COM Participating Faculty
College of Medicine – University Scholars Program
Yenisel Cruz-Almeida, MSPH, PhD
Aging & Geriatric Research, Neuroscience, Community Dentistry & Behavioral Science
My research examines the neural mechanisms in humans accounting for the interactions between pain, cognition and physical function in older adults. We have ongoing research studies in older adults with and without pain using neuroimaging and sensory psychophysics.
Stephen Anton, Ph.D.
- Aging and Geriatric Research
- firstname.lastname@example.org or (352) 273 – 7514
I am interested in the role that lifestyle factors and natural compounds may have in influencing biological mechanisms related to the aging process, as well as age-related metabolic diseases.
Thomas W. Buford, Ph.D.
Department of Aging and Geriatric Research
The main emphasis of our lab is in conducting clinical and translational research dedicated to preserving the health and independence of older adults. Broadly, our work centers around identifying factors which contribute to the onset of age-related physical disability and subsequently identifying novel interventions to rehabilitate older adults with functional impairments and prevent disablement. We strive to work collaboratively to conduct high-quality studies in an attempt to improve quality of life for older adults. Integral to our work are the principles of exercise and skeletal muscle physiology, yet we also incorporate a variety of other discplines – including pharmacology, genetics, and cardiovascular physiology. Currently, we are 1) investigating sources of heterogeneity (independent of adherence) in older adults’ functional responses to exercise, and 2) seeking to identify novel adjuvant therapies or alternative paradigms to improve the efficacy of physical exercise for improving functional status among older adults.
Christy S. Carter, Ph.D.
Assistant Professor, Department of Aging and Geriatric Research
TEL: (352) 273-5727 / e-mail: CCarter@aging.ufl.edu
Dr. Carter’s research focuses on the development of preclinical rodent models for assessing the efficacy of preventative treatments for age-related physical and cognitive decline. These interventions include diet, exercise, as well and nutritional and pharmaceutical approaches.
David Clark, Sc.D.
Aging and Geriatric Research, Institute on Aging and Brain Rehabilitation Research Center, Malcom Randall VA Medical Center.
(352)376-1611 x5244 or email@example.com
My research examines how the neural control of walking is affected by aging and/or by neurological injury. A variety of physiological assessments are used in my research, including electromyography (neuromuscular activity), functional near infrared spectroscopy (brain activity) and biomechanics.
Manfred Diehl, Ph.D.
- Assistant Professor in the Institute on Aging, Department of Health Policy and Epidemiology; Joint appointment in the Department of Psychology
- Phone: (352) 265-0680, ext. 86542; E-mail: firstname.lastname@example.org
My work is in two main areas of aging research. First, my work focuses on how personality contributes to successful aging and psychological well-being in old age. In this area, I have conducted studies on adults’ coping strategies, their self-concept, and on the connections between personality traits and the pursuit of personal goals in everyday life. Recently, I have also started to focus on adults’ cognitive representations of their illness as a factor in adaptation to chronic illness. Second, I conduct work in the area of applied cognitive research. Specifically, I am interested in the cognitive abilities that influence older adults’ medication taking behavior and their adherence or non-adherence to their medication regimen. In addition, I am interested in how older adults’ beliefs in their own efficacy can be used in training programs to alter their fear of falling.
Christiaan Leeuwenburgh, Ph.D.
Department of Aging and Geriatric Research
TEL: (352) 273-5735, email@example.com
Dr. Leeuwenburgh’s major research focus is to better understand the molecular mechanisms of programmed cell death (apoptosis), mitochondrial bioenergetic failure with age, mechanisms of oxidative stress and inflammation with age. The Biochemistry of Aging laboratory investigates transgenic mice, uses rodent models for intervention studies and he directs several funded clinical translational studies on humans. In these later studies, he conducts research on the role of apoptosis in the loss of human skeletal muscle with age and its role in human frailty, specifically on low and high functioning older adults.
Todd Manini, Ph.D.
Assistant Professor, Department of Aging and Geriatric Research
firstname.lastname@example.org TEL: 352-273-5914
Seeking highly qualified candidates to complement a National Institutes of Health (NIH) funded project investigating how aging changes the way people use energy to perform common daily activities. The primary purpose of this study is to determine the age-related differences in the metabolic cost of daily activities. A secondary purpose of this project is to validate wearable technology to estimate people’s energy use. In addition to this project, the successful candidate will have the opportunity to conduct studies on reducing sedentary behavior (e.g. television viewing time) among older adults. Previous scholars in our laboratory have had tremendous success and have gone on to work at the NIH and/or were admitted into nationally recognized medical schools.
- Associate Director for Research, Institute on Aging; Associate Professor, Health Policy and Epidemiology
- Phone: 352-265-0680 ext. 86548; E-mail: email@example.com
The specific project we’re looking for colleagues for concerns the assessment of neuropsychological functioning, and day-to-day consistency of performance, in older adults with and without dementia. We’re interested in whether “inconsistency” (daily variability) of cognition might be an independent diagnostic of impaired cognitive functioning. More broadly, from my website: older adults’ everyday problem solving abilities, their relationship to basic cognitive and intellectual performance and to functional competence, and the role of social partners in cognitive collaboration the range of modifiability (plasticity) in adults’ intellectual functioning, and antecedents (especially sensorimotor) of individual differences in adult cognitive and intellectual functioning.
Amy Mehraban Pienta, Ph.D.
- Assistant Professor in the Institute on Aging, Department of Health Policy and Epidemiology Affiliate Department of Sociology
- Phone: 265-0680 x86504; E-mail: firstname.lastname@example.org
I am a sociologist and a demographer who studies aging. My two main lines of research are (1) social and demographic aspects of retirement and work disability and (2) social and demographic aspects of health and well-being. I primary conduct my research by analyzing nationally representative survey data. I have additional expertise issues related to: women and aging, African American Aging, and Aging in Nepal.
Shinichi Someya, Ph.D.
Department of Aging and Geriatric Research
Tel: 352-294-5167; E-mail: email@example.com
Hearing loss is caused by genetic defects, noise exposure, ototoxic drugs, and/or aging and is the third most prevalent chronic health condition in adults. A major question being studied in our laboratory is how hearing deteriorates with age at the molecular level. We are particularly interested in understanding how cochlear hair cells, spiral ganglion neurons, and/or stria vascularis cells are continually lost throughout life. To answer these questions, we study the molecular basis of hearing loss as well as hearing function under normal/healthy conditions using various transgenic and knockout mice and cultured mouse inner ear cell lines. A second question being studied in our laboratory is can the progression of hearing loss be slowed? To find these answers, we study the effects of calorie restriction and exercise on hearing in mouse models of hearing loss.
Rui Xiao, Ph.D.
Department of Aging and Geriatric Research, Biology of Aging Division, Institute on Aging
TEL: 352-273-9389, firstname.lastname@example.org
We are interested in understanding the fundamental biology of the interaction between genetic factors and environmental factors in the process of animal aging (Xiao et al., (2013), Cell, 152(4):806-17; Xiao et al., (2015), Cell Reports, 11(7):1123-33.). To address this question, we mainly use the genetic model organism C. elegans because of its short generation period and lifespan and powerful genetic tools. Approaches used in the lab including molecular genetics, lifespan and stress assays, calcium and fluorescence imaging, protein biochemistry, and electrophysiology.
Anatomy & Cell Biology
John P. Aris, Ph.D.
Professor of Anatomy and Cell Biology
We study mechanisms of aging that operate at the cellular and molecular level. Currently, we use the budding yeast Saccharomyces cerevisiae as a model eukaryotic cell for our studies. Our recent experiments have focused on the role of amino acid homeostasis in yeast chronological longevity.
Jun Cai, Ph.D.
Research Assistant Professor of Anatomy and Cell Biology
My research has concentrated on the regulatory mechanisms of pathological angiogenesis. I made a number of novel and important findings. Such breakthroughs include a) identifying the role of placenta growth factor (PlGF-one member of VEGF family) as a survival factor to remodel and sustain newly-formed vessels by binding to VEGF receptor-1 (VEGFR1) at the later stages of angiogenesis and b) elucidating the mechanism by which pigment epithelium-derived factor (PEDF), a natural potent angiogenic inhibitor, exerts its inhibitory effects on VEGF-induced angiogenesis via the γ-secretase regulated cleavage and intracellular translocation of VEGFR1. These novel studies have been fundamental in providing evidence that VEGFR1 plays an active role in the regulation of angiogenesis. The clinical achievement with angiogenesis inhibitors in cancer treatment is a milestone in the field of angiogenesis research. However, the clinical benefits are transitory and are followed by a restoration of tumor growth and progression. Recently my research interest is expended on establishing research programs centered in the mechanistic basis of this apparent resistance for the therapeutic targeting of tumor angiogenesis. This year I have been awarded a New Investigator Grant from the BankHead Coley Cancer Program. Within the next three or four years I will focus on studying the underlying mechanisms of the strategies adapted by angiogenic-stimulated endothelial cells to perpetuate aberrant angiogenesis within tumor microenvironment, which may will provide some alternative points of therapeutic intervention in anti-angiogenesis strategies.
Yehia Daaka, Ph.D.
Professor and Chair / Anatomy and Cell Biology
Tel: 352-273-8112; e-mail: email@example.com
A focus of our research is to characterize molecular mechanisms of mitogenic signal transduction initiated by the ubiquitous G protein-coupled receptors (GPCRs), with the goal of elucidating novel approaches for intervention in human pathophysiologic processes with special emphasis on genitourinary (e.g. prostate and kidney) cancers. Specifically, we are using molecular, cellular, and animal models to elucidate the role of the GPCRs and their effectors G proteins and βArrestins in the progression of prostate cancer from androgen-dependent to androgen-independent state, and in the metastasis of kidney cancer. A second line of investigation in the laboratory is centered on studying mechanisms involved in vesicle trafficking, with emphasis on the G proteins dynamin that support constriction and fission of vesicles from the plasma membrane into the cytosol. We have discovered that dynamin is post-translationally modified by tyrosine phosphorylation and S-nitrosylation and we are studying the effect of these modifications on its function in active receptor endocytosis and uptake of infectious bacteria and viruses.
William A. Dunn, Jr., Ph.D.
Professor of Anatomy and Cell Biology
Cells are capable of surviving environmental stresses and chemical insult by promoting autophagy that degrades endogenous proteins within lysosomes for recycling of amino acids and sugars. This pathway has also be shown to promote cell survival by removing damaged organelles and intracellular pathogens. Furthermore, dysfunctional autophagy has been implicated in aging, tumor growth, and in the progression of macular degeneration and neurodegenerative diseases. We are collaborating with other UF laboratories to better define the role of autophagy in these diseased states. Autophagy has been shown to have a major role in tumor growth and in the resistance of cancerous tissue to chemotherapy. This degradative pathway recycles nutrients required for tumor growth and provides the cell an avenue for chemotherapy resistance by removing mitochondria that have been damaged by these agents. Autophagy is an essential homeostatic pathway that protects the cells. However, uncontrolled autophagy can result in cell death. We have been collaborating with Dr Law to identify compounds that will suppress or enhance autophagy. We have identified a number of potential compounds that can inhibit key regulatory proteins of autophagy. The effectiveness of these compounds to inhibit or activate autophagy in osteosarcoma, hepatoma, and glioblastoma cell lines is now being assessed by biochemical and morphological means. The next stage will be to evaluate the effects of these compounds on tumor growth in xenograph models. We project these studies will provide new avenues for drug design and therapeutic intervention that will modulate autophagy thereby limiting tumor growth and enhancing chemotherapy susceptibility.
Alexander M. Ishov, Ph.D.
- Associate Professor, Department of Anatomy & Cell Biology and Shands Cancer Center
- Phone: 273-8202; E-mail: firstname.lastname@example.org
Research Interests: Chemotherapy resistance and new treatments in breast and prostate cancer; chromatin organization and epigenetic.
Daiqing Liao, Ph.D.
- Assistant Professor, Department of Anatomy an Cell Biology
- Phone: 294-7976; E-mail: email@example.com
Deregulation of cellular pathways in transformation and cancer, focusing on how viral oncogenes perturb cellular regulatory circuitry; Molecular genetics of tandemly repeated genes. Students are expected to learn to use cutting-edge techniques in molecular cell biology and genetics for the research project.
Paul J. Linser, Ph.D.
Professor of Anatomy and Cell Biology, Neuroscience, Zoology, Fisheries and Aquatic Sciences and Entomology and Nematology
To date we have characterized 8 of the 12 carbonic anhydrases encoded in the mosquito (Anopheles gambiae) genome. Comprehensive gene expression profiling (i.e. DNA micro array analyses) has also been generated which provides the big pictureof gene expression in relation to homeostasis in the various cell types of the larval gut. New emphases that have emerged from the big picture analyses included a focus on gut function in mediating innate immunity, the role of the salivary glands in gut function and homeostatic ion balance as a function of the activity of the hindgut (rectum) of larvae.
Satya Narayan, Ph.D.
Anatomy and Cell Biology
Mechanism of colorectal carcinogenesis – Recently, for the first time, we have implicated a novel role of adenomatous polyposis coli (APC) in base excision repair (BER). We hypothesized that, after DNA damage, APC level increases and interacts with DNA polymerase beta and flap-endonuclease 1 and blocks BER. Thus, the compromised BER results in the accumulation of mutations that might be a triggering point for the neoplastic transformation of colorectal epithelial cells.
Mechanism of cigarette smoke carcinogen-induced breast carcinogenesis – In recent studies, we have shown that cigarette smoke condensate-treated normal breast epithelial cells gained a growth advantage over untreated cells in vitro and in vivo. Our long-term goal is to establish the mechanism by which cigarette smoke condensate induces breast carcinogenesis.
Chemotherapeutic intervention of colorectal and breast cancers – Currently, we are actively developing structure-based designing of novel small molecular weight inhibitors to combat these deadly diseases. Several lead compounds have been identified and their usefulness has been proven both in vitro and in vivo studies.
Maria Zajac-Kaye, Ph.D.
Associate Professor of Anatomy and Cell Biology; Affiliate appointment in the Department of Medicine
Tel: 352 273-9153 or email: firstname.lastname@example.org
My research interests focus on understanding mechanisms of oncogenic transformation. We have recently studied the role of thymidylate synthase (TS) in tumorigenesis since TS plays a central role in DNA synthesis/repair and high levels of TS have correlated with a poor prognostic outcome in patients with lung, pancreas, colon, and rectal carcinomas. We demonstrated that ectopic expression of catalytically active human TS (hTS) was sufficient to induce a transformed phenotype in mammalian cells both in culture and in transgenic models confirming that it serves as a bona fide cancer therapeutic target. Our current work is focused on defining patterns of cooperation between TS and other cancer genes using a series of defined mouse models. Our goal is to use these transgenic animals to study the in vivo consequences of elevated TS on DNA stability, to test how this relates to tumorigenesis, and to improve the use of TS as a biomarker and therapeutic target.
Abdullah S Ahmad
TEL: 325-294-5107 or email@example.com
Stroke is a medical emergency associated with significant emotional and economic burden. In USA stroke kills more than 143,000 people a year and the estimated cost for stroke-related medical costs and disability in 2010 was $73.7. Unfortunately, effective therapy to prevent or minimize stroke is still elusive. One of the proposed and tested (in our lab) pathway mechanism could be Cyclooxygenase (COX)-prostaglandin pathway. COX is the rate-limiting enzyme for the conversion of arachidonic acid to prostaglandin (PG) E2 (PGE2), PGD2, PGF2α, PGI2, and thromboxane A2 (TxA2), collectively known as prostanoids. The prostaglandins play diverse roles in cell activity through their G-protein-coupled receptors (GPCR). The non-steroidal anti-inflammatory drugs (NSAID) have been widely used to inhibit COX-induced inflammation. By inhibiting COX, the NSAIDs also inhibit the PGs, which play a vital role in cellular physiology and pathophysiology. One of the important PGs is PGD2. Interestingly it is the most abundant PG in the brain. Most of the PGD2 activity is regulated by DP1. By using genetic and pharmacologic approach, we are determining the role of PGD2 in stroke. By using DP1 agonist, antagonist, and DP1-/- mice we are determining the role of DP1 in blood flow. Because “brain attack” is an acute process and usually happens without any warnings, scientists are encouraged to find therapeutic intervention(s) that could limit the brain damage after the attack. Therefore, we are also determining if the use of DP1 selective agonist after stroke can extend the therapeutic window such that the treatment could be provided several hours after the onset. Different strategies are being tested to extend the therapeutic window. We are also determining whether the proposed neuroprotection by using DP1 selective agonist is through improved blood flow and vasculature, or does it have a direct neuronal effect mediated by intracellular mechanisms, or a combination of both. We are also correlating the anatomical outcome with behavioral outcomes.
Azra Bihorac, M.D., FASN
Assistant Professor of Anesthesiology, Surgery and Medicine
Division Chief for Research, Department of Anesthesiology
Phone: (352) 273-9009; Fax: (352) 392-7029; E-mail: firstname.lastname@example.org
My research group is focused on translational and clinical research in the field of critical care medicine with the emphasis on the study of endothelium and microcirculation in sepsis, trauma and surgery-related acute injury. We are using a novel bedside video-imaging technique for the assessment of microcirculation in patients. In collaboration with Dr. Mark Segal’s laboratory we are correlating these findings with the functional status of circulating endothelial progenitor cells in patients with sepsis and trauma. We also have several ongoing epidemiological studies looking for the characteristics and outcomes of acute kidney injury among postoperative and critically ill patients.
Sylvain Doré, Ph.D.
