pathology |
Wang L. (Steve) Cheung, MD, PhD
Assistant Professor, Department of Pathology
Mentors:
Kevin Raney, PhD
Professor and Chair, Department of Biochemistry and Molecular Biology
Alan Tackett, PhD
Associate Professor, Department of Biochemistry and Molecular Biology
Director, UAMS Proteomics Facility
Research Study:
Although melanoma only accounts for 4% of skin cancer, it is responsible for 79% of skin cancer related death. Part of the problem is that we do not understand the pathogenesis of melanoma. To understand the pathogenesis, we are studying the changes in protein expression and epigenetic changes that occur between early and late stage of melanoma. To this end, we are dissecting these lesions from archival melanoma samples (i.e. formalin fixed paraffin embedded tissues) and utilizing mass spectrometry to identify the proteomic and epigenetic markers. Then we will examine whether these markers have prognostic or diagnostic utility in a retrospective studies using clinical specimens.
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| Holly Felix, PhD Assistant Professor, Department of Health Policy and Management, College of Public Health |
Holly Felix, PhD
Assistant Professor, Department of Health Policy and Management, College of Public Health
Mentors:
Delia Smith West, PhD
Professor, Department of Health Behavior and Health Education, College of Public Health
Director, Center for the Study of Obesity
Cornelia Beck, PhD, RN, FAAN
Professor, Department of Psychiatry and Behavioral Sciences, College of Medicine
Glen P. Mays, PhD, MPH
Professor and Chair, Department of Health Policy and Management, College of Public Health
Research Study:
Obesity is a public health problem with more than 66% of US adults overweight or obese. Obesity rates among community-dwelling older adults (≥65 yrs) are particularly high and increasing rapidly. These trends are alarming considering individual and societal impacts of obesity. Given the rising rates of obesity among the elderly, the increasing number of elders in the US population, and the association between obesity, disability and nursing home placement, it is probable that many obese elders are in or will soon be in nursing homes. Given the differences in health care needs, use and quality of care received in medical settings by obese persons, it is probable that obese elders receive poorer quality long-term care (LTC) than non-obese elders. It is, therefore, imperative to begin exploring the association between obesity and LTC outcomes. The overall goal of this project is to examine the impact of obesity among the elderly on the delivery of LTC that can guide the development and evaluation of policy and programmatic interventions targeting the elderly and the LTC system to promote high quality of care with reduced health disparities.
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| Dennis Kuo, MD, MHS Assistant Professor, Department of Pediatrics |
Dennis Kuo, MD, MHS
Assistant Professor, Department of Pediatrics
Mentors:
Mary Aitken, MD, MPH
Professor, Department of Pediatrics
Patrick Casey, MD
Professor, Department of Pediatrics
Research Study:
Dr. Kuo’s research plan will generate important knowledge and understanding about children with medical complexity and their families. Children with medical complexity (CMC) are the highest resource utilizers within the group of children and youth who have special health care needs (CYSHCN). The typical CMC has medical technology dependence, multiple specialty care needs, and therapy and educational requirements. This important group of children is growing in number due to advances in hospital health care and medical technology. Optimal medical management of CMC in the community setting will maximize their growth and development. Such management may also reduce overall medical costs by preventing excess inpatient admissions and emergency room use. The proposed research consists of two studies. The first study is a multi-institutional survey of families of CMC that describes family needs and their expectations of care in the primary care setting. The second study creates a full profile of CMC health service use across multiple settings, identifying reasons for specific outpatient and inpatient health service visits. The results will be used to translate optimal models of chronic care for CMC into the community setting.
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| Sundararaman Swaminathan, MD Assistant Professor, Internal Medicine |
Sundararaman Swaminathan, MD
Assistant Professor, Internal Medicine
Mentors:
Sudhir Shah, MD
Professor, Internal Medicine
Director, Nephrology Division
Robert E. McGehee, Jr. PhD
Professor, Department of Pediatrics
Dean, Graduate School
Research Study:
Diabetes has reached epidemic proportions and worldwide 170 million patients are affected. Increased body iron stores, catalytic iron, and dietary heme intake have been implicated in the pathogenesis of diabetes mellitus and its complications. CD163+ macrophages play a central role in both heme and iron metabolism via the heme oxygenase-1 (HO-1)-H-ferritin-ferroportin pathway and also via the hepcidin-ferroportin pathway. Ferroportin is the only known iron-export protein in the body. The role of the CD163 scavenger receptor pathway and its downstream components in obesity, adipose tissue fibrosis, insulin resistance, and diabetes-related complications has never before been examined. We recently made a novel observation that CD163+ macrophages secrete collagen and that high glucose induces development of collage-secreting CD163+ macrophages expressing angiogenic markers from human peripheral blood mononuclear cells (PBMC) in vitro. This effect is further augmented with low doses of angiotensin II (AT-II). This mechanism leading to iron excess may be crucial to the initiation of diabetes based on data demonstrating that inflammatory mechanisms via adipose tissue recruitment of CD163+ macrophages play a central role in the pathophysiology of insulin resistance, diabetes, and its complications. Preventing macrophage infiltration ameliorates insulin resistance, atherosclerosis, and glomerular changes of experimental Type 2 diabetes in mice. Our overall hypothesis is that there is increased infiltration of collagen-secreting CD163+ macrophages in adipose tissue, pancreas, and kidney in insulin resistance and diabetes. Consequent activation of the CD163-HO-1-ferritin-ferroportin pathway would result in iron accumulation, oxidative stress, and progressive organ damage that facilitates a phenotypic spectrum characteristic of diabetes. Novel therapeutic strategies that inactivate this pathway such as recombinant hepcidin, targeted interruption of the CD163 pathway, or chelating iron exported by this pathway would prevent the entire phenotypic spectrum of diabetes.
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