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Training Faculty Research Interests

(all faculty listed are potential mentors on this T32)

Chris Baylis, Ph.D.
Physiology & Functional Genomics
baylisc@ufl.edu
NIH Biosketch

Control of renal hemodynamics and blood pressure by nitric oxide and angiotensin II. Angiotensin II excess/ Nitric oxide deficiency and endothelial dysfunction in the pathogenesis of hypertension and progressive renal disease. Sexual dimorphism in the aging kidney. Maternal renal adaptions in normal and hypertensive pregnancies. Current studies are underway using animal models (rats, mice), molecular biology approaches (Western blot, Real time PCR, in vivo siRNA delivery) and morphology (immunohistochemistry, histology).
Role in Training Program: Program director. Mentor.

Behnke, Brad Ph.D.
Applied Physiology and Kinesiology
bjbehnke@hhp.ufl.edu
NIH Biosketch

Research interests include the structural and functional plasticity of resistance arteries within, as well as the regulation of blood flow to, skeletal muscle, adipose tissue and tumors. Current research areas include: 1) effects of prolonged mechanical ventilation on diaphragm perfusion and vascular function, 2) age related alterations in vasomotor regulation in adipose tissue and skeletal muscle, 3) effects of exercise training on tumor perfusion, oxygenation, and mitochondrial function, 4) Collaborative studies on the impact of exercise on kidney function.
Role in Training Program: Mentor.

Barry Byrne, M.D. 
Pediatrics/Cardiology
bbyrne@ufl.edu
NIH Biosketch

Molecular genetics and gene therapy of cardiovascular disease. In the area of cardiomyopathy, we are studying gene replacement in an autosomal recessive form of fatal cardiomyopathy in children. The disease is the prototype of lysosomal storage disorders leading to skeletal and cardiac muscle weakness. We have used AAV vectors to achieve sustained correction of the gene deficiency and correction of the phenotype in natural and transgenic mouse models of the disease. This therapy is currently being proposed for human clinical trials. Similar therapies are being used to combat cardiac transplantation rejection. Secondly, we are investigating the ability of mesenchymal stem cells to undergo myocardial specification for the purpose of tissue repair in the heart. Finally, several projects are focused on the use of AAV vectors injected into striated muscle to achieve sustained release of therapeutic proteins, including thrombolytic factors and coagulation factors. Dr. Byrne is the director of the UF Powell Gene Therapy center.
Role in Training Program: Mentor.

Brian Cain, Ph.D.
Biochemistry & Molecular Genetics
bcain@ufl.edu
NIH Biosketch

The Cain laboratory is interested in the molecular regulation of ion transport in the kidney. The primary focus is on aldosterone-dependent induction of the endothelin-1 (EDN1) gene, and its role in the regulation of acid-base and sodium balance. We discovered that aldosterone stimulates the binding of both the mineralocorticoid and the glucocorticoid receptors to mediate induction EDN1 in renal collecting duct cells. Recently, studies of miRNA action on endothelin-1 expression have been initiated. 
Role in Training Program: Mentor.

Kirk P. Conrad M.D.
Physiology & Functional Genomics
kpconrad@ufl.edu
NIH Biosketch

Research interests are in the following areas: Mechanisms underlying vasodilation and increased arterial compliance during normal pregnancy with emphasis on the hormone relaxin; role of relaxin in bone marrow derived progenitor cell mobilization and function; potential therapeutic role of relaxin in preeclampsia; maternal cardiovascular adaptations to pregnancy in women conceiving by ART, as well as obstetrical and neonatal outcomes; local relaxin ligand-receptor expression and function in arteries of males and females, and the impact on cardiovascular homeostasis in vivo and as a function of aging; decidualization, placentation and placental trophoblast cells, and their involvement in the etiology and pathogenesis of preeclampsia and intrauterine growth restriction (IUGR); and potential first trimester biomarkers for preeclampsia and IUGR.
Role in Training Program: Mentor.