Departments of Anesthesiology/Neuroscience
Center for Translational Research in Neurodegenerative Disease
352-273-9663 or SDore@anest.ufl.edu
The goal of the team effort directed by Sylvain is to discover new effective mechanisms that limit neuronal dysfunction associated with ischemic and hemorrhagic Stroke, Alzheimer disease, Aging, and various other neurological disorders. The overall objective is to slow down the progression of the disease, and ultimately stop it. To do so, the aim is to limit neuron death resulting from acute and/or chronic neurodegenerative conditions, re-establish normal cerebral blood flow, limit inflammation, stimulate endogenous repair, and restore regular cellular functions. Using a variety of in vitro and in vivo preclinical models, several new hypotheses and potential therapies are being investigated and developed:
- One objective is focused on understanding the actions of prostaglandin (PG) metabolites generated by the degradation of arachidonic acid by cyclooxygenase enzymes. These enzymes are the rate-limiting steps for the production of PGs, which are key elements in the inflammatory response. The resulting consequences are suggested to play an important role in the loss of normal neuronal functions associated with stroke, aging and neurodegenerative disorders.
- We also intend to understand of the protective role of the heme metabolites in the brain using cellular/molecular techniques and various models of ischemic and hemorrhagic stroke, AD, and aging. New knowledge is gained specifically by investigating the action and the role of activity of the heme oxygenase enzyme and its unique bioactive metabolites, namely, carbon monoxide, iron, biliverdin, and bilirubin.
- Our lab also provides molecular evidence for the potential therapeutic applications of complementary and alternative medicines. Using cultures of neurons it was observed that treatment with a standardized extract of Ginkgo biloba could alter the presence of specific genes/proteins important in neuronal function. The lab is exploring the regulation of the transcriptional factor Nrf2, and the increased expression of phase 2 protective enzymes, notably heme oxygenase. Also results have been obtained using resveratrol and other polyphenols, which appear to be active ingredients concentrated in red wines, and which has been proposed to explain some of the beneficial effects associated with the so called “French Paradox.” Similarly, experiments have provided evidence for a unique protective mechanism for the flavanol epicatechin which can be enriched in dark chocolate. These bioactive nutrients could provide resistance against damage induced by free radicals, the toxins which are generated with aging and are the hallmark of many neurodegenerative processes.
Tammy Euliano, M.D.
Associate Professor of Anesthesiology
TEL: 352-265-0077; TEuliano@anest.ufl.edu
My research interests are in monitoring in obstetrics. We have several projects ongoing including (1) prediction of which women will develop preeclampsia, a potentially lethal disorder of pregnancy, (2) non-invasive maternal fetal monitoring during labor to replace existing devices, and (3) diagnosis of preterm labor. Students working with us consent patients for the research study, collect research data, attend research meetings, and meet with the analysis team to understand the full clinical research process.
Mary A. Herman, MD, PhD
Department of Neuroanesthesia, Department of Anesthesiology
I am an anesthesiologist interested in the long-term effects of anesthesia on patient outcome, including neurocognition. Currently, we are studying the effects of anesthetics on the mortality of women with gynecological tumors. We are studying what patient factors (such as depression, use of different medications, or patient response to anesthetic) may affect long-term outcome. In addition, I am interested in the genetic basis of pain.
Anatoly E. Martynyuk, Ph.D., D.Sc.
Department of Anesthesiology
Telephone: (352) 846-1553, email@example.com
Mechanisms mediating the adverse actions of general anesthetics in the early stages after birth. We test the hypothesis that systemic actions of sevoflurane and isoflurane and resulting neurohumoral and inflammatory signaling are necessary elements in the mechanisms mediating acute and long-term developmental abnormalities caused by the anesthetics in neonates.
Steven Robicsek, M.D., Ph.D.
Department of Anesthesiology
My research interests are in (1) mechanisms and management of secondary injury in patients with traumatic brain injury (2) prevention, detection and management of spinal cord ischemia.
Kevin J. Sullivan, M.D.
The Congenital Heart Center and Department of Anesthesiology
Division Phone: 352-273-5422, E-mail: firstname.lastname@example.org
The Congenital Heart Center at the University of Florida provides comprehensive cardiology and cardiac surgical care to patients ranging from preterm infants, through early childhood and into young adulthood. Care rendered includes correction of congenital heart defects, heart and lung transplantation, and medical management of cardiac disease. Care is rendered in the Pediatric Cardiac Intensive Care Unit in the north Tower and involves all aspects of critical care medicine including artificial heart support, dialysis, and ventilator support. Operative repairs and cardiac catheterization occur in the operating room and the cardiac catheterization laboratory.
Patient outcomes and Quality and Safety Assurance is increasingly recognized as a cornerstone of evidence based medicine, and is a required activity for many physician leaders.The Congenital Heart Center is conducting numerous Quality and Safety studies to track and improve the peri-operative care of this very fragile patient population. The student who wishes to work within our division will have the opportunity to choose between over thirty Quality/Safety initiatives that range from small to large, and simple to complex. As the interested student participates in these activities they will be exposed to all aspects of pediatric cardiac surgery, anesthesia, pediatric cardiology, and pediatric critical care medicine. Finally, students will participate in the formation of recommendations for changes in the processes used to care for our patients.
Patrick Tighe, M.D.
Department of Anesthesiology
Over 60% of surgical patients will suffer from severe acute postoperative pain. While effective non-opioid interventions exist to significantly minimize or even prevent this suffering, such therapies can carry significant costs and risks if not matched to appropriate patients. Our lab applies a variety of machine learning techniques to characterize and forecast severe acute postoperative pain. Active experiments involve content and sentiment analysis of social media, social network analysis, and machine learning of clinical data from UF Health in order to improve our understanding and prediction of severe acute postoperative pain.
Biochemistry & Molecular Biology
Linda Bloom, Ph.D.
Dept. of Biochemistry & Molecular Biology
Email: email@example.com TEL: (352) 294-8379
Research Interests: Our research interests are in DNA replication and repair. We are working on defining molecular mechanisms by which the replication machinery duplicates genomes to support normal cell division, and mechanisms by which the replisome responds to DNA damage that is encountered during replication. In addition to defining these biochemical pathways, we are using what we have learned to work towards the development of antibiotics that target bacterial DNA replication.
Brian Cain, Ph.D.
- Department of Biochemistry and Molecular Biology
- firstname.lastname@example.org or 392-6473
The work in our laboratory focuses on the application of recombinant DNA technology and enzymology to the study of membrane proteins. Most of the research addresses the central enzyme in energy metabolism F1F0 ATP synthase.
Nancy D. Denslow, Ph.D.
- Scientist, Dept. of Biochemistry & Molecular Biology
- Phone: (352) 392-9665; E-mail: email@example.com
I am interested in understanding the molecular mechanisms by which environmental contaminants act as endocrine disruptors and affect biological systems. We use fish as a model for our studies because they are present in the rivers and lakes that are polluted by these compounds. The project would include protein analyses and western blots, isolation of mRNA, northern blotting with appropriate probes and the determination of the extent of induction of specific genes.
Ben M. Dunn, Ph.D.
- Professor, Dept. of Biochemistry & Molecular Biology
- Phone: (352) 392-3362 or (352) 273-1464; E-mail: firstname.lastname@example.org
The Dunn lab in Biochemistry & Molecular Biology offers projects designed to conduct drug discovery for potential therapy of infectious diseases including HIV, malaria, and tuberculosis. This lab offers training in protein chemistry, enzymology, protein crystallography, and structure-based drug design. Former students of the Dunn lab have gone on to careers in academic research, medicine, and pharmaceutical industry.
Susan C. Frost, Ph.D.
- Assoc. Professor, Dept. of Biochemistry & Molecular Biology
- Phone: (352) 392-3207; E-mail: email@example.com
My research laboratory is interested in nutrient control of glucose transport activity in an adipocytes model system. We are currently testing the hypothesis that glucose deprivation induces the synthesis of a novel protein that interacts with the membrane protein responsible for glucose transport to enhance uptake of glucose into cells. This project is funded by the NIH through 2003.
Suming Huang, Ph.D.
Associate Professor of Biochemistry and Molecular Biology
Tel: (352) 273-8199, Email: firstname.lastname@example.org
The overall goal of my research is to delineate the epigenetic pathways that regulate the normal hematopoiesis and to further determine how these networks are perturbed in acute leukemia. I have extensively studied the relationship between chromatin structure and developmentally regulated gene activation in eukaryotes, with particular interest in epigenetic regulation of hematopoiesis.
Michael S. Kilberg, Ph.D.
Professor of Biochemistry and Molecular Biology
email: email@example.com Phone: 392-2711
We are investigating transcriptional and epigenetic regulation of several human genes in response to nutrient stress; either protein/amino acid deprivation, which activates the Amino Acid Response signaling pathway or ER stress, which activates the Unfolded Protein Response pathway. For example, genomic analysis of the human asparagine synthetase (ASNS) gene has allowed us to identify several genomic cis-acting sequences, the corresponding transcription factors, and the assembly mechanisms of the general transcriptional machinery that are responsible for nutrient-dependent transcriptional control. These data have led us to focus on the molecular control of the genes for the nutrient-responsive transcription factors themselves, to understand the mechanisms for “regulation of the regulators.” Among these transcription factors are ATF4, ATF3, C/EBPb, JUN, FOS, and NF-kB.
Joanna R. Long, Ph.D.
Associate Professor of Biochemistry & Molecular Biology
Director, Advanced Magnetic Resonance Imaging & Spectroscopy Facility
TEL: (352)846-1506, e-mail: firstname.lastname@example.org
My research focuses developing magnetic resonance techniques for monitoring proteins, lipids, and metabolites in situ and in vivo to gain a molecular level understanding of their complex behaviors. Current projects include: 1) the structure, dynamics and function of lung surfactant peptides which traffic lipids in pulmonary surfactant; 2) The development of dynamic nuclear polarization (DNP) to examine metabolic flux in vivo; 3) the structure and assembly of proteins in fibril formation and biofilm stabilization; 4) Developing DNP approaches for studying membrane protein structure
Jianrong Lu, Ph.D.
Assistant Professor, Biochemistry & Molecular Biology
Email: email@example.com Phone: 273-8200
Our research is aimed at understanding the mechanisms and functions of epigenetic regulations in cancer metastasis. In particular, we focus on histone post-translational modifications at the E-cadherin gene, which encodes for a suppressor of metastasis and is frequently inactivated in cancer.
Thomas H. Mareci, Ph.D.
Professor of Biochemistry & Molecular Biology
Phone: (352) 392-3375; E-mail: firstname.lastname@example.org
Our research focuses on the study of fundamental questions of tissue structure and biochemical processes in living systems accessible to study with nuclear magnetic resonance (NMR) techniques. To provide a detailed understanding of the living system, we are performing detailed investigations of biophysical processes at the cellular and tissue level, along with the development of NMR measurement, processing methods, and specialized hardware. Our current projects are focused on structure and function in the brain: 1) we are using NMR measurements of water translational diffusion in tissue to map fibers in highly structured white matter in the brain and constructing a network map of brain structure, and 2) we are delivering genetic material to specific parts of the brain in order to introducing light-sensitive proteins to the membranes of neurons in the brain to map brain function connectivity. These proteins respond to specific laser light which allows us to directly simulate function in a specific area of the brain then map functional connections to other areas in the brain. The results of these two projects will then be combined to relate structure to function in the brain.
Matthew E. Merritt, Ph.D.
Associate Professor of Biochemistry and Molecular Biology
My lab focuses on using magnetic resonance based methods to measure metabolic flux quantitatively, in systems ranging from cell culture to whole animals.
Thomas W. O’Brien, Ph.D.
- Department of Biochemistry and Molecular Biology
- Phone: 392-6878; email: email@example.com
Research in our laboratory addresses several questions related to the structure, function, biosynthesis and evolution of mitochondrial ribosomes. Human mitochondrial ribosomes differ unexpectedly from bacterial and cytoplasmic ribosomes, as well as
other kinds of mitochondrial ribosomes. Current projects include
structural/functional characterization of the novel GTP binding ribosomal protein implicated in programmed cell death, localization of several novel proteins in the mitochondrial ribosome, and use of RNA interference to elucidate functional roles of the novel proteins, as candidates for mitochondrial disease.
Thomas P. Yang, Ph.D.
- Assoc. Professor, Dept. of Biochemistry & Molecular Biology
- Phone: (352) 392-6472; E-mail: firstname.lastname@example.org
My laboratory is interested in the general area of eukaryotic gene regulation, and specifically in mechanisms of transcriptional regulation of mammalian genes. We study the transcriptional regulation of genes in two genetic systems of differential gene expression, X chromosome inactivation and genomic imprinting.
Community Health & Family Medicine
Danielle Nelson, MD MPH
Dept. of Community Health & Family Medicine
Use of EHR in improving accuracy of ordering and in improving rates of health maintenance /preventive care, chronic disease management (especially diabetes), and optimization of EHR to improve provider satisfaction and efficiency.
Marie-Carmelle Elie, M.D.
Dept. of Emergency Medicine
TEL: 352-265-5911, 352-265-8075; E-mail: email@example.com
My area of research focuses on improved diagnostics and the prevention of organ dysfunction associated with critical illnesses such as sepsis and shock. The ability of a clinician to avert disease is directly related to whether they can reliably discern which of their many patients are at risk. In the emergency department, prevention is underemphasized. Tools, such as biomarkers and risk stratification calculators, that reliably predict the development of conditions such as severe sepsis, acute respiratory distress syndrome and acute renal failure are underutilized. The consequence is often related to poor outcomes that require prolonged ventilator support, renal replacement therapy, and other resources that impact quality of life, the cost of healthcare, and survival. Current clinical trials enroll emergency department patients with severe illness in an effort to prevent the progression of their disease.
Linda B. Cottler, Ph.D., MPH, FACE
Department of Epidemiology
TEL: 352-273-5468, firstname.lastname@example.org u
Global Health, Addiction, Community Based Research, Mentoring Pedagogy, Interventions, Health Inequalities.
Health Outcomes and Policy
Jiang Bian, Ph.D.
Department of Health Outcomes & Policy
Contact: 352-273–8878; email@example.com
Social media and social web, consumer health, semantics of health knowledge and semantic web technology, data science and data-driven health research, data privacy, and network science.
Michelle Cardel, Ph.D., R.D.
Department of Health Outcomes and Policy
TEL: 273-9703, E-mail: firstname.lastname@example.org
Background: Obesity and cardiometabolic risk disproportionately affects Hispanic American (HA) adolescents relative to their white counterparts. The reasons for such differences appear to be both biological (physiological) and non-biological (environmental). Socioeconomic status (SES) has been consistently used as a proxy for environmental exposure, and an association between lower SES, obesity and cardiometabolic risk has been demonstrated during adolescence and adulthood. In adolescents, recent studies are demonstrating that perceptions of social status are better indicators of obesity risk than traditional SES. However, the nature of perceived social status and its relationship to eating behavior and obesity risk are poorly understood. The objective of this study is to investigate the effect of manipulation of social status condition on eating behavior and obesity risk in 15-18 year old Hispanics.
Hypothesis: Adolescents will consume a greater number of calories, fat, and sugar following the low social status condition when compared to the high social status condition. Obese adolescents will consume a greater number of calories, fat, and sugar following the low social status condition when compared to normal weight adolescents.
Methods: This aim will be accomplished using a randomized crossover design to place adolescents in experimental high and low social status conditions. We will evaluate how much adolescents eat in an ad libitum buffet meal following the manipulation of social status.
Role of medical student: The medical student(s) will be expected to assist in the data collection and data analysis to examine the role of psychosocial outcomes on eating behavior and obesity risk in youth. Expected outcomes include a poster presentation at UF and possibly national meetings and manuscript preparation. In addition, the student(s) will gain joint mentorship and exposure from faculty with the Institute for Child Health Policy, the Department of Health Psychology, the Department of Health Outcomes and Policy, and the Department of Pediatrics.
Funding and relevant publications: Current internal efforts by Health Outcomes and Policy allow for this integrated research. Previous funding for pilot study allotted from University of Colorado and University of Alabama’s Nutrition Obesity Research Centers.
- Cardel MI, Johnson SL, Beck J, Dhurandhar E, Keita AD, Tomczik A, Pavela G, Huo T, Janicke D, Peters JC, Hill JO, Allison DB. The Influence of Experimentally Manipulating Social Status on Acute Eating Behavior: A Pilot Study. Physiology and Behavior (under review as of December 1, 2015).
- Cardel M, Bellows L, Boles RE, Davies P, Gavin W, and SL Johnson. Self-Concept and Obesity Risk in Low Income Diverse Preschoolers. Presented as an oral presentation at American Society of Nutrition, 2015.
Matthew J. Gurka, Ph.D.
Department of Health Outcomes and Policy
TEL: 352-627-9088, E-mail: email@example.com
I am currently researching the metabolic syndrome in children and adults, and how this syndrome leads to future disease (cardiovascular disease, type 2 diabetes). I am specifically interested in better ways to measure this syndrome and its severity. I am also involved in research related to childhood obesity.
William Hogan, M.D.
Dept. of Health Outcomes & Policy
My research interests including biomedical ontology, use of electronic health record and administrative data for research, and informatics in support of research in general.
Mildred M Maldonado-Molina, Ph.D.
Health Outcomes and Policy
Areas of interest: Preventing consequences associated with alcohol and drug abuse among youth, including drugged driving and prescription drug abuse.
Keywords: Alcohol and drug prevention, youth, research methodology, policy evaluations, applied statistics, health outcomes, epidemiology, cohort and national studies, longitudinal data.
Ramzi G. Salloum, Ph.D., MBA
Dept. of Health Outcomes & Policy
Contact: (352)294-4997 or firstname.lastname@example.org
We are currently conducting research in various aspects of tobacco control, ranging from the identification of targets for the regulation of waterpipe (hookah) smoking and e-cigarettes, to the development of effective interventions to screen for and treat tobacco use within clinical settings.
Stephanie Staras, Ph.D.
Health Outcomes and Policy
My research focuses on preventing cancer through maximizing use of the human pappillomavirus (HPV) vaccine. My work focuses on decreasing missed clinical opportunities with an in-clinic health information technology system and increasing community demand with parent reminders and education.
Dorina Avram, M.D.
