Organ systems

Dr. Leslie V. Farland is a reproductive epidemiologist in the Department of Epidemiology and Biostatistics at the Mel and Enid Zuckerman College of Public Health. She has training in biology (AB; University of Chicago) and reproductive epidemiology (MSc, ScD; Harvard T.H. Chan School of Public Health). Prior to joining the faculty at UofA, she was an Instructor in the Department of Obstetrics and Gynecology at Harvard Medical School and served as the Director of Epidemiologic Research at the Center for Infertility and Reproductive Surgery at Brigham and Women's Hospital. Her current research portfolio capitalizes on her training and focuses on three major themes: i) the intersection between women’s reproductive health and chronic disease risk, ii) etiology and risk factors for reproductive and gynecologic diseases and iii) disparities in infertility care and fertility treatment utilization.

Stern lab research aims to understand the role of glucagon signaling in the pathogenesis of obesity, type II diabetes mellitus, and aging. Glucagon Signaling in Obesity and Type II Diabetes: Insulin resistance and elevated insulin are key to the metabolic disturbances in type II diabetes mellitus (T2DM). Yet, elevated glucagon, common to diabetes, may be equally important in the metabolic abnormalities in T2DM. Dr. Stern has shown that nutritional state differentially affects glucagon secretion in obesity. In turn, the glucagon:insulin ratio is dysregulated in obesity. Current Stern lab research aims to understand the metabolic consequences of a dysregulated glucagon response to fasting and re-feeding. Glucagon Signaling and Aging: More than 25% of the U.S. population greater than 65 years old has Type II diabetes mellitus, representing the highest prevalence of diabetes of any age group. Most research aimed at understanding the consequences of obesity in aging have focused on insulin and downstream signaling cascades, overlooking a potential role for glucagon. Given that many prominent diabetes treatments target glucagon or glucagon signaling pathways, it is essential to understand the role of glucagon in aging. Stern lab research examines 1) the tissue specific effects of glucagon signaling, 2) the role of glucagon signaling in obesity-accelerated aging, and 3) the role of glucagon signaling in healthspan extension promoted by calorie restriction. This work will close a significant gap in our understanding of how glucagon alters aging, while allowing us to assess the potential risks associated with inhibition of glucagon signaling. Other Stern Lab Research Foci: Sleep disturbance and metabolic dysfunction Obesity related cancer development and progression

Fragile-X syndrome, which includes mental and physical defects and is the most common form of inherited mental retardation. Keywords: Neurodegeneration, ALS, Aging

Dr. Jennifer Teske, PhD is an Assistant Professor in the Department of Nutritional Sciences. Her primary research interest is the study of the metabolic consequences of environmental noise stress as it relates to the whole-organism stress response and human health.

Sean W. Limesand, PhD, is an Associate Professor in the School of Animal and Comparative Biomedical Sciences at the University of Arizona in the College of Agriculture and Life Sciences. He is also a member of the UA’s BIO5 Institute and Department of Obstetrics and Gynecology. Dr. Limesand is nationally and internationally recognized for his work studying fetal endocrinology and metabolism in pregnancy and in pregnancies compromised by pathology such as intrauterine growth restriction and diabetes. His research is focused on defining developmental consequences resulting from a compromised intrauterine environment. Specifically, he is focused on fetal adaptations in insulin secretion and action that when altered in utero create lifelong metabolic complications. Dr. Limesand has lead the charge on prenatal origins of –cell dysfunction as the Principal Investigator for a number of federal and foundation grant awards and published more than 40 peer-reviewed articles on topics related to this research. Keywords: Diabetes, Pregnancy, Perinatal Biology

I am a senior research scientist and oversees medicinal chemistry research at BIO5 Institute's drug discovery initiative. I oversee group of medicinal chemistry involved in the development of small molecule therapeutics for idiopathic pulmonary fibrosis (IPF), neuropathic pain, acute lung injury and cancer. I am co-founder of Reglagene and Regulonix - two biotech companies with startup technology from the University of Arizona. I have 15 years' experience in medicinal chemistry with expertise in translational drug development. I am also a co-inventor of small molecules targeting hTERT and MYC for the treatment of glioblastoma, melanoma, lymphomas and prostate cancer. Our work in the area of neuropathic pain has led to successful funding from Tech Launch Arizona and will result in STTR funding from NIH.