Rhonda Cooper-Dehoff, Pharm.D.
Pharmacotherapy and Translational Research
Division of Cardiovascular Medicine
dehoff@cop.ufl.edu
NIH Biosketch

Dr. Cooper-DeHoff is an expert in clinical pharmacology, pharmacogenomics and clinical trials, with particular focus in the area of hypertension and antihypertensive drugs – both blood pressure response and adverse metabolic responses. She has particular expertise in the pharmacogenomics of thiazide diuretics and beta-blockers. She has had funding and numerous publications in the areas of response and adverse response and pharmacogenomics associations of antihypertensive drugs. Currently, she is M-PI of the hypertension-focused research group within the NIH Pharmacogenomics Research Network (PGRN), with work focused on short-term blood pressure and adverse metabolic responses, along with long-term adverse cardiovascular outcomes and new onset diabetes. She has effectively co-led this collaborative research group, spread over 6 institutions in the US for a decade. She also served as the Director of the International Pharmacy Coordinating Center for the INternational VErapamil Trandolapril STudy (INVEST) which was a network of over 800 research sites in 14 countries. She served successfully in that capacity for more than five years. She has also served as the leader of International Consortium for Antihypertension Pharmacogenomics Studies (ICAPS) since 2012, facilitating and presiding over all consortium activities to date. 
Role in Training Program: Mentor.

David Gilland, Ph.D.
Nuclear and Radiological Engineering
gilland@ufl.edu
NIH Biosketch

The area of specialization is medical imaging, in particular, positron emission tomography (PET) and single photon emission computed tomography (SPECT). Research efforts have included the development of novel instrumentation and image processing algorithms for these imaging modalities. (PET) and single photon emission computed tomography (SPECT). Research efforts have included the development of novel instrumentation and image processing algorithms for these imaging modalities. Ongoing studies include analysis and imaging of the spatial and temporal nonlinear dynamics of hearts during atrial and ventricular fibrillation. In addition, a monitoring method is in development that can detect and quantify bleeding in the abdominal cavity as a consequence of the blunt trauma suffered in motor vehicle accidents.. 
Role in Training Program: Mentor. Member of Program Recruitment and Review committee.

Julie Johnson, Pharm.D.
Pharmacy Practice
Johnson@cop.ufl.edu
NIH Biosketch

Dr. Johnson is an expert in clinical pharmacology and pharmacogenomics, with particular focus on the pharmacogenomics of cardiovascular drugs, particularly beta-blockers, a drug class that she has been working with since the mid-1980’s. She has an extensive record of funding and publication in pharmacogenomics. She is PI of the hypertension-focused research group within the NIH Pharmacogenomics Research Network, with work focused on short-term blood pressure and adverse metabolic responses, along with long-term adverse cardiovascular outcomes and new onset diabetes. She is the chair of the new NHGRI genomic medicine implementation network called IGNITE and is PI of a genomic medicine implementation grant, focused on pharmacogenomics, in that network. She has an extensive track record of training the next generation of scientists, including undergraduate students, for whom she has mentored a minimum of 3 per summer for the last 10 years, graduate students (8 awarded PhD as chair of PhD committee), and postdoctoral trainees (20 total). Most of her PhD and post-doctoral trainees have pursued research careers in academia, with a large number who have been successfully funded, promoted and tenured. Her former trainees include numerous tenured faculty, full professors, a department chair, and the Director of the Office of Clinical Pharmacology, Center for Drug Evaluation and Research, US Food and Drug Administration. 
Role in Training Program: Mentor; Internal Advisory Board.

Michael J. Katovich. Ph.D. 
Pharmacodynamics
katovich@cop.ufl.edu
NIH Biosketch

Investigation of components of the endocrine renin-angiotensin system (RAS) and their effects on hypertension and associated cardiovascular organ damage. We have utilized gene therapy approaches to enhance and/or modify certain aspects of the RAS in order to reduce cardiovascular risks in hypertension and diabetes. We utilize in vivo animal models as well as cell culture to evaluate the physiological, pharmacological and morphological effects of manipulations of the RAS. Currently we are over-expressing components of the RAS such as the AT2R, ACE2 and Ang-(1-7) in models of systemic hypertension, pulmonary hypertension, stroke, and various models of heart disease to determine the “beneficial” effects of these RAS components on various end organs. Utilization of gene therapy and stem cell approaches and classical physiological methods (such as vascular smooth muscle reactivity, in vitro heart perfusion, metabolic studies, cardiac imaging, etc) aid in not only the understanding of the mechanism of actions of existing therapeutic agents but also leads to new innovative therapeutic effects in treating cardiovascular and metabolic diseases.
Role in Training Program: Mentor.