Professor of Medicine
Dorina Avram’s research interest is in immune regulation, mostly at mucosal sites. Her work has an important impact in the control of autoimmune diseases such as multiple sclerosis and inflammatory bowel disease, as well as in airway inflammation.
Mark Brantly, M.D.
Professor of Medicine, Molecular Genetics and Microbiology
Phone 352-392-7861; e-mail: email@example.com
We study the molecular basis of the conformational disease alpha-1-antitrypsin deficiency, and develop therapies to treat the lung and liver disease associated with this disorder. In our lab students have an opportunity to work on projects that potentially have a direct impact on the health of individuals with this disorder. We conduct clinical studies to evaluate novel therapies develop our lab. See our web site for more information about our research group. http://www.alphaone.ufl.edu
Michael R. Bubb, M.D.
Associate Professor, Dept. of Medicine
Phone: (352) 273-9681; E-mail: firstname.lastname@example.org
My laboratory uses cell biological and biophysical techniques to study actin polymerization and cell movement. We are particularly interested in understanding the intracellular regulation of the traffic of molecules within the crowded confines of the interior of cells. The processes of intracellular traffic and cellular movement are relevant to many human disease s such as in development of cancer and of autoimmunity. We also study pharmacologic agents that target the regulation of actin polymerization. These agents have a broad range of applications, including modulation of apoptosis, angiogenesis, immunology, neurodevelopment and cancer biology.
Donna Carden, M.D.
Department of Emergency Medicine
TEL: 352.265.5911 and email@example.com
Emergency Department (ED) crowding represents a major threat to the nation’s health care safety net. The reasons for ED crowding are complex and include increased use of EDs for both emergent as well as non-urgent conditions. However, there is little agreement in the published literature regarding the definition of a non-urgent ED visit.
The overall purpose of this project is to define ED visit urgency in order to begin to address the causes and health outcome consequences of ED crowding.
Christopher R. Cogle, M.D.
Department of Medicine, Division of Hematology and Oncology
Dr. Cogle is a physician and scientist with research focus on blood cancers. Dr. Cogle is seeking undergraduate and graduate students to participate in research involving two separate projects: (a) drug development, and (b) health policy. The drug development project involves in vitro leukemia cell assays and related data analyses. Students are expected to produce data for co-authoring meeting abstracts, presentations, publications and grant applications. The health policy project will examine the use of computational biology systems in the clinical diagnosis and treatment of patients with cancer. Students will participate in state-level and national-level meetings and produce written reviews for co-authored publications in peer-reviewed medical journals.
Kenneth Cusi, M.D.
Medicine / Endocrinology, Diabetes and Metabolism
My work involves cutting-edge research in adult diabetes and metabolism, both on clinical and basic research aspects related to the role of obesity, insulin resistance and lipotoxicity (fat-induced cellular damage) in the development of type 2 diabetes and its complications, in particular, the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Because we have a broad spectrum of clinical and basic research projects I would be glad to discuss them personally with the interested candidate (contact me directly at 352-273-8661 or 7236). I have enjoyed training many undergraduate students over the past 20 years and have recently moved to UF to develop a vibrant research program. A more detailed description can be found in our website at http://com-dom-endo.sites.medinfo.ufl.edu
Michelle L. Gumz, Ph.D.
Assistant Professor of Medicine (Nephrology) and Biochemistry & Molecular Biology
The long term goal of my lab is to characterize the role of Per1, a circadian clock protein, in the regulation of blood pressure and cardiovascular function. Our current focus is on the mechanism of Per1 action in the kidney. Current projects in the lab include (1) whole animal experiments to study the blood pressure phenotype and renal sodium handling defect in Per1 knockout mice, and (2) in vitro experiments to understand the molecular regulation of Per1 target genes in mouse kidney collecting duct cells.
Coy Heldermon, M.D., Ph.D.
Assistant Professor of Medicine
My interests are as follows:
- Treatment of Inherited Disorders through gene and stem cell therapies
- Assess factors that modulate the exchange of stem cells between mother and offspring during gestation.
- Develop breast cancer biomarkers using Breast cancer xenografts.
Nicole M. Iovine, M.D., Ph.D.
Department of Medicine
office: 376-1611 ext 4265
Currently, there are two active projects in my lab, both of which involve innate host defense against Gram negative bacterial infection; 1) Autophagy as an innate immune defense against C. jejuni and 2) The Bactericidal/Permeability-Increasing Protein: A Neutrophil-Derived Antibiotic with Activity Against Multi-Drug Resistant Gram-Negative Bacteria.
Christian Jobin, Ph.D.
Professor of Medicine
E-mail: Jobin@medicine.ufl.edu Tel:352-294-5148
Dr. Jobin’s research focuses on establishing mechanisms controlling host-bacteria interaction in the intestine. His laboratory is especially interested in the functional impact of bacteria in intestinal injury repair, inflammation and colorectal cancer. Using genetically engineered mice and zebrafish, germ-free and gnotobiotic technology in combination with microbiome analysis, he is studying the role of innate signaling on homeostasis and disease process.
Jonathan D. Licht, M.D.
Department of Medicine
Director- The University of Florida Health Cancer Center
The Marshall E. Rinker, Sr. Foundation and David B. and Leighan R. Rinker Chair
TEL: 352-273-8143, Email: firstname.lastname@example.org
We study how mutations in epigenetic regulators lead to wide-ranging defects in gene regulation and the development of blood and other malignancies.
Margaret C. Lo, M.D.
- Assistant Clinical Professor, Dept of Medicine
- Phone: (352) 265-0651; E-mail: email@example.com
Our research interest is clinically based, focusing on improvement in internal medicine (IM) resident education and performance of core clinical measures of diabetes as a chronic illness. Specifically we are studying the effectiveness of an ambulatory rotation through a multidisciplinary resident diabetes clinic (MRDC) (which includes an endocrine attending, 2 medicine attendings, a clinical diabetic educator, a clinical nutritionist, and a pharmacist) on learning and practice behaviors of PGY-1 and 2 IM residents, and on the quality of care that they subsequently give to the uncontrolled diabetic patients in their own longitudinal clinics. We will be comparing patient outcomes (hemoglobin A1c, blood pressure, LDL-cholesterol) among uncontrolled diabetic patients managed by PGY-1 AND 2 IM residents before and after resident exposure to the MRDC.
Michael MacMillan, MD
Department of Orthopaedics
We are the Strength Science Lab where we apply resistance training to certain orthopaedic conditions and preventative programs. We are also pursuing support for ACL injury prevention and certain tendonopathies. We are also interested in the health aspects of resistance training.
Rajesh Mohandas MD, MPH
Department Affiliation: Assistant Professor of Medicine and Physiology and Functional Genomics
Phone: 352-273-5355 Email: firstname.lastname@example.org
My research interests focuses on the cardiovascular complications of kidney disease. It includes clinical as well as basic laboratory research. My clinical research examines cardiovascular outcomes in patients with kidney disease. My laboratory focuses on elcudiating the molecular basis of vascular stiffness and how stiffness of the extracellular matrix affects vascular smooth muscle function. In addition to the usual molecular biology tools such as PCR and western blot, our lab performs arteriography of the microvasculature (which involves canulating vessels that are thinner than a hair), murine echocardiography and atomic force microscopy to measure stiffness of cells and matrix.
Stratford May, MD, PhD
Department of Medicine
Phone 273-8012; email email@example.com
Mechanisms of programmed cell death, cell cycle regulation and metastasis; identification of novel signal transduction pathways related to protein kinases, cysteine proteases, Bcl2 family members, and tumor progression; DNA damage/repair
Yuri Y. Sautin, Ph.D., D.Sc.
- Associate Professor Division of Nephrology, Hypertension and Transplantation
- Phone: (352) 273-5805 E-mail: Yuri.Sautin@medicine.ufl.edu
Our group is involved in basic research in the field of the metabolic syndrome, obesity and kidney disease. We are particularly interested in the mechanisms of signal transduction involving several lipid and protein kinase cascades and NADPH oxidase, which are responsible for oxidative stress, inflammation and prediabetic phenotype in adipocytes, hepatocytes and renal epithelial cells in cell culture and animal models of the metabolic syndrome and obesity. We use a variety of techniques, such as immunofluorescence, live cell imaging by confocal microscopy, RNA interference, recombinant viruses, immunoprecipitation, real-time PCR and immunoblotting to characterize gene expression, etc. We use also animal models of the metabolic syndrome.
Mark Segal, M.D.
- Professor and Division Chief, Dept. of Medicine
- Phone: 352-392-4008; E-mail: firstname.lastname@example.org
The Segal Lab is focused on understanding the mechanism of the increased cardiovascular risk in unique populations. These populations include patients with chronic kidney disease, patients with lupus nephritis, patients receiving high doses of erythropoietin, women who have complicated pregnancies, and patients who suffer from acute kidney injury. Our hypothesis is that the mechanism of the increased risk in these populations can be determined by analysis of components of the peripheral blood. Our lab has focused on utilizing circulating endothelial cells as a marker of increased endothelial injury and bone marrow derived angiogenic cells as a mechanism of endothelial repair.
With regard to women with complicated pregnancy, dramatic changes occur in the maternal systemic circulation during pregnancy epitomized by massive vasodilation, reduction in systemic vascular resistance and reduction in global arterial compliance. In addition to changes in arterial tone and remodeling, another potential mechanism for the decrease in systemic vascular compliance and increase in global arterial compliance is vasculogenesis and angiogenesis (formation of new or increased branching of existing blood vessels, respectively) or arteriogenesis (increase in compliance by arterial remodeling) via the mobilization of bone marrow derived angiogenic cells. The pregnancy hormone, relaxin, secreted by the corpus luteum during pregnancy, has been shown to replicate the maternal circulatory changes in pregnancy when administered to non-pregnant rats and humans. We were the first to demonstrate that relaxin is a mobilizer of bone marrow derived endothelial cells. Currently we are studying the levels and function of circulating endothelial cells and bone marrow derived endothelial cells in women during spontaneous pregnancies and pregnancies in women who conceived through artificial reproductive technology. We are studying two types of artificial technology: 1) Standard artificial reproductive technology in which the women have supraphysiologic levels of relaxin; and 2) Egg donor artificial reproductive technology in which the women have absolutely no detectable level of relaxin. We are investigating the question as to whether the health of the blood vessels during pregnancy affects future risk of heart disease.
Ashutosh M Shukla, M.D.
Assistant Professor, Division of Nephrology, Hypertension & Transplantation
TEL: (352) 273-8821, Ashutosh.Shukla@medicine.ufl.edu
Peter W. Stacpoole, Ph.D., M.D.
- Professor of Medicine, Biochemistry and Molecular Biology
- E-mail: email@example.com
My research summary can be found in the websites for the Dept of Medicine or Dept of Biochem and Mol Biol. In brief, it involves laboratory and clinical research into the causes and treatment of both acquired and congenital mitochondrial diseases. I have mentored over 35 undergraduate pre-professional students and currently have 3 undergraduates working with my group.
Roland Staud, M.D.
Professor of Medicine, Division of Rheumatology & Clinical Immunology
Phone: (352) 273-9682; E-mail: firstname.lastname@example.org
Chronic widespread musculoskeletal pain (CWP) is highly prevalent in the general population (20%) and represents a major cause for dysfunction and loss of income [2; 3] . There are few pharmacological and non-pharmacological therapies available, which generally are of small effect size. Central pain processing abnormalities, including abnormal pain modulation, play an important role for the pathogenesis of this disorder but specific details are lacking . We hypothesize that excessive central pain facilitation is a major factor for patients’ increased pain and pain sensitivity. This hypothesis will be tested by quantitative sensory testing (QST) and functional MRI (fMRI). The student will interact with chronic pain patients and healthy controls and will consent, obtain questionnaires and perform QST (heat and pressure stimuli) on the subjects. He/she will be trained to perform these tasks reliably and how to avoid bias. The student will observe fMRI and will help prepare the subjects for the procedure. The study is funded by NIH and UF funds.
 Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 2009;10(9):895-926.
 Papageorgiou AC, Silman AJ, Macfarlane GJ. Chronic widespread pain in the population: a seven year follow up study. Annals of the Rheumatic Diseases 2002;61(12):1071-1074.
 Staud R. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol 2011;25(2):155-164.
Amy Y. Vittor M.D., Ph.D.
Dept of Medicine, Division Infectious Disease & Emerging Pathogens Institute
I am intrigued by various factors that drive disease emergence. To this end, I study the influence of factors such as immunity, deforestation and climate change on the emergence of mosquito-borne viruses such as chikungunya, Mayaro, Venezuelan equine encephalitis, and South American eastern equine encephalitis. I also find the mechanisms behind the tendency of these viruses to jump hosts and become adapted to humans fascinating, and am looking at the host response to viral infection in various types of human cells to better understand what allows a zoonotic virus to take hold and spread in humans.
Gary P. Wang, M.D., Ph.D.
Department of Medicine, Division of Infectious Diseases
Research in my Lab focuses on understanding virus-host interactions, in particular the mechanisms by which viruses evade host immune responses and antiviral drug selective pressures. Specifically, the lab studies hepatitis C virus and Human Immunodeficiency Virus, using a combination of methods including high throughput next-generation sequencing, bioinformatics, as well as traditional methods of molecular biology and virology. As a deeper understanding of viral population dynamics and evolution is critical to many aspects of HIV and HCV treatment and prevention, the lab studies the genomic consequences of HIV and HCV infection in patients in the face of antiviral pressure, with the dual goal of understanding mechanisms and developing strategies for antiviral therapy. Please see http://wanglab.medicine.ufl.edu for more information.
Charles Wingo, M.D.
- Department of Medicine
- Email: email@example.com
Studies in the Wingo lab focus on the molecular physiology of H,K-ATPase’s of the kidney and the ion channels and signal transduction proteins that regulate this class of pumps. These pumps are important in potassium conservation (potassium reabsorption) during potassium depletion and have been hypothesized to play a role in certain forms of hypertension. We are also interested in the distribution and function of these pumps in other tissues and the role of hormones which affect blood pressure such as angiotensin II, bradykinin, and dopamine in the regulation of these transporters.
We utilize a variety of techniques including physiological studies in knockout animals, patch clamp analysis of intact and cultured collecting duct cells, heterologous expression studies of ion channels and ATPase subunits with analysis of their activities, and immunohistochemical studies at the light and EM level. Expertise within the laboratory includes, protein chemistry and molecular biology, patch clamp analysis and confocal microscopy, and microperfusion, intracellular pH and intracellular calcium measurements.
Elena Yarmola, Ph. D.
- University of Florida Department of Medicine
- Tel. (352) 376-1611 ext. 4305; E-mail: firstname.lastname@example.org
Dynamic remodeling of actin cytoskeleton is vital for development and immune system function. Actin-binding proteins tightly regulate actin cytoskeleton in response to extracellular stimuli.
We study molecular mechanisms of actin regulation proteins both theoretically and experimentally. Please visit http://www.medicine.ufl.edu/rheuma/yarmola.asp to find more details about our research.
Ellen M. Zimmermann, M.D.
Professor of Gastroenterology
Associate Vice Chair for Research, Department of Medicine
Our labs studies Crohn’s disease and ulcerative colitis, two chronic diseases of the intestine that affect all ages but particularly young adults. Our research focus is on mechanisms of tissue inflammation that lead to tissue fibrosis with particular interest in genes that contribute to specific disease phenotypes. We use cell culture and animal models to study inflammatory mechanisms and effects of therapy on inflammatory mediators. We also perform clinically oriented studies on MRI imaging of the intestine and on aspects of the disease including natural history, patient quality of life, and response to therapy. Our lab is collaborative and collegial and there are many opportunities for students to participate.
James R. Zucali, Ph.D.
- Professor, Dept. of Medicine
- Phone: (352) 392-2991; E-mail: email@example.com
We are interested in studying the insertion of chemoresistant genes using lenti viral gene transfer into normal hematopoietic stem cells to increase resistance to elevated chemotherapy in bone marrow transplantation. We are also interested in creating mixed chimeras to determine whether graft versus host disease can be prevented while preserving graft versus tumor effects in an allogeneic bone marrow transplant setting.
Molecular Genetics & Microbiology
Henry V. Baker, Ph.D.
- Professor and Chair, Dept. of Molecular Genetics & Microbiology
- Phone: (352) 392-0680; E-mail: firstname.lastname@example.org
My research is aimed at understanding the nature of the combinatorial interactions that occur between transcription factors to regulate gene expression. We use a variety of molecular techniques to study how proteins are recruited to their regulatory sequences on the DNA. We are also using a genomic approach to define regulatory networks that exist within the cell.
David C. Bloom, Ph.D.
- Professor, Department of Molecular Genetics
- Phone: 392-8520; E-mail: email@example.com
My lab’s overall goal is to understand how Herpes Simplex Virus type 1 (HSV-1) is able to go latent in nerve cells, and how stress causes it to reactivate and cause recurrent disease. My current research is focused in three major areas: 1) Characterizing viral genetic elements that regulate latency and reactivation, 2) Identifying molecular determinants of HSV latent gene expression and silencing of lytic genes, and 3) Developing novel therapeutic approaches to reducing the ability of HSV to reactivate.
Barry J. Byrne, M.D., Ph.D.
- Asst. Professor, Dept. of Molecular Genetics & Microbiology
- Phone: (352) 846-1531; E-mail: firstname.lastname@example.org
My laboratory is actively involved in developing new genetic therapies for cardiovascular disease. In the area of cardiomyopathy, we are studying gene replacement in an autosomal recessive form of fatal cardiomyopathy in children. Additional projects are focused on transplant rejection and heart failure as well as hemophelia. In these projects we use AAV vectors to achieve sustained correction of the gene deficiency and correction of the phenotype in mouse models of disease.
Lung-Ji Chang, Ph.D.
- Assoc. Professor, Dept. of Molecular Genetics & Microbiology
- Phone: (352) 392-3315; E-mail: email@example.com
Analysis of lentiviral transgene functions, modification of dendritic cell immunity, HIV gene therapy and immunogene therapy using mouse and cat cancer models.