Janet L. Funk, MD, FACP, is a Professor of Medicine at the University of Arizona College of Medicine. Dr. Funk leads a federally-funded research team that is focused on identifying new treatments for chronic diseases that have strong inflammatory components, including metabolic bone diseases, such as arthritis, bone tumors and osteoporosis, and cardiovascular diseases, including diabetes. Recent studies have focused on the use of medicinal plants that have historically been used to treat inflammatory conditions, such as arthritis. By understanding whether and how these plants work in blocking inflammatory pathways in the body, we are striving to harness the power of nature and the wisdom of our ancestors to indentify new treatments for diseases that are common in our modern society. Discoveries we have made at the lab bench have allowed us to move forward into the clinics, building upon the old to discover the new.

Dr. Thomas Doetschman, PhD, Biochemistry & Biophysics, University of Connecticut, has been involved in cardiovascular research for over a decade through investigations into the cardiovascular roles of the three TGFβ ligands and FGF2 ligand isoforms in genetically engineered mice. These mice have determined that TGFβ2 plays major roles in heart and vascular development and for maintenance of valvular and large vessel integrity in the adult and that both the TGFβ1 and FGF2 are involved in adult heart disease.His work has also demonstrated roles of TGFβ in cancer and immunology. He found that a major function of TGFβ1 is to inhibit autoimmunity and to establish homeostatic balance between immune regulatory and inflammatory cells. He has shown that an imbalance in the latter is critical in the tumor suppressor function of TGFβ in the colon.Dr. Doetschman has also played an important role in the development of the mouse genetic engineering field. He has been responsible for the establishment of 3 mouse genetic engineering facilities, in Cincinnati OH, Singapore and the University of Arizona’s BIO5 Institute. Keywords: "Cancer", "Microbiome", "Mouse Genetic Engineering", "Connective Tissue Disorder"

Thomas Davis, PhD, and his lab continue its long-term CNS biodistribution research program, funded by NIH since 1981, by studying the mechanisms involved in delivering drugs across the blood-brain barrier to the C.N.S. during pathological disease states. Recently, Dr. Davis and his lab discovered specifica drug transporters which can be targeted to enhance delivery. They are also interested in studying the effect of hypoxia/aglycemia/inflammatory pain on endothelial cell permeability and structure at the blood-brain barrier. Dr. Davis has recently shown that short-term hypoxia/aglycemia leads to significant alterations in permeability which can be reversed by specific calcium channel antagonists. This work has significant consequences to the study of stroke. Additionally, he has discovered that peripheral pain has significant effects on BBB tight junction protein cytoarchitecture leading to variations in the delivery of analgesics to the CNS.

Clara Curiel-Lewandroski, PhD, is the director of the Pigmented Lesion Clinic and Multidisciplinary Cutaneous Oncology Program, both part of the University of Arizona Cancer Center Skin Cancer Institute. She completed two research fellowships, the first in the Department of Dermatology at Harvard Medical School, and the second at the Ludwig Boltzman Institute and Immunobiology of the Skin at Miinster University in Germany. Dr. Curiel is certified by the American Board of Dermatology.Dr. Curiel-Lewandroski’s research focus is on melanoma chemoprevention, early detection of melanoma, cutaneous T cell lymphomas and skin cancer. She studied the extended use of non-steroidal anti-inflammatory drugs, particularly aspirin, and their ability to possibly decrease the risk of cutaneous medanoma (CM) development. CM is responsible for more than 77 percent of skin cancer deaths.