Maureen Keller-Wood. Ph.D. 
Pharmacodynamics
kellerwd@cop.ufl.edu
NIH Biosketch

The research in the laboratory is focused on understanding the normal role of increased maternal cortisol in the pregnant state, and the effects of over- or under-secretion of cortisol in pregnancy on the mother and the fetus. Present studies in the laboratory focus on the effects of increased maternal cortisol on fetal growth and metabolism, fetal cardiac maturation, and fetal adaptation to the stress of labor and delivery, as well as postnatal effects on cardiac function and blood pressure. Current studies use an in vivo animal model (pregnant sheep) with use of telemetry to assess fetal blood pressure, heart rate and ECG over the last month of gestation, a period of rapid fetal growth and cardiac terminal differentiation, and during labor and delivery, as well as during induced perturbations. These are combined with biochemical, molecular and metabolic analysis of the hearts using immunohistochemistry, transcriptomics (using gene array and q-rtPCR), biochemical (mitochondrial function and enzyme assays), and metabolomic techniques. 
Role in Training Program: Mentor.

Eric Krause, Ph.D.
Pharmacodynamics
ekrause@cop.ufl.edu
NIH Biosketch

My laboratory utilizes a systems approach to investigate the neuronal circuits that promote resiliency or susceptibility to stress-related diseases. In particular, we are interested in brain mechanisms that contribute to the co-morbidity of psychopathologies like anxiety and depression with cardiovascular disorders. To this end, we generate mutant mice and deliver agents into distinct brain nuclei to selectively target different neuronal phenotypes and determine their role in promoting resiliency or susceptibility to these stress-related pathologies. Currently, the laboratory is conducting pre-clinical studies investigating oxytocin and angiotensin-related peptides as potential therapeutics for co-morbid anxiety and cardiovascular disorders. 
Role in Training Program: Mentor.

Christiaan Leeuwenburgh, Ph.D.
Department of Aging
cleeuwen@aging.ufl.edu
NIH Biosketch

Senescent aging involves both programmed changes in gene expression and detrimental cellular changes due to oxidative stress, inflammation, glycoxidation products, diminished repair mechanisms and apoptosis. The mitochondria play a key role in regulating cellular oxidative stress and apoptosis due to chronic oxidant production and/or the accumulation of mitochondrial mutations. Apoptosis in tissues occurs with age, but the mechanisms have not been thoroughly investigated. To better understand the role of apoptosis, mitochondrial function and mitochondrial mutations in muscle and the brain we have created mutator mice (Pol-G) and p66sch deficient mouse models. Pol-G mice show an accelerated aging phenotype and p66sch deficient mice show an extended life-span and enhanced resistance to mitochondrial induced apoptosis. Furthermore, in normally aging rats we are examining specific interventions (life-long caloric restriction, dietary interventions, and life-long exercise) which are able to attenuate cellular oxidative stress and apoptosis. If the precise mechanisms underlying age-associated cell loss and cellular deterioration of myocytes and endothelial cells can be identified, it could help allow targeted interventions. 
Role in Training Program: Mentor.

Marian Limacher, M.D.
Cardiovascular Medicine
marian.limacher@medicine.ufl.edu
NIH Biosketch

Research expertise includes cardiovascular risk factors, cardiac disease in women, and clinical outcomes research. She is the PI for the University of Florida Clinical Center for the Women’s Health Initiative (WHI) with access to its large data repositories. She is also Director of the UF CTSI Training and Professional Development Program (TPDP). As Director of the TPDP, she has a key role in overseeing those trainees in the CTSI pre-doctoral and junior faculty programs who are pursuing didactic courses and mentored research. CTSI and other UF trainees have the opportunity to obtain a Certificate or Master’s degree in Clinical and Translational Science. 
Role in Training Program: Mentor.

Alex Lucas, M.D.
Cardiovascular Medicine
alexandra.lucas@medicine.ufl.edu
NIH Biosketch

My research group is investigating immunomodulatory viral serpins and their role in identifying pathways central to inflammatory vascular disease. We are also examining the potential of three viral immune modulating proteins, two serine proteinase inhibitors (serpins) and a chemokine modulating protein. The two serpins, Serp-1 and Serp-2, target highly important but divergent coagulation (Serp-1) and apoptotic/ inflammmasome (Serp-2) pathways. The chemokine modulating protein M-T7 inhibits chemokine to GAG interactions. Serp-1 has recently been successfully tested in a clinical trial of acute unstable coronary disease with stent implants with a demonstrated significant reduction in markers of myocardial damage. We are currently funded as a co-investigator to study vasculitic syndromes secondary to transplant rejection as well as oral pathogens and their role in driving inflammatory aortic plaque growth. We are currently funded as a PI to study the role of chemokine : GAG interactions in transplant vasculopathy. We are extending our current work to look at a new virus derived inflammasome inhibitor and the effects of this protein on vascular disease. We continue to expand our prior studies on the anti-inflammatory serpins in inflammatory vasculitic syndromes, transplant vasculopathy and giant cell arteritis as well as more recent work on viral sepsis and pancreatic cancer models.
Role in Training Program: Mentor.