Paul A. Gulig, Ph.D.
Molecular Genetics & Microbiology
firstname.lastname@example.org TEL: 294-5544
Oxalobacter formigenes is an obligate anaerobic bacterium that is a component of the gut microbiota of humans and other animals. Its sole carbon and energy source is oxalate, the major component of most kidney stones. O. formigenes can decrease urinary oxalate and prevent kidney stones by stimulating the gut epithelium to excrete oxalate from the blood into the intestinal lumen, where the bacteria consume the oxalate. We are using a molecular genetic approach with O. formigenes in a mouse model to elucidate the mechanism by which the bacteria stimulate oxalate excretion and the biology of intestinal colonization. We are combining bacterial genomics and bioinformatics to construct mutations is specific O. formigenes genes, and we examine the mutants for their ability to decrease urinary oxalate in mice fed a high oxalate diet. When genes of interest have been identified, we will determine if they can be expressed in other probiotic bacteria of if their products can be used to treat hyperoxaluria (high urinary oxalate).
Stephanie Karst, Ph.D.
Molecular Genetics & Microbiology
Our laboratory studies the interactions between the host mucosal immune system and enteric pathogens, specifically using the enteric noroviruses as a model system. The noroviruses are particularly interesting to us because people fail to develop a lasting protective immune response upon a primary exposure – thus, people can be repeatedly infected by noroviruses. This failure of the host mucosal immune system to maintain protection against a pathogen is also observed with other mucosal pathogens. We believe that the failure can be explained by an aberrant recognition of the pathogen by the mucosal immune system such that it responds as it would to non-pathogenic commensal organisms. This information is critically important to the design of effective vaccines against mucosal pathogens. A second major project in the lab aims to elucidate the mechanisms by which noroviruses cause disease, specifically testing the hypothesis that they encode virulent enterotoxins.
Alfred S. Lewin, Ph.D.
Dept. of Molecular Genetics & Microbiology
Phone: (352) 392-0676; E-mail: email@example.com
Dr. Lewin’s group uses the tools of gene therapy or drug therapy to prevent blindness caused by inherited retinal degeneration or by age related macular degeneration (AMD). Inherited retina degeneration includes retinitis pigmentosa (RP) which causes progressive loss of vision beginning in the teenage years. Age related macular degeneration develops late in life and leads to loss central vision in >10% of people older than 70. Projects include development of viral vectors to block the expression of mutant forms of rhodopsin; development of viral vectors to prevent oxidative stress and inflammation that contribute to both AMD and RP; and repurposing approved drugs to prevent cell death in both of these diseases. Methods will include molecular cloning, tissue culture, immunochemistry and microscopy. Treatment of experimental animals (mice) will be involved, and student researchers will analyze vision and retinal structure in these animals using advanced imaging and electrophysiology techniques.
Chythanya Rajanna, Ph.D.
Assistant Professor of Molecular Genetics and Microbiology
(phone and/or e-mail): firstname.lastname@example.org / 352-505-1328
My main focus is on bacterial pathogenesis particularly of Yersinia pestis. I am interested in studying the diversity of Y. pestis strains isolated from different regions of world and to develop phage based techniques for surface decontamination and detection. I am also investigation role of bacterial biofilm in environmental persistence and virulence of Y. pestis.
Rolf Renne, Ph.D.
Professor, Department of Molecular Genetics
Phone: 273-8204; E-mail: email@example.com
My laboratory studies how Kaposi’s sarcoma-associated herpesvirus (KSHV) also called Human Herpesvirus Type 8 (HHV8) contributes to tumorigenesis. We are focused on understanding the molecular mechanisms by which latency-associated gene products such as the latency-associated nuclear antigen (LANA) and 12 viral-encoded microRNAs contribute to viral pathogenesis. We are utilizing a wide range of molecular biology, genetic. ribonomics, and high throughput methods to investigate miRNA function and epigenetic regulation of both the viral and host cellular genome during tumorigenesis.
Maurice S. Swanson, Ph.D.
Professor, Department of Molecular Genetics and Microbiology
Tel: (352) 273-8076, E-mail: firstname.lastname@example.org
Our laboratory focuses on the co/post-transcriptional regulation of gene expression and the roles of simple sequence repeats, or microsatellites, in neurological and neuromuscular disease. We use a combination of in vivo model systems, high-throughput sequencing and computational biology techniques to uncover novel mechanisms of gene regulation, RNA processing and human disease pathogenesis.
Margaret (Peggy) Wallace, Ph.D.
Professor, Dept. of Molecular Genetics & Microbiology
TEL: (352) 392-3055 / e-mail: email@example.com
The Wallace laboratory is involved in molecular and cellular studies of human diseases that are hereditary in origin or have a genetic predisposition. These studies employ patient samples and mouse models. There are several ongoing projects. One project involves neurofibromatosis type 1 (NF1), a common dominant condition characterized by localized overgrowth/abnormal growth of many tissues (resulting in features such as neurofibromas, skeletal dysplasia, and other tumors such as myeloid leukemia, and GIST in the gut). Studies are underway investigating roles of the NF1 gene protein (neurofibromin) in several tumor types and other NF1 phenotypes. Mutations/expression changes in other genes in these tumors are also being studied. A recent project is genetic association in the depigmentation disorder vitiligo. We have also been involved in gene mapping and mutation analysis in hereditary heart conditions such as primary cardiomyopathy and Pompe disease. Also, we are collaborators in projects identifying genetic polymorphisms that contribute to taste preferences, and baseline pain differences and chronic pain disorders. Thus, this laboratory performs basic and translational research, and works closely with clinicians to obtain patient and family samples.
Lizi Wu, Ph.D.
- Molecular Genetics & MIcrobiolgy
Our laboratory is interested in understanding transcriptional events of signal transduction pathways critical for normal development and human diseases and one of our current major focuses is a highly conserved cell fate determination pathway mediated by Notch receptors. Aberrant Notch signaling is associated with T cell leukemia as well as a growing number of solid tumors. However, it remains elusive how Notch signaling regulates the growth, survival, and interactions of the tumor cells and its microenvironment during cancer development. Therefore, we aim to elucidate molecular regulation underlying normal and pathological Notch signaling and hope that the knowledge from our research may point to the mechanisms that transform normal cells to cancerous cells, and thus aid in developing novel cancer therapies.
Lei Zhou, Ph.D.
Associate Professor of Molecular Genetics and Microbiology
The overall objective of my research is to understand how the regulatory pathways controlling cellular suicide (apoptosis) are activated in response to cellular stresses and virus infection. Apoptosis is a gene-controlled process that leads to the destruction of obsolete, damaged, or pathogen-infected cells. The destruction of the cell is largely achieved by the activation of a group of proteases called Caspases. Caspases are synthesized as dormant enzymes in essentially all cells, their activation is controlled by several interrelated pathways. While the downstream effector components of these pathways are expressed ubiquitously, the upstream pro-apoptotic regulators are regulated at the transcriptional level. The expression of these upstream pro-apoptotic genes acts as the “trigger” for initiating selective cellular destruction. In mammalian systems, genes encoding BH3-only proteins such as Noxa, Puma, and Bim are the transcriptional targets of P53. In Drosophila, P53 induces apoptosis through transcriptional activation of the RHG (reaper, hid, grim) genes.
Michael Weiss, M.D.
- Division of Neonatology, Pediatrics Department
- Phone: (352) 392-4195; E-mail: firstname.lastname@example.org
Currently our laboratory focuses on the role of amino acid transporters in the pathophysiology of Hypoxic-Ischemic Encephalopathy (HIE). HIE occurs with an incidence of 1 in 1000 births. We hope, that by gaining a better understanding of how amino acid transporters modulate the transport of glutamine and glutamate, to develop treatments for this neurologically devastating disease.
Glen Finney, M.D.
Assistant Professor of Neurology
email@example.com , 352-273-5550
I am interested in research in memory and cognitive disorders, brain-behavior relations, the neurobiology of creativity, neurology and health policy, and neurology education.
Vishnumurthy S Hedna, M.D.
Stroke Division, Neurology Department
TEL: 353-273-5550, VHEDNA@MAIL.UFL.EDU
Brain edema management; subarachnoid hemmorhage; vasopressin in stroke; atrial fibrillation and stroke, transcranial dopplers in stroke.
Kenneth M. Heilman M.D.
Distinguished Professor, Department of Neurology and the GRECC at the VAMC
Email: firstname.lastname@example.org TEL: 352-376-1611 Extension 6898
Our research is neurobehavioral (neuropsychology-behavioral neurology) and we investigate the neurobehavioral deficits associated with diseases such as dementia, head trauma and stroke causing disorders such as aphasia, spatial inattention (neglect), memory disorders, loss of skilled movements (apraxia), disorders of emotional communication and mood, changes in creativity, as well as many other cognitive domains. We also perform research on healthy older and younger volunteers. Our goals are to: 1) learn how the brain works; 2) how diseases alter cognitive functions; 3) how these disorder can best be diagnosed and treated. Examples of our research can be found by searching Pubmed with the term “Heilman K” Many former student have participated in our research program and have been authors of published papers.
Yuqing Li, Ph.D.
Professor of Neurology
My research is mainly focused on pathophysiology and experimental therapeutics of dystonia and restless legs syndrome. I am also broadly interested in animal models of movement disorders and in molecular and cellular mechanisms of synaptic plasticity during development and learning. My lab’s expertise is to perform conditional mutagenesis in mouse where selected genes are altered in specific neurons or circuits in the brain and in defined period during animal’s development. This powerful approach allows us to apply functional genomics and other multidisciplinary approaches to understand the pathogenesis of neurological disorders and to develop effective treatment.
Carolina B. Maciel, M.D.
Assistant Professor of Neurology. Division of Neurocritical Care. Neurology Department
Email: email@example.com TEL: 352-273-6165
Dr. Maciel’s interests include the humbling task of predicting neurologic outcome following acute brain injury, the mechanisms related to secondary brain injury in the neurocritically ill, and the critical care management of the potential organ donor. Dr. Maciel’s research focuses on improving neuroprognostication techniques and understanding the impact of cortical electrical phenomena (seizures and cortical spreading depression) after acute brain injuries. Dr. Maciel is working to elucidate mechanisms responsible for transient neuronal dysfunction and secondary brain injury which could lead to delayed or incomplete recovery, so that accuracy of neuroprognostication assessments can improve.
Nikolaus McFarland, M.D./Ph.D.
Department of Neurology
Research: My research focuses on Parkinsonian disorders and pathological mechanisms, in particular the role of alpha-synuclein and other neurodegenerative proteins.
Kimford J. Meador, M.D.
- Department of Neurology, McKnight Brain Institute
- Phone: (352) 273-5550; E-mail: firstname.lastname@example.org
Active areas of research include cerebral lateralization, dementia, epilepsy, mechanisms of attention and memory, neglect syndrome, neurodevelopmental effects of antiepileptic drugs, and the pharmacology and physiology of cognition.
Diego E. Rincon-Limas, Ph.D.
Department of Neurology
Phone: 273-9689, Email: email@example.com
My laboratory applies a variety of techniques to study the molecular pathways associated with several neurodegenerative diseases and to discover potential therapeutic targets. To do so, we use a multidisciplinary approach combining Drosophila genetics, neuroscience, molecular biology, biochemistry and optogenetic technologies.
- H. Subramony M.D.
Professor of Neurology
I have clinical research projects in the field of genetically determined cerebellar degenerations.
Michael F. Waters, M.D.,Ph.D.
Asst. Prof. of Neurology and Neuroscience
Chief, Neurovascular Division
Director, University of Florida Stroke Program and Associate Medical Director NeuroICU
Our research interests include genetic mechanisms of stroke, including cerebral cavernous malformations, CADASIL, and sickle cell anemia. In addition, he has active research in gene discovery and the pathophysiology of dominant cerebellar ataxias. Dr. Waters is a member of the American Academy of Neurology and the American Society of Human Genetics.
Jacob Ayers, Ph.D.
Assistant Professor of Neuroscience
Phone: (352) 293-8679; Email: firstname.lastname@example.org
The goal of my laboratory is to better understand the mechanisms involved in neurodegeneration and how these diseases propagate and spread throughout the body. Our lab utilizes a number of transgenic mouse models along with ex vivo and in vitro techniques to study proteins involved in Amyotrophic Lateral Sclerosis (ALS), Parkinson’s Disease, and Alzheimer’s Disease, in the hope to develop therapies which could prevent these toxic processes from occurring.
David R. Borchelt, Ph.D.
- Department of Neuroscience
- Phone: 352-294-0105 or email: email@example.com
My laboratory works to understand the basic mechanisms by which specific populations of neurons lose function and degenerate in neurodegenerative disease. Our studies mainly focus on genetic forms of Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.
Paramita Chakrabarty, Ph.D.
Dept of Neuroscience
firstname.lastname@example.org ; 352-273-7271
My key research focus is to explore how the activation of the innate immune system affects unique sets of pathological hallmarks in different neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Using recombinant adeno-associated virus mediated gene targeting in mouse models of these human neurodegenerative diseases, I am a) analyzing the effect of immune activation on the neuropathology, and b) designing and testing bioengineered innate immune modulators as therapeutic strategies in these mouse models. Some of the techniques that I frequently use in AAV based modeling and therapeutic studies are: behavioral analysis, high throughput biomarker studies (Nanostring and proteome arrays), biochemical analysis of neuropathological epitopes and MRI. Other secondary techniques, for example, primary neuroglial cultures and flow cytometry are also frequently used. More recently, my research has focused on understanding how specific innate immune mediators affect intrinsic vulnerability of neurons, leading to regionally selective neurodegeneration.
Shawn Dotson, Ph.D.
Assistant Professor of Neuroscience and Psychiatry, Division of Addiction Medicine
Dr. Dotson’s laboratory is interested in the functional organization of the gustatory system in the periphery, with a particular focus on the receptor basis of taste specificity. Mammals utilize several distinct populations of taste receptor cells to detect chemical cues that contain important information about the quality of foods. Exactly how these various cell populations contribute to the process of translating the physical properties of taste stimuli into neural activity still remains somewhat of a mystery. My laboratory uses sophisticated animal psychophysical testing to evaluate these processes in animals that have genetically or otherwise manipulated nervous systems. These studies may lead to the design of food additives that could benefit individuals suffering from conditions that are linked to excessive intake of foodstuffs (e.g., alcoholism, type 2 diabetes).
Kevin M. Felsenstein, PhD.
Associate Professor of Neuroscience
TEL: 352-294-5308, email@example.com
The primary emphasis of my research is to identify novel therapeutic targets for neurodegenerative disorders including but not limited to Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease. The identification of these targets is just the first step in a long drug discovery process which includes assay development, development of high throughput screens, and screening of diverse chemical collections including natural product extracts to identify compounds that specifically interact with the target of choice. These so-called ‘hits’ will form the basis of a synthetic chemistry effort, eventually, resulting in the elucidation of an optimized lead candidate with appropriate in-vitro and in-vivo activity. The optimized lead potentially could go on to preclinical/clinical development. Throughout this process the specificity of the interaction is investigated with the potential mechanism of action (MoA) identified. The identification of the MoA in itself may form the foundation of 2nd and 3rd generation drug discovery identification efforts. In parallel, we are also attempting identify biomarkers and be able to assay them routinely from blood or cerebrospinal fluid that could be used not only to determine target engagement but also potentially disease modification. While these translational efforts form the majority of our work we also aim to elucidate potential unifying mechanisms that underly neurodegeneration in general. One such potential mechanism may involve perturbation of mitochondrial dynamics and we are looking at ways to stabilize mitochondria as a potential therapeutic approach.
Pedro Fernandez-Funez, Ph.D.
Assistant Professor of Neurology and Neuroscience
e-mail: firstname.lastname@example.org Tel: (352) 273-5557
I am interested in understanding the molecular basis of complex neurodegenerative diseases such as Alzheimer’s disease. To identify new genes and cellular networks with a key role in the neurodegenerative process, we use fruit fly models of several diseases. For this, we express human genes (wild type and mutant) that cause neurodegeneration in the brain of flies and, then, try to identify new genes that lessen the cell loss. In the laboratory we use classic genetics, molecular genetics, RNA/DNA analysis, PCR, Western blot, protein biochemistry, immunofluorescence, cell culture and histological analysis.
Thomas C. Foster, Ph.D.
Professor of Neuroscience
Synaptic plasticity is thought to mediate the associative and information storage properties of neurons, and intracellular Ca2+ levels occupy a pivotal position in regulating synaptic plasticity by determining whether synaptic strength increases or decreases in response to neuronal activation. Changes in synaptic strength involve biochemical cascades and ultimately changes in gene regulation. One area of research in my laboratory is directed toward examining age-related changes in this signaling cascade from synaptic plasticity to transcription. The other area involves examining age-relate changes in estrogen. Many effects of estrogen are opposite to those observed during aging; however, the efficacy of the hormone is reduced if therapy is initiated several years after the onset on menopause or after the symptoms of Alzheimer’s disease are manifest.
Todd E. Golde, M.D.
Professor of Neuroscience
Director of the Center for Translational Research In Neurodegenerative Disease
Current Projects in the Golde Lab and the staff who lead these projects are described below.
- Immunotherapeutic approaches for Alzheimer’s disease and other amyloid disease (Yona Levites, PhD, Pedro Cruz PhD). Aggregation and accumulation of the amyloid β protein in the brain is thought to trigger a complex degenerative cascade that results in Alzheimer’s disease. These studies build on ~10 years of research in the labaoroty and are designed to develop novel active and passive immunotherapies that safely and effectively target AB amyloid in AD. Notably these therapies may have benefit in other amyloid diseases. Funded by the NIH/NIA http://projectreporter.nih.gov/project_info_description.cfm?aid=7796588&icde=5525743
- Gamma-Secretase Modulators and the role of short amyloid pep tides in Alzheimer’s disease. (Thomas Ladd, Brenda Moore PhD). A longer species of Aβ, Aβ42, is thought to be the key pathogenic molecular in AD. It is critical for deposition of Aβ. Thus, lowering levels of Aβ42 could have a major impact on the development of AD. In collaboration with Dr. Edward Koo’s laboratory (UCSD), we previously demonstrated that select drug and drug-like compounds could modulate A42 production and that this effect was attributable to direct alteration of -secretase activity. Drug with this type of effect oon Aβ are now referred to as a -secretase modulators (GSMs). These studies provided the rationale for clinical testing of GMSs by the commercial sector. Our current collaborative studies are designed to examine more closely how GSMs work, and whether short Aβ peptides are protective. Funded by the NIH/NIA. http://projectreporter.nih.gov/project_info_description.cfm?aid=8111733&icde=5525743
- Therapeutic Targeting of Intramembrane Cleaving Protease. (collaborations with Dr. Wolfe Harvard, Drs. Osborne (U. MASS), Miele (Loyola/U. Miss), M. Bouton (U. FL) and Greenbaum ( U. Penn)). Presenilin is the catalytic component of a multisubunit protease called -secretase that cleaves membrane proteins within their transmembrane domains. -Secretase cleaves a number of proteins and mediates signal transduction by many of these. In 2003, in collaboration with Dr. Chris Ponting, we identified a family of intramembrane proteases (signal peptide peptidase) that were related to -secretase. We are evaluating targeting these proteases in cancer, immunologic disease, and malaria. Funded by the NIH/NIA. http://projectreporter.nih.gov/project_info_description.cfm?aid=8098929&icde=5525743
- Proteinopathy induced Senescence Reponses in Neurodegenerative Disease (Wei Kou PHD, Paramita Chakrabarty PhD). We are exploring an alternative way in which protein accumulation in the brian might lead to brian organ failure. We hypothesize that protein misfolding and aggregation triggers a self-reinforcing cycle of chronic stress (sub-lethal toxicity), pro-inflammatory signals and a senescence response (Golde and Miller, Alz Res Ther 2009). We will examine whether under stress, neurons can undergo changes that phenocopy aspects of replicative senescence and whether these senescent changes are accelerated in AD and other CNS proteinopathies. To avoid confusion over semantics, we will refer to a putative stress response in non-dividing, terminally differentiated cells that mimics phenotypes seen in replicatively senescent cells as a senescence response. Funded by the Ellison Senior Scholar Award
- Somatic Brian transgenesis and AAV based models of Neurodegeneration (Yona Levites, PhD, Carolina Ceballos-Diaz, and Paramita Chakrabarty PhD). We have developed a method using viral vectors to transduce large portions of the neonatal brain. We refer to this technique as somatic Brain transgenesis. Using this technique we can much more rapidly model various aspects of neurodegenerative disease for a fraction of the costs associated with traditional transgenics. We have established over a dozen collaborations based on this technique.
- Inflammatory and Immune Mediators in Neurodegeneration. (Paramita Chakrabarty, Carolina-Ceballos Diaz, Pedro Cruz PhD, Wie Kou PhD). Recent work from our lab has challenged a long-standing hypothesis that inflammatory processes in AD accelerate Aβ deposition. Unpublished studies also reveal a potential novel role of interferon in nigrostriatal degeneration. Using the somatic brain transgenic technology described above we plan to more broadly explore immune modulators as mediators of neurodegenerative pathways.
Habibeh Khoshbouei, Ph.D., Pharm D.
The overall goal of my research program is to understand how the dopamine transporter (DAT) regulates biological responses, and how thisregulation is modulated by structural differences in ligands acting at DAT and by DAT-interacting proteins. As an example, by discovering the mechanisms by which the DAT substrate methamphetamine induces its unique addictive qualities, we will not only reveal novel therapeutic targets for intervention/prophylaxis of disorders associated with dysregulation of the dopaminergic system, but almost certainly ascertain new molecular mechanisms for transporter-effected signal transduction. Finally, I also intend that my research laboratory will provide an outstanding venue for the training of undergraduate and graduate trainees.
Michael King, Ph.D.
- Research Associate Professor, Department of Neuroscience, and VAMC
- Phone: (352) 376-1611×6499; E-mail: email@example.com
Our lab uses anatomical, electrophysiological, and biochemical/molecular techniques to study progressive neurodegenerative disease. The neuropathological effects of prolonged alcohol consumption are studied to figure out mechanisms by which damage results in impaired learning and memory. Gene transfer techniques are being used to develop better animal models for human neurodegenerative diseases, and potential therapeutic approaches to such diseases.
Ashok Kumar, Ph.D.
Neuroscience, McKnight Brain Institute
The overall goal of my research is to understand the relationship of cognitive impairment with brain aging and age-associated neurodegenerative diseases. Towards this goal, a central focus of my research involves delineating the basic mechanisms contributing to age-related cognitive decline and assess the role of various interventions such as environmental enrichment, exercise, and viral-vector mediated upregulation of target proteins in restoring and or rescuing impaired cognition, synaptic plasticity, and cell excitability.
Michael Lane, Ph.D.
Research Assistant Professor of Neuroscience
In collaboration with Dr. Paul Reier, also in the Department of Neuroscience, my research interest lies in the anatomical and functional changes that occur following spinal cord injury. We use a range of neuroanatomical and functional measurements to examine natural repair mechanisms (underlying plasticity) following spinal cord injury, and the potential for further repair. We are also evaluating the therapeutic potential for neural tissue transplantation, alone or in combination with pharmacological and gene delivery approaches, to modify the lesion environment, minimize damage and enhance repair processes.
Jada Lewis, Ph.D.
Associate Professor of Neuroscience, Center for Translational Research in Neurodegenerative Disease
Office: (352) 273-9666 Lab: (352) 294-5160
My lab focuses on generation and characterization of in vivo model systems of Alzheimer’s Disease, Frontotemporal Dementia, Parkinson’s Disease and Amyotrophic Lateral Sclerosis. Individuals in my lab will gain experience in a wide range of tasks in molecular biology, neuropathology, and biochemistry.
Jeremy McIntyre, Ph.D.
Assistant Professor, Department of Neuroscience
Phone (352) 294-8266 Email: firstname.lastname@example.org
Olfactory disorders affect a significant portion of the population. Disorders in the sense of smell can be caused by aging, traumatic injuries, infections and genetic mutations. Defects in ion channel function underlie an emerging class of human genetic diseases, termed channelopathies. In addition to other sensory defects, channelopathies can cause the loss of the sense of smell. Our research aims to identify mechanisms by which specific ion channels regulate olfactory signaling, how these are disrupted in disease states and the ability to correct channel defects. The ultimate goal of this work is to demonstrate functional recovery of olfactory function in channelopathy models for the further development of treatments for human patients.
Additionally, my lab studies the role of primary cilia on the neurons present in the olfactory bulb. Primary cilia are a type of cellular “antenna” that function to sense cues in the extracellular environment. However the precise roles for these organelles on neurons in the brain remain unknown. Many of these cilia possess G-protein coupled receptors for neuromodulatory signals. The aim of this project is to elucidate the role for cilia in modulating neuronal function in the olfactory bulb.
Harry S. Nick, Ph.D.
- Professor, Dept. of Neuroscience
- Phone: (352) 392-3033; E-mail: email@example.com
Our laboratory studies the molecular mechanisms that control the regulation of gene expression during the inflammatory response. We study the regulation of a subset of genes regulated by pro-inflammatory cytokines that play a cytotoxic or cytoprotective role in the inflammatory response in the brain, lung and kidney.
Lucia Notterpek, Ph.D.
Professor and Chair
Dr. Notterpek investigates how the loss of glial insulation around axons, called myelin, contributes to the pathogenesis of neural disorders. Diseases that are specifically linked with defects in myelin include peripheral neuropathies, such as Charcot-Marie-Tooth diseases and multiple sclerosis. Recent studies also suggest an involvement of myelin damage in underlying the painful symptoms of trigeminal neuralgia. Current research is focused on understanding the subcellular changes within neural cells that underlie the progressive nature of these disorders and to identify approaches to restore myelin and neural function. The laboratory is equipped with models and reagents, including small molecule therapeutics and genetic modifications to attain these goals. Other areas of active investigation include the role of gene regulatory mechanisms in peripheral nerve development, and the effects of aging on neuromuscular function.
Matt Sarkisian, Ph.D.
Dept of Neuroscience
My lab is interested in the development of the cerebral cortex and its pathogenesis which frequently is associated with neurological disorders such as seizures, mental retardation, autism and abnormal learning and memory. Primarily, we approach this in animal models by introducing new or mutated genes into neural progenitors in the embryonic cerebral cortex. This enables us to track subsequent genetic, neuroanatomical, physiological and behavioral changes during brain development.
Sue Semple-Rowland, Ph.D.
- Associate Professor, Dept. of Neuroscience
- Phone: (352) 392-3598; E-mail: firstname.lastname@example.org
The research in my laboratory is focused on two problems. The first is development and analyses of gene replacement strategies for treatment of inherited retinal disease using viral vector technology. The second is understanding the phototransduction cascade through which light signals entrain the circadian clocks located in the neural retina. Our experiments are carried out using molecular, biochemical, histological, embryological and cell culture techniques.
Wolfgang J. Streit, Ph.D.
- Professor, Dept. of Neuroscience
- Phone: (352) 392-3910; E-mail: email@example.com
Research concerns functions of microglial cells in the regenerating and degenerating central nervous system. Understanding microglial biology is important for developing strategies to repair the injured CNS, and also for understanding primary neurodegenerative disease, such as Alzheimer’s disease.
Loic P. Deleyrolle, Ph.D.
Dept. of Neurosurgery
TEL: 352-682-1961 E-mail: firstname.lastname@example.org
My research interest lies in understanding mechanisms contributing to brain tumor heterogeneity and developing novel therapeutic paradigms to treat glioblastoma, including metabolic interventions and immunological targeting.
Maryam Rahman, M.D.
Department of Neurosurgery
Research interests: novel therapies for brain tumors, immunotherapy for adult glioblastoma, quality improvement and patient safety.
Vinata Vedam-Mai, Ph.D.
Neurosurgery & Movement Disorders and Neurorestoration (UFCMDNR)
Email: email@example.com; TEL: 273-8583
Research is focused on neurodegenerative diseases, particularly Parkinson’s disease and improving its current therapies (including immunotherapy). Trying to comprehend the effect of chronic electrical stimulation such as DBS on neurogenic niches of the brain. Using metabolomic techniques, assessing the minute fluxes within the metabolome of diseased brain.
Obstetrics & Gynecology
Nancy S. Hardt, M.D.
- Ob-Gyn and Pathology
- 352-273-5460 office
We work on the city, county, state, and federal level to improve the health of Floridians. For example, we study and monitor health disparities using GIS mapping, we train students in advocacy through monthly visits to Tallahassee, we work on a number of county and state level committees in the areas of mother/baby health, maternal mortality, domestic violence, and child abuse; and we work on federal health policy in the areas of graduate medical education, reimbursement for Medicaid, and coverage of pregnancy and interconceptional health. This choice would be perfect for an undergraduate student in biological sciences, psychology, or political science who would like to go to graduate school in the health professions.
Gregory Schultz, Ph.D.
- Professor, Dept. of Obstetrics & Gynecology
- Phone: (352) 273-7560
- E-mail: firstname.lastname@example.org
Excessive scarring of corneal wounds causes impaired vision. Therapies currently used to reduce corneal scarring use non-specific drugs, including anti-inflammatory steroids or anti-proliferative cancer drugs like 5-fluorouridine (5FU) or mitomycin-C that can cause severe, long-term side effects. We are developing antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) that specifically target mRNAs for the two growth factors, transforming growth factor beta (TGFb) and connective tissue growth factor (CTGF), that are known to regulate scarring in the cornea and in other tissues in the body. Initial studies with these new drugs show significant reduction of the target mRNAs in cultures of corneal fibroblasts and reduced corneal scarring in rabbit models following excimer ablation of corneas. In this project, the student will participate in experiments using gene-targeted therapy to reduce corneal scarring. The student will assist in surgery creating corneal wounds, measure expression of TGFb and CTGF mRNA and proteins, and measure corneal scarring (haze) in photographs of rabbit corneas. The student should have basic understanding of biochemistry and molecular biology techniques and be willing to work with laboratory animals.
Lisa Beth Spiryda, M.D., Ph.D.
Obstetrics and gynecology
- Translational research on Identifying molecular markers involved with Human Papillomavirus acquisition and persistence and role in cervical dysplasia and cancer as well as other cancers. 2. Health Disparities, Women’s Health – breast feeding, routes of surgeries.
Shannon E. Boye, Ph.D.
Ophthalmology (primary), Molecular Genetics and Microbiology (secondary)
TEL: (352) 273-9342; email: email@example.com
Dr. Boye’s lab focuses on the development of viral vectors for the treatment of inherited retinal disease. The retinal disorders she currently studies include, but are not limited to, Leber congenital amaurosis (LCA1, LCA2 and CEP290-LCA) and Usher syndrome. Because of its importance to human vision, much of Dr. Boye’s work focuses on cone photoreceptor-targeted therapy. The three major goals of her research program are:
1) Developing an AAV-based therapy for the treatment of GUCY2D-LCA1. Dr. Boye manages the pre-clinical, proof-of-concept and safety studies aimed to bring this treatment from bench to bedside within the next couple of years.
2) Optimizing AAV vectors to successfully treat diseases which involve mutations in large genes (something recently considered outside the scope of standard AAV gene therapy).
3) Developing novel viral vectors capable of delivering therapeutic genes to the outer retina (photoreceptors) following a surgically less invasive, intravitreal injection.
Qiuhong Li, Ph.D.,
Associate Professor of Ophthalmology
TEL: 352-392-0747, Email: firstname.lastname@example.org
Our research is mainly focused on retinal renin angiotensin system. The renin-angiotensin system (RAS) plays a vital role in the cardiovascular system. Angiotensin II (Ang II), a key peptide hormone of RAS, has been known to regulate a variety of hemodynamic physiological responses, including fluid homeostasis, renal function, and contraction of vascular smooth muscle. In addition, elevated level of Ang II is capable of inducing a multitude of non-hemodynamic effects, such as the induction of reactive oxygen species (ROS) and expression proinflammatory cytokines, leading increased oxidative stress and inflammation. Classically, RAS is considered a circulating hormone system consisting of a linear cascade of Ang II generation. However local RAS exists in almost every organ including the CNS and eye, and plays vital role in neuro-vascular function and modulating local immune responses. Furthermore, the discovery of angiotensin-converting enzyme 2 (ACE2) has resulted in the establishment of a novel axis of RAS involving ACE2/Ang-(1-7)/Mas. ACE2 is able to cleave Ang II to form Angiotensin-(1-7) (Ang-(1-7)). Ang-(1-7) binds to a G-protein coupled receptor, Mas, and activates signaling pathways that counteract the effects of Ang II. Thus the ACE2/Ang-(1-7)/Mas axis has emerged as a critical regulator of Ang II/AT1R signaling. Accumulating evidence has also demonstrated that enhanced expression of Ang-(1-7) and ACE2 reduces inflammation, oxidative damage, inhibits pathologic angiogenesis, and confers protection against a variety of pathological conditions including metabolic syndrome, diabetes and its complications; neuro-vascular dysfunctions and neurological diseases. Our current research projects are primarily focused on this protective axis (ACE2, Ang-(1-7) and Mas receptor).
Two main aspects of our current research projects, funded by NIH, American Diabetes Association and BrightFocus foundation, are: (1) Translational studies- to enhance this protective axis using various approaches, including local ocular gene delivery via recombinant adeno-associated viral vectors, pharmacological and oral delivery of proteins expressed and bioencapsulated in plant cells, to treat (both prevention and possibly reversal) a number of retinal diseases including diabetic retinopathy, age-related macular degeneration, and inherited photoreceptor degeneration in animal models; (2) Basic research studies- although the protective effects of Ang-(1-7)/Mas signaling are well-established in many organs under many different pathological conditions including the CNS, the signaling mechanisms and downstream target genes are largely unknown. Our long term goal is to further elucidate these signaling mechanisms and downstream genes involved in the protective actions of Ang-(1-7) in the retina and their interactions with other pathways implicated in the pathogenesis of retinal diseases in order to develop more effective and targeted therapeutics.
- Clay Smith, Ph.D.
Shaler-Richardson Associate. Professor of Ophthalmology
Eyes are exquisitely sensitive detectors, capable of registering a single photon of light. In my lab, we focus on how eyes achieve this amazing quantum detection ability. Our primary interests cover the biochemistry and cellular biology of the early events in this process– how the eye captures photons, and how this information is reliably translated into a signal that can be utilized by the brain to form an image. Since defects in this process often lead to visual complications, such as retinal degeneration and stationary night blindness, we anticipate that our studies will lead to therapies for these associated diseases. In my lab, we utilize the tools of molecular biology, protein chemistry, structural biology, and cell biology to delve into these questions.
Orthopaedics and Rehabilitation
Laurel C. Blakemore, M.D.
Chief and Associate Professor, Orthopedic Surgery
TEL: 352-273-7435, Email: email@example.com
We have a variety of projects in pediatric orthopedics and pediatric spine surgery
Bryan P. Conrad, Ph.D.
Assistant Professor of Orthopaedics
The driving mission of my lab is to improve the health and well-being of those with musculoskeletal disease through innovative biomechanical research. Our work encompasses three broad areas: clinical research, implant testing and sports performance. The main focus of our clinical research is in the area of spine biomechanics: to improve management and care of individuals with spine trauma and to better understand the biomechanics of low back pain.
Heather K. Vincent, Ph.D.
Department of Orthopaedics and Rehabilitation
Phone: 273-7459 firstname.lastname@example.org
Research Interests: obesity and disability, rapid weight loss and changes in gait and quality of life, effect of exercise and nutraceuticals on obesity related disability and pain, effect of hyaluronic acid viscosupplementation on knee pain and physical function in obese adults with knee osteoarthritis, eccentric resistance exercise effects on metabolic rate and muscle soreness, running and gait mechanics.