Paul Oh, Ph.D.
Physiology and Functional Genomics
ohp@ufl.edu
NIH Biosketch

A major part of my research focuses on the elucidation of pathogenetic mechanism underlying human vascular diseases such as hereditary hemorrhagic telangiectasia (HHT) and pulmonary hypertension, and on development of transgenic and knockout animal models for such diseases. We utilize these animal models to evaluate potential therapeutic drugs for their efficacy. As a collaboration project with Dr.Raizada, we are developing a mouse model to test whether overexpression of ACE2 gene in a specific tissue can ameliorate pulmonary hypertension.
Role in Training Program: Mentor.

Carl J. Pepine, M.D. 
Cardiovascular Medicine
pepincj@medicine.ufl.edu
NIH Biosketch

Major research interests focus on the pathophysiology of ischemic heart disease and coronary and systemic vascular hemodynamic mechanisms underlying the disease. Current work includes investigator-initiated clinical trials research. Ongoing studies include optimization of control of blood pressure in coronary artery disease patients which includes genotyping for pharmacogenomics in collaboration with Dr. Julie Johnson. Another project is part of the NHLBI-Women’s Ischemia Syndrome Evaluation (WISE) to investigate vascular function in women with suspected ischemic heart disease. We also have ongoing work in resistant hypertension (RHTN) among CAD patients as well as women with and without IHD. These projects have identified a prevalence of RHTN, its high risk for adverse outcomes including death, and multiple predictors of risk. We also are performing detailed imaging (cMRI) and measures of coronary vascular smooth muscle function (eg, flow reserve with adenosine) and endothelial function (response to acetylcholine), and we have collected DNA on ~800 of these women. The core lab for the coronary flow reserve and intravascular ultrasound (IVUS) data resides at UF. We have developed an animal model for RHTN and have initiated collaboration with the Raizada Lab examining gut microbiota as a mechanism for RTHN.
Role in Training Program: Mentor.

Mohan K. Raizada, Ph.D.
Physiology and Functional Genomics
mraizada@ufl.edu
NIH Biosketch

Elucidation of the cellular and molecular mechanisms involved in neural control of cardiovascular functions with emphasis on the brain Renin-Angiotensin System (RAS). Ongoing areas of investiagtion include: signal transduction mechanism of Ang II-induced Norepinephrine (NE) neuromodulation; mechanisms of Ang II-regulated NE neuromodulation in the neurons of the SHR; gene profiling techniques to identify known and unknown genes that are regulated by Ang-II in the brain and hypertension related genes; lentiviral and adenoviral-vector mediated gene transfer techniques to chronically regulate expression of altered genes in the brain and determine the outcome in cardiovascular functions in hypertensive rats; genetic Targeting of the RAS for the Control of Hypertension.
Role in Training Program: Mentor.

Peter P. Sayeski, Ph.D. 
Physiology and Functional Genomics
psayeski@ufl.edu
NIH Biosketch

Research is focused on the intracellular signaling pathways of angiotensin II with particular emphasis on the angiotensin II-mediated growth effects via increasing the transcription of growth-promoting genes within the nucleus of the cell. Current research is on the angiotensin II mediated activation of intracellular tyrosine kinases such as Jak2, Pyk2, Fak, Fyn and Src. These are the same molecules that have been implicated in certain types of cancers and are also critical for development. Studies are determining the importance of these tyrosine kinases in mediating angiotensin II-dependent growth responses and determining whether the catalytic activity of these tyrosine kinases is altered in disease states. A variety of cellular, molecular, genetic and biochemical techniques are used for these studies.
Role in Training Program: Mentor; Associate PD.