Kevin P. Raisch, Ph.D.
Department of Otolaryngology
Ph: 352-273-7783, email: email@example.com
With the increasing association of Human Papillomavirus (HPV) and the oral cancers, my studies involve screening healthy adults and head and neck cancer patients for HPV infection. HPV-positive tumors have been more responsive to cancer treatment options than HPV-negative tumors, therefore we are studying the molecular biology of HPV-induced tumors. For the treatment of head and neck cancer patients, my research involves screening compounds (small molecular inhibitors, novel agents, or single-chain antibodies) for anti-tumor activity and analyzing the compounds for synergistic activity with radiation and chemotherapeutic agents. These investigations include mechanistic studies to understand the anti-tumor activity of these novel agents.
Pathology, Immunology & Laboratory Medicine
Todd M. Brusko, Ph.D.
Assistant Professor, Department of Pathology, Immunology and Laboratory Medicine
For more information, http://bruskolab.diabetes.ufl.edu/
Dr. Brusko and his team of diabetes researchers at the University of Florida are dedicated to the development of safe and effective therapies to prevent and reverse type 1 diabetes. His laboratory works in close collaboration with Michael Haller, M.D., and Desmond Schatz, M.D., to conduct mechanistic studies in ongoing clinical trials and generate novel avenues for therapeutic intervention.
Martha J. Burt, M.D.
Pathology, Immunology, and Laboratory Medicine
My current research projects are: drug use and abuse in deceased pregnant and recently pregnant women, and in domestic violence fatalities. Most of my research is retrospective and includes collaboration with professionals in several colleges on campus.
Jason H. Byrd, Ph.D.
Pathology, Immunology and Laboratory Medicine
Dr. Byrd’s laboratory is involved in the forensic sciences. Specifically, forensic entomology, forensic botany, postmortem interval estimations, DNA analysis, crime scene analysis and veterinary forensic sciences.
Martha Campbell-Thompson, DVM Ph.D.
Pathology, Immunology, and Laboratory Medicine
Our research focuses on understanding several key areas of beta cell biology in both health and diabetes particularly related to inflammatory and neural mechanisms for loss of beta cells in type 1 diabetes.
Michael Clare-Salzler, M.D.
Professor and Chair, Pathology, Immunology and Laboratory Medicine
Research interests include Cellular and Molecular Immunology, Autoimmune diseases
Antigen presenting cells, Dendritic cell biology, Type 1 interferon biology and immunogenetic regulation of interferon responses, Inflammation, Eicosanoid metabolism, and Inflammation resolving lipids (resolvins).
Abdoreza Davoodi-Semiromi, Ph.D.
- Research Asst. Professor, Dept. of Pathology & Immunology
- Phone: (352) 392-0397; E-mail: firstname.lastname@example.org
I am interested in molecular pathogenesis of type 1 diabetes by using an animal model of human type 1 diabetes namely NOD mouse. Currently, I am investigating impact of a kinase inhibitor on generating regulatory T-cells and wanted to shown de-novo generated regulatory T-cells are capable to prevent/delay onset of diabetes in NOD mouse. In the course of this study a variety of different techniques such as flow cytometry, beads-based assays using Luminex technology, gene cloning and many other techniques will be used.
Timothy J. Garrett, Ph.D.
Department of Pathology, Immunology, and Laboratory Medicine
Phone: 352-273-5050; email: email@example.com
I’m interested in the application of mass spectrometry in clinical research. We are working on global and targeted metabolomics in which we are developing methods and instrumentation for identifying and quantifying as many metabolic markers to understand what is happening with individual metabolism in disease. Mass spectrometry is employed because it has sufficient sensitivity, mass resolution, and accuracy to measure a few thousand small molecules in a single plasma sample.
Bruce A. Goldberger, Ph.D., DABFT
Director of Toxicology and Professor, Department of Pathology,
Immunology & Laboratory Medicine, Department of Psychiatry
Phone: (352) 265-0680 x72001; E-mail: firstname.lastname@example.org
Dr. Goldberger’s laboratory supports Medical Examiner Offices in seven districts throughout the State of Florida with an approximate yearly caseload of 3000. Dr. Goldberger’s laboratory also provides analytical services for governmental, academic, and private organizations. Dr. Goldberger’s research includes: ( 1) the study of the role of illicit and prescription drugs (especially cocaine and opioids) in the death of individuals investigated by medical examiners; (2) the study of the dietary influences of caffeine; and (3) the identification and measurement of alcohol and drugs in breath.
Marguerite Hatch, Ph.D.
- Department of Pathology
- email@example.com or 392-0013
A number of diseases are associated with kidney stone formation which is a very painful condition and damaging to kidney function. My research involves studying animal models and investigating basic mechanisms that are responsible for excreting the stone-forming compounds.
Saeed R. Khan, Ph.D.
- Professor, Dept. of Pathology, Immunology & Lab Medicine
- Phone: (352) 392-3574; E-mail: firstname.lastname@example.org
Investigating the role of renal epithelial injury in modulation of crystallization in the kidneys. Molecular biological, biochemical and microscopic techniques are used to investigate the production of various urinary proteins by renal epithelial cells in culture as well as in animal models in response to various stimuli.
Chen Liu, M.D., Ph.D.
- Professor of Pathology, Department of Pathology, Immunology and Lab Medicine
- Phone: 392-2886; E-mail: Liu@pathology.ufl.edu
My lab is interested in the pathogenesis of hepatitis C virus infection, particularly the role of cellular factors in viral replication. We are also interested in oncogenic cell transformation.
Clayton E. Mathews, Ph.D.
Professor, Departments of Pathology, Immunology, and Laboratory Medicine
Phone (Office) 352-392-9803; email email@example.com
Dr. Mathews’ studies have forged a new path in the understanding of autoimmune diabetes. While the majority of the field focuses on identifying defects in cells of the immune system, the guiding hypothesis of Dr. Mathews’ research is that insulin secreting pancreatic beta cells are active contributors to the autoimmune process in T1D. The initial publications from Dr. Mathews demonstrating that pancreatic islets had down regulated self-defenses, and that this reduction was important in the initiation of diabetes. The extension of this work strongly supported the hypothesis that beta cells play an active role in the pathogenesis of diabetes. The findings demonstrated that islets varied in their resistance to autoimmune destruction and further that islets from different donors ranged from highly susceptible to extremely resistant to damage. These novel findings proved to be influential because, prior to this paper, there was no evidence suggesting that beta cells could resist autoimmune destruction. Dr. Mathews’ investigations have provided the proof of concept for many subsequent therapy studies y both his and other groups. These findings also led Dr. Mathews a postulate that there are genetic factors expressed at the level of the pancreatic islet that provide resistance to autoimmune diabetes. His successive publications have supported this hypothesis and have identified a gene (mt-Nd2) that is responsible for protection as well as to the identification of the signaling pathways that can be blocked inhibiting beta cell death without modifying beta cell insulin secretory activity. The discovery of genes that pancreatic islets employ to ward off autoimmune effector mechanisms have important ramifications for transplantation, stem cell engineering, and future genetic and pharmacological diabetes preventative therapies.
Laurence Morel, Ph.D.
Department of Pathology, Immunology, and Laboratory Medicine
Tel # (352) 273-5638, firstname.lastname@example.org
Dr. Morel’s research focuses on the genetic analysis of lupus susceptibility using a mouse model and validates the findings obtained in the mouse with immune cells obtained from lupus patients and healthy controls. The long-term goal of this research is to identify the genes responsible for lupus susceptibility and to characterize their contribution to autoimmune immunopathology. This is a multifaceted project combining immunological and genetic approaches that has established her expertise in lupus genetics and more generally in the genetics of autoimmune diseases and in mouse models of autoimmune pathogenesis. The complexity of lupus genetics stems from the fact that it is a polygenic disease and that no single gene is required for disease development. Dr. Morel has made a significant contribution to the field of complex trait genetics, and lupus genetics in particular, by showing that lupus susceptibility was inherited as a threshold liability of a combination of four susceptibility alleles. Dr. Morel has defined a conceptual approach, the congenic dissection, which is now widely used to analyze complex traits in animal models. In the process, they have updated the production of congenic strains to molecular screens and develop the “speed-congenic” method, which is now considered to standard approach for the production of congenic strains.
Dr. Morel has made considerable progress toward the identification of lupus susceptibility genes and in their functional characterization. She has shown that lupus pathogenesis was reconstituted by the combination of three chromosomal regions from the lupus-prone strain in a triple congenic strain. This was a landmark study in the field that has not been achieved in any other models. This BcN/LmoJ triple congenic strain is now the basic model to study lupus immunogenetics and mechanisms of tolerance in Dr. Morel’s lab. This BcN/LmoJ strain has now been licensed and it is distributed by the Jackson Laboratories to numerous investigators and companies. Dr. Morel’s research now focuses of characterizing the contribution to autoimmune pathogenesis of several genes that she has positionally cloned as lupus susceptibility genes in the NZM2410 mouse. These genes, which include homeobox protein (Pbx1), orphan nuclear receptor (Esrrg), cell cycle regulator (Cdkn2c), SAP family adaptor (Sh2d1b1) and growth factor receptor (Csf3r), are very diverse in function and cellular target of expression. Finally, Dr. Morel is conducting research on the genetic regulation of cellular metabolism in immune cells and how it can be used to treat lupus with metabolic inhibitors.
Naohiro Terada, M.D., Ph.D.
- Professor, Dept. of Pathology
- Phone: 352-392-2696; E-mail: email@example.com
Induced pluripotent stem cells (iPSCs) are a newest type of stem cells artificially generated by transiently expressing a set of exogenous transcription factors in somatic cells such as skin fibroblasts. The iPSCs can differentiate into all the cell types in our body such as neurons and cardiomyocytes as embryonic stem cells (ESCs) do. Since Yamanaka (2006) originally reported the method for iPSC induction, the field has been rapidly expanding with great expectation. Essentially, the clinical implications of iPSCs are in two fold; first, as a cellular resource for transplantation therapy, and second, as a system to model human diseases. In my laboratory, in collaboration with many clinical investigators, we focus on utilizing patient-derived iPSCs for understanding disease mechanisms and for drug discovery. We welcome highly motivated and innovative undergraduate students to join our effort.
Changqing Xia, M.D., Ph.D.
- Research Assistant Professor, Department of Pathology, Immunology and Laboratory Medicine
- Phone: 846-0585, Fax: 352-392-5393
- E-mail: firstname.lastname@example.org
My research field is immunology, especially focusing on autoimmune type 1 diabetes. We are developing a program using tolerogenic dendritic cells or other approaches to prevent type 1diabetes by restoring self immune tolerance.
Lijun Yang, Ph.D.
- Asst. Professor Dept. of Pathology
- Phone: 392-0005; E-mail email@example.com
On-going research in my laboratory focuses on major areas of adult stem cell plasticity for a cure/management of type 1 diabetes mellitus (T1DM). Over the past several years, we have made great progress by discovering ways to transdifferentiate adult stem cells (bone marrow, liver stem cells, and splenocytes) into functional insulin-producing pancreatic islet-like cells extrinsically by manipulating culture microenvironments and intrinsically by over-expressing those transcription factor(s) playing critical roles in pancreatic beta-cell development. In addition, we are pursuing two additional research projects: (1) Explore molecular mechanism of ATRA-induced cell differentiation in acute promyelocytic leukemia; and (2) Generate tumor-antigen-specific cytotoxic T-cells for the treatment of multiple myeloma.
George Aslanidi, Ph.D.
My research is focuses on the production and application of adeno-assosiated virus (AAV) vectors in application of gene and cell therapy, adaptation of AAV delivery methods to dendritic cells based immunotherapy, and mechanisms of maturation of dendritic cells (DC) and peripheral T-cell activation. In all cases, these strategies have focused on the use of viral vectors (AAV) to regulate therapeutic transgenes and on efforts to retargeting such AAV vectors to provide a more specific and efficient means for gene therapy.
Manuela Corti, PT, Ph.D.
Department of Pediatrics
E-mail: firstname.lastname@example.org TEL: 352-294-5779
Dr. Manuela Corti is currently an Assistant Professor at the University of Florida in the Child Health Research Institute and Powell Gene Therapy Center. Dr. Corti is a clinical scientist engaged in translational research focusing on understanding the contribution of neurological impairment in neuromuscular disorders by combining expertise in clinical assessment with novel therapies that rely on correcting the fundamental genetic defect. Her specific research is dedicated at developing AAV gene therapy programs for neuromuscular diseases and immunomodulation strategies to allow for multiple AAV dosing. Her research interests also include outcome measures and clinical trial readiness for neuromuscular diseases.
Sam Xianjun Cheng, MD, Ph.D.
Department of Pediatrics
TEL: (352)273-9358, Email: email@example.com
My lab is currently working on several projects with the goal of defining novel therapeutic approaches to inflammatory bowel disease, irritable bowel syndrome, and secretory diarrhea.
Curt DeGroff, M.D.
Clinical chart review study – We would like a student to look at whether the use of a new micro-mini size transesophageal echo probe we use in the operating room on patients receiving congenital heart surgery has improved post operative feeding issues.
Willa H. Drummond, M.D.
Professor, Dept. of Pediatrics
My research will be in areas relating to developing effective clinical computer systems and in using data derived from computerized systems to study the physiology of ECMO (extracorporeal membrane oxygenation) and the neonatal cardiopulmonary diseases that cause need for ECMO (mainly pulmonary hypertension, failure and septic shock).
Marilyn Dumont-Driscoll, MD, PhD
Medicine- General Pediatrics
TEL: 352-334-1340 or firstname.lastname@example.org
My focus is on clinical research (non-laboratory) in the area of childhood obesity including aspects of prevention, early identification of risk factors including genetic predisposition for obesity and associated physical and mental health co-morbidities, with clinical assessment, management and follow-up in the context of a medical home. My other area of interest is in resident and student medical education, genetics in primary care, quality of care in pediatrics, and patient/family satisfaction and strategies to improve adherence.
Darin J. Falk, Ph.D.
TEL: (352) 273-6549; E-mail: email@example.com
The major interest of the laboratory is to determine the primary mechanism by which respiratory muscles display decreased activation or force-generating capacity in models of neuromuscular disease. A specific example is Pompe disease which affects the central nervous system, neuromuscular junction, and skeletal muscle; ultimately resulting in respiratory and ambulatory dysfunction. Our studies have focused on identification of each of these aspects to determine their contribution to loss of proper maintenance and function in these systems. To accomplish this, our approach incorporates an array of molecular, biochemical, and physiological measurements. In addition, we have found that recombinant adeno-associated viral (rAAV) vectors can be tailored to provide adequate gene expression in skeletal muscle and the CNS in a mouse model of Pompe disease. Specifically, rAAV therapy has reversed the disease associated phenotype and restored motoneuron and respiratory muscle function. Further optimization of rAAV vectors has led to improved transduction efficiency and may allow for a reduction in viral particles required to provide a therapeutic benefit. This may be critical in reducing potential immunoreactivity to the rAAV capsid and/or transgene and provide improved outcomes in affected patients. http://falk.research.pediatrics.med.ufl.edu/
Suman Ghosh, M.D.
Assistant Professor in the Department of Pediatrics, Division of Pediatric Neurology. Joint Assistant Professor in the Department of Neurology.
TEL: 352-265-8250, email at firstname.lastname@example.org
My clinical research focuses on etiologies and treatment of cerebral palsy, co-morbidities associated with pediatric traumatic brain injury and neurodevelopmental outcomes in children with congenital heart disease.
Michael Haller, M.D.
TEL: 352.273.9264, email@example.com
My research focus is pediatric type 1 diabetes. Our group uses a bench to bedside (translational) research approach in efforts to better understand type 1 diabetes and to develop therapies to prevent and ultimately reverse the disease. We have opportunities that span the entire spectrum of research from basic science in the laboratory to animal model experiments, to large clinical trials.
Brad E. Hoffman, Ph.D.
Department of Pediatrics, Division of Cellular & Molecular Therapy
TEL: (352) 273-8152, firstname.lastname@example.org
I am a cellular immunologist with a long-standing interest in tolerance induction using adeno-associated virus (AAV) gene therapy. My laboratory is particularly interested in the mechanisms surrounding the generation of antigen-specific regulatory T-cells (Tregs), and the role they have in tolerance induction following gene transfer. One major focus of the laboratory is aimed at exploiting the unique molecular and cellular mechanisms of liver-directed AAV gene therapy in order to modulate immunological tolerance to specific antigens as a preventative or therapeutic intervention in autoimmune neurological diseases such as Multiple Sclerosis.
Peter B. Kang, M.D.
Department of Pediatrics (Division of Pediatric Neurology)
Contact: email@example.com or 352-273-8920
My laboratory focuses on the genetics of muscular dystrophy, in particular the limb-girdle muscular dystrophies. We use exome sequencing to screen families for potential mutations and then use various approaches to confirm or exclude candidate mutations. Certain genes of interest are selected for more in-depth analysis and long term study.
Chen Ling, Ph.D.
Department of Pediatrics,
TEL: 352-273-6174, firstname.lastname@example.org
Dr. Ling’s research focuses on adeno-associated virus (AAV) virology, gene therapy and traditional Chinese medicine (TCM). His laboratory has made contributions to the above fields including: identification of a novel function of the inverted terminal repeat in the AAV genome and a new method applied by AAV to reduce its endogenous gene expression; elucidation of cellular receptor/co-receptor for AAV serotype 3; development of human liver targeting recombinant AAV gene therapy vector; identification of small molecules isolated from TCM to enhance gene therapy outcome; and delivery of cytotoxic genes isolated from TCM for the purpose of cancer gene therapy. The current emphasis of Dr. Ling’s research is on combining the treatment of rAAV-based cancer gene therapy and of TCM for human hepatocellular carcinoma.
David Markusic, Ph.D.
TEL: 273-8149, email@example.com
Using novel adeno-associated virus (AAV) vectors for gene therapy to treat hemophilia. To model and identify strategies to minimize immune responses against human factor VIII, factor IX, and AAV following gene transfer. To translate effective strategies in hemophilia models that induce tolerance and reverse pre-existing immunity to coagulator factor to treat autoimmune disease.
Josef Neu, M.D.
Contact information (phone and/or e-mail): 273-8982; firstname.lastname@example.org
The Neonatal Gastroenterology and Biochemical Nutrition Laboratory most recently has been involved in studies of the intestinal microbiome and how it relates to the development of neonatal necrotizing enterocolitis and sepsis. We are also studying the relationship of how different microbes related to later health and disease.
Don Novak, Ph.D.
- Professor and Chief, Department of Pediatrics
- Phone: 392-6410; E-mail: email@example.com
Our laboratory is interested in the pathophysiology of normal fetal development, particularly as related to fetal nutrition. Our primary focus is upon placental function and the passage of nutrients across the placenta from mother to fetus. We utilize a variety of models (in vivo animal models, isolated cells, human placenta) and techniques in our efforts. The eventual goal of our research is to understand the mechanisms and regulation of nutrient transfer from mother to fetus, thus allowing the development of effective therapies for common disorders such as intrauterine growth retardation, which currently adversely impact the health of infants worldwide.
Christina A. Pacak, Ph.D.
Department of Pediatrics
Our primary focus is to develop adeno-associated virus (AAV) mediated gene therapy and mitochondrial transplantation therapy to treat disorders that affect mitochondrial function. The lab has deep expertise in the use of various serotypes of AAV combined with tissue specific promoters to achieve robust transgene expression for the treatment of genetic disorders. We are particularly interested in developing treatments for the following two genetic diseases:
Barth Syndrome – an X-linked mitochondrial disease that causes dilated cardiomyopathy, neutropenia, muscle weakness, growth delay and exercise intolerance. The underlying problem is a mutation in the tafazzin gene which causes a decrease in cardiolipin synthesis.
Cockayne Syndrome – a multi-system autosomal recessive neurodegenerative disorder characterized by growth failure, nervous system impairment, photosensitivity, eye abnormalities, liver dysfunction, and a variety of other symptoms caused by premature aging. A defect in transcription-coupled DNA repair and its consequences in the repair of mtDNA contribute to the pathophysiology of this disease.
Additionally, recent collaborative work demonstrated that ischemia reperfusion injury can be prevented by injecting mitochondria isolated from healthy unaffected tissue into a heart model of regional cardiac ischemia. The hearts that received mitochondria displayed a significant decrease in apoptosis and infarct size as well as an increase in regional function as compared to controls. Based upon these exciting results we are now developing the same concept of mitochondrial transplantation therapy to ameliorate mitochondrial impairment in neuronal cells caused by cerebral hypoxia in newborns.
Liya Pi, Ph.D.
Department of Pediatrics
TEL: 352-294-5679, Email: firstname.lastname@example.org
My current research focuses on the patho-physiology of the liver, particularly the mechanisms involved in fibrotic response during hepatic progenitor cell activation and liver cancer development. Alcohol and high fat diet (HFD) influence the function of a wide range of cells and tissues. They can interact with cellular components or indirectly affect systemic oxidative and inflammatory states via intermediate metabolites. Persistent damage causes chronic injury leading to hepatic progenitor cell (HPC) activation and life-threatening fibrotic diseases such as alcoholic cirrhosis and nonalcoholic steatohepatitis (NASH). Dynamic extracellular matrix (ECM) remodeling is involved in these fibrotic diseases via transcriptional regulators, growth factors and proteases. Connective tissue growth factor (CTGF) is an extracellular signaling modulator in the CCN (Cyr61/CTGF/Nov) family important for hepatic progenitor cell activation and liver repair. Overexpression of CTGF is a hallmark in fibrotic disorders. Two regulators of CTGF, ADAMTS7 (a disintegrin and metalloproteinase with thrombospondin type I repeat 7) and the transcriptional coactivator YAP (Yes-associated protein), have been identified. We are currently using our established alcohol and NASH models to investigate the roles of ADAMTS7 and YAP in CTGF mediated HPC activation, alcohol fibrosis and NASH diseases. Some of our recent publications are below.
- Wu Q, Pi L, Trinh T, Zuo C, Xia M, Jiao Y, Puszyk W, Pham K, Nelson D, Robertson K, Ostrov D, Xia C, Liu C. Vaccine targeting glypican-3 induces tumor regression in a murine hepatocellular carcinoma model. (2017) Molecular Therapy. 25(10):2299-2308.
- Bria A, Sun X, Zhou JM, Jorgensen M, Petersen BE, Pi L. Hepatic progenitor cell activation in liver repair. (2017) Liver Research Journal. https://doi.org/10.1016/j.livres.2017.08.002
- Pi L, Jorgensen M, Oh SH, Protopapadakis Y, Gjymishka A, Brown A, Robinson P, Liu C, Scott EW, Schultz GS, Petersen BE. (2015) A disintegrin and metalloprotease with thrombospondin type i motif 7: a new protease for connective tissue growth factor in hepatic progenitor/oval cell niche. American Journal Pathology. 185:1552-1563.
- Pi L, Robinson PM, Jorgensen M, Oh SH, Brown AR, Weinreb PH, Trinh TL, Yianni P, Liu C, Leask A, Violette SM, Scott EW, Schultz GS, Petersen BE. (2015) Connective tissue growth factor and integrin αvβ6: a new pair of regulators critical for ductular reaction and biliary fibrosis in mice. Hepatology. 61:678-691.
Jeffrey Roth, Ph.D.
Program Director and Research Associate Professor of Pediatrics
TEL: 352.334.1360, E-mail: email@example.com
Our research interests include:
- Anti-obesity initiative in local schools. This project involves developing fun after school activities with interdisciplinary UF graduate and undergraduate students. Work with students 2x – 4x a month at schools. Obtain baseline and periodic measures of health. Analyze data.
- Reduce foster care placement for at-risk youth. Local child welfare agencies want to link their data with our Center’s data. Develop aggregate descriptive statistics, key indicators of health, and generate GIS maps for sharing with social service agencies.
- Develop health report cards for Alachua County and share with the community. Create maps of these health indicators.
- Assist construction of a maternal and child health data warehouse. Conduct needs assessment. Develop tools to query data electronically and dynamically.
Sachin S. Talathi, Ph.D.
- Pediatrics (Primary), Neuroscience (Joint), Biomedical Engineering (Affiliate)
- firstname.lastname@example.org / 352-870-0229
Epilepsy Neural Engineering, Dynamical Principles in Neuroscience.
Lindsay Thompson M.D. M.S. and Erik Black Ph.D.
Through multidisciplinary work in medicine, public health/ health services research and education, we, as investigators with the Division of General Pediatrics, employ techniques of observational research to understand outcomes in health and well-being. We are currently involved in several projects in education and medicine, although we specifically are seeking help in investigating online profiles and their relationships to health. We argue that the degree of overlap between high-risk behaviors depicted in online social networking profiles (eg: Facebook, MySpace) and real-life, high-risk behaviors (alcohol, drug, tobacco consumption, sexual practices, etc) is unknown. Our research aims to explore two related objectives: first, it aims to establish a rubric, or tool, to reliably quantify the content of online social networking profiles. Second, it aims to test whether high-risk behaviors depicted in individual online social networking profiles are associated with participation in real-life, high-risk behaviors, and to establish how personal characteristics such as age, gender and race/ethnicity affect this relationship.
Christopher C. Wendler Ph.D.
Assistant Professor of Pediatrics
TEL: 352-294-5675, email@example.com
Increasing evidence indicates that alteration of the normal prenatal environment affects development and can influence an individual’s lifetime risk of developing obesity and cardiovascular disease. Thus, understanding how in utero exposure to chemical agents lead to increased susceptibility to adult diseases is the goal of my research. Previously, we have demonstrated that adenosine A1 receptor (A1AR) signaling protects the embryo from hypoxic conditions in utero. In addition, we have revealed that in utero caffeine exposure has long-term effects on cardiac function and morphology in adult offspring, and that these effects are mediated by A1AR action. Recently, we have demonstrated that in utero caffeine treatment leads to changes in DNA methylation patterns in adult hearts. And we are currently pursuing research to determine if these changes in DNA methylation mediate the changes we see in adult hearts. In addition, we have begun to examine whether caffeine exposure in utero has transgenerational effects on heart function.
Pharmacology & Therapeutics
Jeffrey K. Harrison, Ph.D.
Professor, Department of Pharmacology & Therapeutics
Email: firstname.lastname@example.org Tel: 352-627-9208
Glioblastoma is one of the most challenging adult brain tumors to treat. Therapeutic targeting of the immune system, i.e. immunotherapy, in cancer is an active area of investigation. Despite some early success, additional combinatorial approaches will be needed for immune-based therapies to be more effective. Our lab uses pre-clinical mouse models to study the biology of glioma and to identify new therapeutic targets. We are primarily interested in understanding the mechanisms of communication between glioma and immune cells within the tumor microenvironment and how specific chemokines and chemokine receptors function in these interactions.
William Kem, Ph.D.
- Professor, Dept. of Pharmacology & Therapeutics
- Phone: (352) 392-0669; E-mail: email@example.com
My lab investigates naturally occurring toxins that act upon nerve and other excitable cells. We sue these toxins as chemical probes to investigate receptors and ion channels of biomedical interest. Currently there are two major projects. One involves the design of nicotinic receptors in the brain and may be useful in therapy of Alzheimer’s and other neurodegenerative diseases. The second project utilizes a sea anemone peptide as a molecular model for developing new immunosuppressant drugs for treating organ transplants and autoimmune disorders. Students electing to do research in the laboratory would gain experience in chromatography and electrophoresis of proteins and their biological characterization.
Michael King, Ph.D.
- Associate Scientist, Department of Pharmacology & Therapeutics, and VAMC
- Phone: (352) 376-1611×6499; E-mail: firstname.lastname@example.org
Our lab uses anatomical, electrophysiological, behavioral, and biochemical/molecular techniques to study progressive neurodegenerative diseases such as Alzheimer’s. Gene transfer techniques are being used to develop better preclinical models for human neurodegenerative diseases, and potential therapeutic approaches for treating such diseases. Models we have developed can reproduce key neuropathological phenomena and progressive dementia to permit experimental focus on specific mechanisms and interventions. The lab also studies age-related memory loss apart from disease, particularly in relation to neuronal function in a temporal lobe structure known as the hippocampus.
Brian Law, Ph.D.
Pharmacology & Therapeutics
TEL: (352) 273-9423; email@example.com
We have two ongoing projects:
- Investigating the role of The CUB Domain-Containing Protein 1 (CDCP1) in breast cancer metastasis- We have discovered that the transmembrane protein CDCP1 activates several biochemical pathways that allow cancer cells to survive in the detached state during the process of metastasis. Current efforts involve understanding how CDCP1 activates these different downstream pathways through the tyrosine phosphorylation of different residues in the CDCP1 cytoplasmic domain, identifying CDCP1-associated proteins using affinity chromatography/mass spectrometry approaches (i.e. proteomics), and testing new therapeutic strategies for neutralizing CDCP1 function to prevent breast cancer metastasis.
- Characterization and optimization of a novel class of anticancer agents that downregulate the EGFR, HER2, and HER3 receptor tyrosine kinases- We have identified a new class of compounds that inactivate the oncogenic Epidermal Growth Factor Receptor (EGFR) family of proteins EGFR, HER2, and HER3 by disrupting the disulfide bonds present in the conserved cysteine-rich extracellular domains of these proteins. These agents, which we term Disulfide bond Disrupting Agents (DDAs) are promising anticancer agents in that they exhibit anticancer activity in vivo and exhibit no detectable toxicity. This is a collaborative project between the Castellano Laboratory in the Chemistry Department and the Law Laboratory in the Pharmacology Department. Approaches used in this project include: Chemical synthesis and characterization, testing compounds in cell culture studies, and using protein chemistry/proteomics approaches to validate EGFR, HER2, and HER3 as DDA targets and to identify additional targets of these anticancer agents.
Steven D. Munger, Ph.D.
Professor and Vice-Chair of Pharmacology and Therapeutics
TEL: 352-294-5749, Email: firstname.lastname@example.org
My lab uses molecular biological, genetic and behavioral approaches to understand how chemosensory receptors contribute to the body’s detection of, and response to, odors, tastes and food components.
Edgardo Rodriguez, Ph.D.
Department of Pharmacology and Therapeutics
Contact: email@example.com, (352) 294-5781
A significant number of adult-onset neurological diseases, including Alzheimer’s, Parkinson’s and Huntington’s disease are characterized by the aberrant and toxic accumulation of proteins in affected neurons. Our group relies on the use of model systems to test novel gene-based therapies that prevent, halt or reverse these “proteinopathies”. In particular, we develop Adeno-Associated virus-based gene therapies to suppress the expression of these proteins in affected neurons. Recently, using models of spinocerebellar ataxias, we have demonstrated that suppressing the expression of toxic proteins, even after disease onset, can lead to significant recovery of neuronal function and halt the progression of pathology. A new exciting area of gene therapy research in our group focuses on the development of “gene-editing” tools that can be used to modify inherited mutations in adult neurons.
Thomas C. Rowe, Ph.D.
- Assoc. Professor, Dept. of Pharmacology & Therapeutics
- Phone: (352) 392-3541; E-mail: firstname.lastname@example.org
Our lab is interested in the cellular function of nuclear and organellar DNA topoisomerases and their role as targets for cancer and malarial chemotherapy. DNA topoisomerases are an ubiquitous class on enzymes which regulate the structure and function of cellular chromosomes and are established targets for antimicrobial and anticancer drugs. We are using molecular, biochemical, and genetic approaches to investigate how these drugs interfere with the regulation and functions of topoismoerases in tumor cells and the human malarial parasite Plasmodium falciparum.
Physiology & Functional Genomics
Abdel A. Alli, Ph.D., MPH
Assistant Professor of Physiology and Functional Genomics
Tel: (352) 273-7877 Email: email@example.com
My laboratory is interested in understanding the role of nanometer-scale cell-derived vesicles called exosomes in the regulation of sodium transport mechanisms in the kidney during diabetic nephropathy and salt-sensitive hypertension. We are also interested in identifying novel proteolytic-dependent regulatory mechanisms in the kidney that contribute to blood pressure disorders. We use a multidisciplinary approach that integrates molecular biology, biochemistry, proteomics, and electrophysiology in order to examine complex regulatory mechanisms of membrane transporters in both cellular and animal models. This allows for the identification of novel drug targets and the development of specific therapeutics.
Kirk P. Conrad, M.D.
Professor of Physiology and Ob/Gyn
Research interests are in several areas of Reproductive & Perinatal Biology including: mechanisms underlying maternal renal and systemic vasodilation, and increased arterial compliance during normal pregnancy with emphasis on the ovarian hormone relaxin and the underlying vascular cellular and molecular mechanisms; maternal cardiovascular and renal adaptations to pregnancy in women conceiving by Assisted Reproductive Technologies (ART), as well as the perinatal outcomes and remote consequences of ART on offspring; the potential role of impaired decidualization in the etiology of preeclampsia and other placental syndromes. Combined preclinical and clinical research is applied to translate discoveries in animal models, tissues and cells to humans or vice versa.
Annette de Kloet, Ph.D.
Physiology and Functional Genomics
TEL: (352)-294-8490; email: firstname.lastname@example.org
A major goal of my research program is to elucidate mechanisms underlying obesity and co-morbid conditions such as hypertension and diabetes. A particular emphasis is placed on the interactions among neural circuits that regulate energy balance with those that control blood pressure, and also on the impact that the renin-angiotensin system has on these circuits. Some specific research topics currently being explored include: (1) examining the role of angiotensin-II and related peptides in the neuroendocrine regulation of energy balance; (2) optogenetic targetting of angiotensin-sensitive neurons of the nodose ganglion to combat obesity and hypertension; and (3) evaluating mechanisms by which angiotensin-sensitive neurons of the median preoptic nucleus coordinate physiological and pathophysiological responses to hypertensive stimuli. In order to explore these and other research topics, we use a mutli-level approach that spans the use of several molecular, genetic, physiological and behavioral techniques. Some examples of the approaches used are: telemetry and indirect calorimetery, which are used to assess cardiovascular parameters and energy expenditure respectively; optogenetics, fiber photometry, neuronal tract tracing, mRNA in situ hybridization, and immunohistochemistry, which are used to characterize the structure and function of specific sets of neurons involved in these processes; and genetic recombination and virally-mediated gene transfer techniques, which allow for the manipulation of gene expression in specific cellular phenotypes.
Karyn Esser, Ph.D.
Professor of Physiology and Functional Genomics and Assistant Director of the Myology Institute
Email: email@example.com Phone: 352-273-5728
Circadian rhythms are well known daily patterns in sleep/wake cycles and core body temperature. Recent discoveries have uncovered that the molecular clock mechanism underlying circadian rhythms exists in all cells in the body. My lab is currently pursuing three main areas of research related to circadian rhythms and skeletal muscle. Using targeted genetic mouse models, we have found that the clock mechanism in skeletal muscle modulates fat/carbohydrate metabolism, muscle structure/function in the presence of normal circadian function in the brain. We are pursuing these observations to define the transcriptional and translational networks regulated by the molecular clock in skeletal muscle that regulate both metabolism and function. The second area of study is based on the recent work that has shown that time of activity/exercise can function as a cue to “set” the clocks in skeletal muscle independent the brain. We are using cell culture models of muscle contraction combined with unique exercise paradigms to define the mechanisms by which activity can regulate the molecular clock. Lastly, we are working to develop analytic techniques to use biometric data obtained from wearable devices to define “circadian health” in human populations.