Philip J. Scarpace, Ph.D.
Pharmacology and Therapeutics
scarpace@ufl.edu
NIH Biosketch

Studies are concentrated on age-related obesity and development of leptin resistance. Studies include use of recombinant adeno-associated viral mediated leptin (rAAV-leptin) gene delivery to chronically elevate central leptin in young lean and aged-obese rats. Current studies suggest that although there are initial robust responses to leptin gene delivery, over time lean rats become completely refractory to leptin (endogenous pharmacological administration) independent of obesity. Aged rats demonstrate a more rapid onset of this leptin resistance following leptin gene therapy, yet rats of both ages are fully responsive to downstream activation by alpha-melanocyte stimulating hormone (alpha-MSH) agonist, suggesting the leptin resistance lies within the first order hypothalamic neurons expressing leptin receptors. The primary goal is to determine the mechanisms of leptin resistance in aging which has a major impact in obesity associated cardiovascular disease including hypertension.
Role in Training Program: Mentor.

Debbie Scheuer, Ph.D.
Physiology and Functional Genomics
scheuerd@ufl.edu
NIH Biosketch

The effect of stress and stress hormones on blood pressure regulation by the central nervous system. Central nervous system renin angiotensin aldosterone system mechanisms in blood pressure regulation. Techniques include measurement of blood pressure in conscious rats, measurement of plasma hormones, models to induce acute and chronic stress, microinjection of viral vectors to provide for long-term modulation of neuronal gene expression, chronic delivery of hormones and receptor antagonists to specific brain regions, Real time PCR, immunohistochemistry, tract tracing, radioimmunoassay.
Role in Training Program: Mentor.

Mark Segal, M.D., Ph.D.
Nephrology, Hypertension and Transplantaion
segalms@medicine.ufl.edu
NIH Biosketch

Our focus is in understanding the mechanism of increased risk of cardiovascular disease in unique patient populations, such as women undergoing artificial reproductive technology, patients who suffer from acute kidney injury, and patients receiving erythropoietin. We investigate the role of circulating cells (bone marrow derived angiogenic cells, endothelial colony forming cells, and circulating endothelial cells) in determining vascular health through the use of animal models, cell culture experiments, and translational research.
Role in Training Program: Mentor; Member of Program Recruitment and Review committee

Colin Sumners, Ph.D.
Physiology and Functional Genomics
csumners@ufl.edu
NIH Biosketch

My current work encompasses two major areas. (1) Studies on the role of angiotensin II (Ang II) and other renin-angiotensin system components in the brain in the neural control of blood pressure and neurogenic hypertension. Current topics of study include: Role of angiotensin type 2 receptors (AT2R) in CNS cardiovascular control centers; Anti-inflammatory effects of Ang II/AT2R and angiotensin-(1-7)/Mas in hypertension. (2) Investigations into the beneficial actions of angiotensin peptides and receptors in ischemic and hemorrhagic stroke, with a view to uncovering novel therapeutic avenues. 
Role in Training Program: Mentor.

Nihal Tumer, Ph.D.
Pharmacology & Therapeutics
ntumer@ufl.edu
NIH Biosketch

Research is focused on catecholamines, stress and aging. A fundamental question in aging research is whether aging systems respond and adapt to physiological and pathological challenges as well as younger systems. Catecholamine biosynthesis with age in the rat is an excellent model to study the potential loss of plasticity with age. In the catecholaminergic system, there are a number of changes with age in the steady-state concentrations of various components, and more importantly, there are specific failures in homeostatic regulation. The research addresses mechanisms involved in catecholamine biosynthesis, especially the induction of tyrosine hydroxylase (TH) assessed at the molecular level by determining cAMP-mediated signal transduction with age under normal, exercise training or cold-stress conditions in the adrenal medulla and in the brain. The exact factors contributing to the increase in TH gene expression with age are unknown but may involve some peptides, cholinergic agonists, angiotensin II (Ang II), NPY or various agonists that increase PKA or PKC pathways. 
Role in Training Program: Mentor. Member of Program Recruitment and Review committee

Glenn A. Walter, Ph.D. 
Physiology & Functional Genomics
glennw@ufl.edu
NIH Biosketch

Noninvasive imaging of cell metabolism, structure, and physiology in vivo. Basic biophysical properties related to real time in vivo imaging of organ systems (cardiac, skeletal muscle, brain) and their physiology under both normal and pathological conditions. Advanced techniques in magnetic resonance imaging, optical imaging and spectroscopy, and nuclear magnetic resonance spectroscopy. Expertise in the biology and physiology of muscle regeneration and disease following viral (adeno-, and adenoassociated virus) and cell mediated gene correction. 
Role in Training Program: Mentor.

David Weiner, M.D.
Nephrology, Hypertension & Transplantation/Medicine
weineid@ufl.edu
NIH Biosketch

Acid-base homeostasis, ammonia metabolism and transport in the kidneys, liver, CNS and intestinal tract, mechanisms and regulation of proton and bicarbonate transport, regulation of expression of the ammonia transporter family members, Rhbg and Rhcg, and the role of glutamine synthetase in renal ammonia metabolism. Other interests examine the evaluation and management of primary aldosteronism in patients with refractory hypertension. 
Role in Training Program: Mentor.

Charles Wingo, M.D.
Nephrology, Hypertension & Tranplantation/Medicine
cswingo@ufl.edu
NIH Biosketch

Molecular regulation of transporters in the collecting duct that determine final renal excretion of solutes and water and thence control of body fluid homeostasis and blood pressure. Particular emphasis is on Na+ and K+ regulation and current work is focused on interactions between aldosterone and endothelin in the IMCD, control of level and activity of Na+, H+- and K+-ATPases.
Role in Training Program: Mentor.

Charles E. Wood, Ph.D.
Physiology and Functional Genomics
woodc@ufl.edu
NIH Biosketch

The research performed in the Wood laboratory is focused on the mechanisms controlling the responses to stress (hypoxia and hypotension) in the fetus in utero and on the mechanisms controlling the timing of birth. This laboratory has published research results which have played a leading role in elucidating the function of the fetal arterial baroreceptors and chemoreceptors in the control of fetal cardiovascular and endocrine function. Other research performed in this laboratory has identified the cardiovascular neural receptors which are involved in the integrated cardiovascular and endocrine response to alterations in blood gases and blood pressure in the fetus.

Present work in this laboratory focuses on three projects: 1) the role of glutamatergic signaling in response to hypoxia and hypercapnia in the upregulation of neuroinflammation and apoptosis in the fetal brain; 2) the influence of estrogens on the fetal brain regions which are important for cardiovascular and endocrine responsiveness to stress; and 3) the biological consequences of exposure to endocrine disruptors during pregnancy.

This laboratory has reported that prostaglandins generated within the fetal brain exert a profound influence on fetal reflex responsiveness to stress. The fetal response to hypotension, for example, is partially blocked using an inhibitor of prostaglandin biosynthesis. Hypotension stimulates the biosynthesis of the inducible form of the enzyme critically important for prostaglandin biosynthesis, cyclooxygenase-2 (COX-2), within the pathways in the fetal brain which impinge on the paraventricular nucleus, which sits at the head of the HPA axis. The expression of COX-2 is dependent on the activity of NMDA-mediated glutamatergic neurotransmission. Blockade of NMDA receptors blocks the upregulation of COX-2 and greatly downregulates the neuroendocrine response to fetal stress. Application of genomics and systems biology techniques has revealed that the COX-2 is but one part of an inflammatory cascade in the fetal brain that is associated with apoptosis. We are currently investigating whether blockade of NMDA receptors with ketamine and other clinically-relevant drugs can reduce damage within the fetal central nervous system after hypoxic insult.

We have discovered that estradiol, circulating in fetal plasma in late gestation, is a critical component of the mechanisms controlling fetal stress responsiveness and the timing of birth in sheep. Increases in fetal plasma estrogen concentrations augment fetal hypothalamus-pituitary-adrenal axis activity, augmenting the neuroendocrine systems that are critical for fetal survival of stress and that initiate and support parturition. We are currently investigating the role of sulfoconjugated estrogens as endogenous prohormones, and that they play an important role in the determination of the vigor of the fetal stress response and that they are involved in the timing of birth.

Fetal estrogen activity is altered by various endocrine disruptors in the environment. We are funded to investigate the role of triclosan, an organochlorine added to personal care products as an antibacterial agent, as an endocrine disruptor in pregnancy. Specifically, we have found that triclosan potently inhibits estrogen sulfotransferase (SULT1E1), and we are actively investigating whether it alters estrogen bioavailability in the fetus or mother.

All of these studies, which are funded on multiple extramural grants, interrelate to each other and will provide a mechanistic understanding of fetal neuroendocrine and cardiovascular stress responses.

Role in Training Program: Mentor. Member of Internal Advisory Board.