Hideko Kasahara, MD, PhD
Physiology and Functional Genomics
TEL: 846-1503, firstname.lastname@example.org
Our laboratory focuses on molecular mechanisms of cardiac diseases including congenital heart disease, and heart failure (http://physiology.med.ufl.edu/faculty/kasahara/). Specific studies include cardiac physiological analyses using genetically engineered mice with heart disease combined with basic molecular biology experiments.
Mohan K. Raizada, Ph.D.
- Professor, Dept. of Physiology & Functional Genomics
- Phone: (352) 392-9299; E-mail: email@example.com
Regulation of angiotensin receptor-mediated neuromodulatory actions in the brains of normal and hypertensive rats. This involves studies in various signal transduction pathways and participation of signaling kinases. Use of antisense gene therapy for a permanent control of hypertension.
Peter Sayeski, Ph.D.
- Professor, Dept. of Physiology & Functional Genomics
- Phone: (352) 392-1816; E-mail: firstname.lastname@example.org
The research performed in my laboratory is focused on understanding the role of Jak2 tyrosine kinase in human diseases. A variety of cellular, molecular, genetic, biochemical and bioinformatic techniques are used for these studies.
Debbie Scheuer, Ph.D.
- Dept. of Physiology and Functional Genomics
- Office Phone: 352-392-2783 e-mail: email@example.com
Our lab studies the effects of stress and stress hormones on the central nervous system regulation of blood pressure. Our long-term goal is to determine how stress hormones act within the brain to cause high blood pressure and cardiovascular disease. We utilize whole animal approaches including in vivo viral vector-mediated gene delivery in combination with in vitro assays and histology.
Colin Sumners, Ph.D.
- Professor, Dept. of Physiology, and Program Director
- Phone: (352) 392-4485; E-mail: firstname.lastname@example.org
Our research focus is in two major areas. 1) Understanding the intracellular signaling mechanisms by which angiotensin II alters the activity of brain neurons, and how these mechanisms may be impaired in hypertension. 2) Studying the role of the angiotensin type 2 receptor (AT2) in neural and cardiovascular function.
Charles E. Wood, Ph.D.
- Professor, Dept. of Physiology & Functional Genomics
- Phone: (352) 392-4488; E-mail: email@example.com
The research performed in this laboratory is focused on the mechanisms controlling the responses to stress in the fetus in utero and on the mechanisms controlling the timing of birth.
Adrie W. Bruijnzeel, Ph.D.
- Assistant Professor, Department of Psychiatry
- Phone: (352) 294-0421; E-mail: firstname.lastname@example.org
Role of corticotropin-releasing factor (CRF) in the depressive-like signs associated with drug withdrawal We use the rat intracranial self-stimulation procedure to investigate the effects of CRF in nicotine withdrawal. This entails the implantation electrodes in the medial forebrain bundle of rats and the daily assessment of brain reward thresholds. Withdrawal from drug of abuse increases the brain reward threshold (i.e. depressive like state) and we try to reverse this by using CRF antagonists and other novel pharmacological treatments for mood disorders. The student will become experience with the following techniques: Surgical techniques: Implantation of electrodes and cannulae in the brain; implantation and removal and subcutaneous minipumps that contain drugs of abuse. Injection procedures: Subcutaneous, intraperitoneal and intracranial administration of drugs. In addition the student will gain extensive knowledge about animal care, how to conduct scientific experiment and drug dependence research. This projected will be conducted in close collaboration with Dr. Mark Gold.
Jacqueline A. Hobbs, MD, PhD, FAPA
Assistant Professor of Psychiatry and Pediatrics
My clinical/research interest is women’s mental health. My laboratory focuses on the role of viruses such as parvovirus B19 and human herpesvirus 6 in inflammatory diseases including autoimmunity and cancer. Target diseases are postpartum depression/psychosis, pregnancy-related mental illness, bipolar disorder, schizophrenia, autism, thyroid cancer, Hashimoto’s thyroiditis, and Grave’s disease. Target organs of interest are brain, thyroid, skin, testis, and lymph nodes.
Khurshid A Khurshid, M.D.
Dept. of Psychiatry
Neuromodulation, sleep disorders. Transcranial Magnetic stimulation for insomnia. Transcranial direct current for depression. ECT for depression.
Mark H. Lewis, Ph.D.
Professor and Assistant Chair
My lab works with animal models of autism and related neurodevelopmental disorders. Specifically we are focused on the abnormal repetitive behavior (e.g., stereotyped behavior, compulsions, rituals, insistence on sameness) characteristic of children and adults with these developmental disorders. We are investigating the neurobiology underlying the development and expression of abnormal repetitive behavior in several animal models. Our research with deer mice involves examining the brain changes associated with the development of abnormal repetitive behavior and its prevention by early experience. These studies include examination of developmental trajectories and the temporal organization of repetitive behavior and associated changes in key pathways in cortical basal ganglia circuitry. These biochemical and pharmacological studies have not only identified neurobiological mechanisms but have identified potential therapeutic targets for the treatment of these behaviors. Other work with an inbred mouse strain is focused on identifying genetic loci that mediate the development and expression of repetitive behavior.
Lisa Merlo, Ph.D., MPE
Department of Psychiatry
My research focuses primarily on impaired healthcare professionals (i.e., physicians, pharmacists, etc. with addiction or other disruptive behavior problems); I also study addiction in other populations. My main interests are psychosocial correlates of the addiction and recovery processes. I use primarily survey and interview data collection methods.
Amber Muehlmann, Ph.D.
Department of Psychiatry
We study basal ganglia circuitry dysfunction as it relates to maladaptive behaviors that are phenotypic for psychiatric (e.g. OCD) and neurodevelopmental disorders (e.g. autism, intellectual disabilities), using mouse models. Our mice exhibit high rates of repetitive behaviors as a consequence of genetic manipulations or environmental impoverishment. Our experiments utilize molecular techniques as well as psychopharmacology and drug development to investigate neuropathology and targeted drug treatments.
Sara Jo Nixon, Ph.D.
Departments of Psychiatry & Psychology
TEL: 352-294-4920, email@example.com
Dr. Nixon’s research focuses on the neurobehavioral concomitants of substance use and dependence/addiction. Her work uses comprehensive behavioral assessments including neuropsychological testing, brain electrophysiology (electroencephalography and event-related potentials), and clinical research interviews. A recurrent theme in her work has been the exploration of sex/gender differences in both the psychosocial and neurobiological aspects of addiction.
Barry Setlow, Ph.D.
Professor of Psychiatry
Email: firstname.lastname@example.org / 352-294-5203
In my laboratory, we use a range of behavioral, pharmacological, biochemical, electrophysiological, and optogenetic techniques in rodent models to investigate the neural mechanisms of impulsive and risky decision making, and how they are altered by drugs of abuse such as cocaine, alcohol, and marijuana.
Song Lai, Ph.D.
Professor of Radiation Oncology; Director, CTSI Human Imaging Core
Phone: 352-294-5597; Email: email@example.com
My research is devoted to the advancement of magnetic resonance imaging (MRI) technology for applications in health and disease in humans, with a focus on brain functional MRI (fMRI). Going beyond the traditional strength of MRI for providing images of the structure/anatomy of the body in health and disease, fMRI allows for imaging the human brain at activity (e.g., thinking, seeing, hearing, etc.) by detecting cerebral hemodynamic responses (i.e., microscopic blood flow or perfusion, and oxygen consumption by brain tissues) accompanying brain activity. fMRI can also be applied to studying/monitoring effects of a treatment, therapy or intervention. We offer excellent opportunities for students to participate in our exciting research, with a particular emphasis on translational MRI research in humans.
Dietmar W. Siemann, Ph.D.
Professor, Dept. of Radiation Oncology
Phone: (352) 395-0287; E-mail: firstname.lastname@example.org
Research in our laboratories is focused on improving conventional anticancer therapies such as radiation and chemotherapy. Our current focus is on the use of drugs which damage the tumor vasculature which cripples the blood supply to the tumor and leads to the death of the tumor cells.
Walter O’Dell, Ph.D.
Assistant Professor ,Radiation Oncology/BME
Phone 273-9030, Email email@example.com
Our team recently solved the technical challenges of extracting and characterizing the structure of lung vessels in 3D from medical images, and we have two patents pending for these new tools. The long-term purpose of our current work is to apply and optimize these tools for use in 3 classes of patients: (1) children born before their lung vessels have fully deformed; (2) teenagers with pulmonary vessel insufficiency (often as a result of being born prematurely); and (3) adults with chronic pulmonary hypertension (PAH). Our clinical objectives are to (1) characterize the development of the pulmonary vessels over time in prematurely-born infants; (2) determine the time-course of progressive vessel disease in these children as they age into young-adulthood; and (3) to study vascular remodeling with chronic PAH. In parallel with the clinical work, our technological objectives are to (4) characterize and validate the accuracy and sensitivity of the method, (5) compare our results against competing approaches; and (6) optimize and streamline the analysis algorithms to position ourselves strongly for additional funding.
Scott Berceli, M.D., Ph.D.
Professor of Surgery
Phone: (352)376-1611, extension 6470; E-mail: firstname.lastname@example.org
Work in Dr. Berceli’s lab is focused on the process of the vascular response to injury, with a specific interest in understanding the role of biomechanical forces in mediating these events. Although these concepts are also seen in vascular problems such as atherosclerosis and arteriogenesis, our current basic science and translational research projects examine the dynamic interplay among the various forces that lead to luminal narrowing following vein bypass grafting. Integrating mathematics, engineering, and vascular biology, research opportunities in our laboratory offer a range of experiences, from bench top testing to in vivo experimentation to the development of in silico computational models.
Atif Iqbal, M.D.
Research focus centers on colorectal cancer, health disparities, quality improvement in colorectal surgery and robotic education with various other ongoing projects in colon and rectal surgery. Projects that are appropriate for entry level research include retrospective chart review, abstract and manuscript construction and participation in presentations. The aim is to mentor investigators on how to do clinical research, write manuscripts and have them published in peer reviewed journals.
Kristina Giles, M.D.
Department of Surgery, Division of Vascular Surgery and Endovascular Therapy
Outcomes and comparative effectiveness studies in vascular surgery with a focus on database and registry studies, quality initiatives, and cost comparisons.
Zhihua Jiang, Ph.D.
Department of Surgery
TEL: (352) 294-5688 or email@example.com
Using both transgenic animal models and cell culture system, we have been exploring the mechanisms that are responsible for occlusive arterial diseases, such as restenosis of arteries and bypass vein grafts. Recently, we have developed projects focusing on the role of TGF-beta signaling pathways in the development of aortic aneurysms. Students in the lab will learn to perform various cellular and molecular assays while gaining knowledge on vascular biology. Those who were trained in our group have been accepted by either Medical School or Dental School at UF. We currently have two open seats for UF undergraduates.
Adam J. Katz, M.D.
Associate Professor of Surgery
Work in Dr. Katz’s lab is focused on understanding the biology and therapeutic potential of adipose tissue-derived stem cells and related factors; developing novel approaches to tissue repair, replacement and regeneration using adipose tissue as a biological resource; and translating promising discoveries and applications to the clinic. Studies are pursued with a bench to bedside approach, with emphasis on translational and regulatory perspectives and considerations. Cell biology, molecular biology, human tissues, animal models, and clinical studies.
Charles T. Klodell, Jr, M.D.
Departments of Surgery and Anesthesiology
TEL: 352-273-5501, firstname.lastname@example.org
–Research focus centers on mechanical cardiac support (LVADs), aortic surgery, and other various side projects in thoracic and cardiovascular surgery. Major interest in translational research that leads to either improved quality of life as it relates to procedures, or patient safety improvement. Many projects that are appropriate for entry level research include retrospective chart review, abstract construction, and participation in national presentation. We have a strong track record of mentoring young investigators to published authors in peer reviewed journals.
Shawn D. Larson, M.D.
Division of Pediatric Surgery/Department of Surgery
Email: email@example.com Office: (352) 273-8761
My interests are in necrotizing enterocolitis (NEC) which is a disease process affecting the GI tract of premature and newborn infants. The condition is associated with significant morbidities and in severe cases, death. Our laboratory is interested in the following projects: investigating innate immune responses secondary to sepsis/NEC with both cell cultures and mouse models, development of an animal model to investigate immune function in NEC, and developing a human tissue bank of intestinal tissue to investigate factors contributing to NEC.
Tiago N. Machuca, M.D., Ph.D.
Dept. of Surgery, Division of Thoracic and Cardiovascular Surgery
My areas of research are lung preservation for transplant, ex vivo lung perfusion and porcine models of lung transplantation. I also do clinical research aiming to improve outcomes in lung transplantation.
Alicia M. Mohr, MD
Associate Professor of Surgery
TEL: 352-273-5670, firstname.lastname@example.org
My research focus is on basic and translational research in the field of trauma and prolonged critical illness with an emphasis on the understanding on injury-associated persistent anemia as a manifestation of bone marrow dysfunction. We are using a novel rodent model to study the effects of chronic adrenergic stimulation following injury and hemorrhagic shock on erythropoiesis and hematopoietic progenitor cell mobilization. Our basic research findings can be correlated with clinical studies persistent anemia and abnormal healing of injured tissue. The student will develop insight on how basic science research can be applied in the clinical arena.
Peter R. Nelson, M.D., M.S.
Assistant Professor of Surgery and Molecular Genetics and Microbiology
Tel. (352) 376-1611 X 6470 / Email: email@example.com
Our research focuses in two main areas – translational biology and outcomes research. We have had students contribute significantly in both of these areas during past experiences.
Translational Research: We study the functional genomics and proteomics linking systemic inflammation to success or failure of vascular surgical procedures, currently lower extremity stenting and/or bypass surgery. This project involves genetic analyses using state of the art microarray technology, high throughput proteomics, and sophisticated bioinformatics to investigate whether or not a person’s innate immunity pre-operatively or their inflammatory reaction to the procedure itself can predict the success or failure of that intervention and therefore be used to improve treatment strategies.
Clinical/Outcomes Research: Here we use our local UF experience combined with large administrative databases to understand and compare local/regional and national trends in vascular surgery. Projects focusing on lower extremity revascularization, abdominal aortic and thoracic aortic aneurysm repair, and venous disease are underway to identify the impact of new technology and to better define expected outcomes in these areas. We are also involved in a number and variety of clinical trials relevant to vascular surgery.
Lori P. Rice, Ph.D.
- Assistant Research Scientist, Dept. of Surgery
- Phone: (352)392-2382; E-mail: firstname.lastname@example.org
Our research program goals are to determine the effects of various antiproliferative agents on prostate cancer cells and to identify target genes or metabolic pathways that may be useful in drug design or diagnostic tools in cells and patient tissue. We are interested in the mechanisms of cancer progression and metastasis and in chemoprevention. Assays currently used in the lab include traditional molecular and cell biology protocols, laser capture microscopy, electron microscopy, animal xenograft studies and microarray analyses. We have an interdisciplinary program with collaborators are based in various departments and colleges, including IFAS, Statistics, Radiology, Pathology, Pharmacology, Molecular Genetics and Surgery.
Winston T. Richards, M.D.
- Clinical Assistant Professor of Surgery, Division of Acute Care Surgery
- Phone: (352) 273-5670; E-mail: email@example.com
My research interests include outcomes analysis of burn and hand injuries as well as developing mathematical models for the clinical characteristics of skin grafting on the hand. I am currently involved in projects describing the need for hand surgery centers of excellence in the State, The need for increased awareness of the pending population changes from the baby boom and their effect on burn care for elderly patients, and a model for the scar contractures that can be expected after skin grafting hand burns.
Jose G. Trevino, M.D.
Department of Surgery
Phone: (352) 265-0761; Fax: (352) 265-1060; E-mail: firstname.lastname@example.org
My research interests involve basic and translational research in pancreatic cancer. My basic science interests are primarily investigating the role of particular onco-proteins/genes on tumorigenic properties. Additionally, I am striving toward translating my work into animal models and provide clinical relevance by correlating our proteins of interest to resected human tumor tissues. Although I am a clinical surgeon, I truly believe that the future of therapies in cancer will be targeted so new developments in basic science with a translatable component.
Victoria Y. Bird, M.D.
Department of Urology
Research interests include infections of the urinary tract, biofilm, catheter associated UTI, surface nanotechnology to mitigate biofilm and bacteria, prostate cancer epidemiology.
Benjamin K. Canales, M.D., MPH
Assistant Professor, Urology
TEL: 352-273-6815, email@example.com
A brief description of your research interests: The focus of our laboratory is a basic-science, translational approach to kidney stone disease utililizing MS technologies of 2D DIGE and qualitative iTRAQ isobaric reagent peptide labeling as well as gene array expression. We have an established knock-out mouse model of hypercalciuria and a hyperoxaluric obese rat model of gastric bypass sugery, all of which have potentials for further exploration. In the summer of 2008, a student completed a 3 month research project involving dissolution of urinary crystals and kidney stones using a novel enzymatic approach.
Philipp Dahm, MD, MHSc
- Department of Urology
- phone: (352) 273-8239 email: firstname.lastname@example.org
The focus of interest of our clinical research group is the development of evidence-based resources and knowledge translation services with an emphasis on urologic surgery. Recently completed projects include a critical appraisal of the quality of evidence supporting the widespread use of robotic-assisted prostatectomy and a formal assessment of the methodological quality of prostate cancer guidelines.
Sergei Kusmartsev, Ph.D.
Assistant Professor, Department of Urology
Tel. 352-273-8235, Email: email@example.com
Our studies are focused on mechanisms of tumor-induced immune suppression and immune tolerance. We are trying to dissect the role of CD11b myeloid cells in the regulation of anti-tumor immune response in both cancer patients and tumor-bearing mice. Currently, several projects are underway, including characterization of myeloid suppressor cells population in peripheral blood of cancer patients with bladder and renal cell carcinoma. Another interest concerns regulatory mechanisms of local immune response in tumor microenvironment. We investigate several genes and transcription factors which are affected in tumor-infiltrated myeloid cells and precursors of antigen-presenting cells. The ultimate goal of our research is correction of tumor-induced dysfunction, activation of immune system and induction of therapeutic immune response.