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Training Faculty

The following faculty members are active researchers who are able to supervise dissertations and theses.  Please click on the name of each member to learn more about them. 

Gene Alexander, PhD. (Neuroscience: Aging, Brain-Behavior, Neurodegenerative Disease)

Program Affiliations:  Psychology, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626 1704, gene.alexander@arizona.edu

Research Interests:  Neuroscience/Aging: brain-behavior relationships in the context of aging and age-related, neurodegenerative disease 

  • My research and academic interests focus on the study of brain-behavior relationships in the context of aging and age-related, neurodegenerative disease. I use neuroimaging techniques, including structural and functional magnetic resonance imaging (MRI) and positron emission tomography (PET), in combination with measures of cognition and behavior to address research questions on the effects of healthy aging and Alzheimer’s disease on the brain and on the mechanisms of human cognitive aging. A major focus of my research program includes the use of univariate and multivariate network analysis techniques with multiple neuroimaging methods and measures of neuropsychological function, health status, and genetic risk to understand how these factors interact to influence cognitive function as we age. My research also includes the application of these techniques to non-human animal models of aging and age-related disease. I direct the Brain Imaging, Behavior & Aging Lab in the Department of Psychology, have an appointment in the Evelyn F. McKnight Brain Institute, and direct the MRI Morphology Core of the Arizona Alzheimer’s Research Center.

Parker B. Antin, PhD. (Cardiovascular Disease: Embryogenesis, Tyrosine Kinases, Hepatocytes)

Program Affiliations: Cell Biology and Anatomy, Cellular and Molecular Medicine, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-7201, pba@email.arizona.edu

Research Interests:  Cardiovascular Disease: Embryogenesis, Tyrosine Kinases, Hepatocytes

  • Research in our laboratory is focused on understanding the molecular regulation of early developmental processes in vertebrate embryos. We primarily use the chicken embryo as a model organism, and approach research questions from the dual perspective of how individual molecules function and how their functions can be integrated into network models. One present research emphasis is concerned with understanding epithelial to mesenchymal transition (EMT) during avian gastrulation. Microarray studies have shown that more than 1800 genes are upregulated in the epiblast adjacent to the primitive streak. Many of these genes are regulated by FGF signaling, including members of several other signaling pathways and at least thirty differentially expressed transcription factors. Fgf signaling therefore appears to be a key upstream regulator of EMT. Studies are investigating the intracellular signaling pathways downstream of Fgf receptor activation, including the MAPK, PI3K and AKT pathways. The MAPK pathway in particular directly regulates downstream gene transcription via activation of several transcription factors, including members of the Ets and T Box families. Studies are investigating downstream transcriptional targets of these factors.
  • Another long standing research interest in the lab is the mechanisms controlling early stages of cardiac myogenesis, from the emergence of premyocardial cells during gastrulation to formation of the primitive heart tube. Bmp and Fgf signaling are well known activators of genes in the cardiogenic pathway, however relatively few direct transcriptional targets of these signaling pathways have been identified. By combining classical experimental embryological approaches with genome wide microarray analyses, we are working to generate a large-scale model of cardiac myogenesis.
  • These studies are integrating with a parallel effort to generate broad approaches for developing network models of biological processes in vertebrates. This involves high throughput in situ hybridization and microarray gene expression analysis and large scale-collation of published information to generate preliminary network models. Models are then tested through parameter space using software tools such as Ingeneue. Results are integrated with an artificial intelligence software environment that evaluates results and can suggest network modifications for retesting. Promising candidate network models are then tested in vivo. Through successive reiterations between computational network modeling and model testing in vivo, progressively more representative networks can be generated. Initial efforts are focused on modeling EMT during gastrulation and cardiac myogenesis.
  • Our laboratory also hosts the GEISHA in situ hybridization database and website (http://geisha.arizona.edu (link is external)). The GEISHA project (gallus expression in situ hybridization analysis) began in 1998 to investigate using high throughput whole mount in situ hybridization to identify novel, differentially expressed genes in chicken embryos. An initial expression screen of approximately 900 genes demonstrated feasibility of the approach, and also highlighted the need for a centralized repository of in situ hybridization expression data. Funding was eventually obtained for this purpose. The goals of the GEISHA project are to obtain whole mount in situ hybridization expression information for all differentially expressed genes in the chicken embryo between HH stages 1-25, to integrate expression data with the chicken genome browsers, and to offer this information through a user-friendly graphical user interface

E. Fiona Bailey, PhD. (Motor Control, Respiratory Physiology, and Hypertension)

Program Affiliations:  Bio5 Institute, Physiology, Physiological Sciences

Website and Publications:  Bailey Lab Homepage

Contact Information:  (520) 626-8299, ebailey@email.arizona.edu

Research Interests:  Motor control, respiratory physiology, and hypertension

  • The research focus in the Bailey laboratory is on the neural control of breathing in human and nonhuman mammals.  The first work in this area assessed the role of pulmonary stretch receptors and central chemoreceptors in the genesis and relief of dyspnea or shortness of breath in healthy adults.  These studies subsequently led to studies in the mammalian (rodent) airway that explored the modulation of upper airway muscles activities by chemical and pulmonary afferent feedback and the potential for selective electrical stimulation of the cranial nerve XII to alter airway geometry and volume (NIH/NIDCD RO3).  Beginning in 2005, with the support of an NIH/NIDCD K23 I began work in neural control of upper airway muscles using tungsten microelectrodes to record from single motor units in adult human subjects. This work led in turn, to studies of regional (or segmental) muscle and motor unit activities in human subjects under volitional, state-dependent (i.e., wake/sleep) and chemoreceptor drives in health and disease (NIH/NIDCD RO1). 
  • On the basis of the experimental work in muscle and motor units we pursued additional lines of enquiry focused on clinical respiratory dysfunction in two specific populations a) infants at risk for SIDS and b) adults diagnosed with obstructive sleep apnea (OSA).  Both lines of enquiry are highly innovative and have immediate diagnostic and clinical applications. 
  • One such line of enquiry explores the potential for a non-pharmacologic intervention daily to lower blood pressure and to improve sleep in patients diagnosed with mild-moderate obstructive sleep apnea.  This training protocol shows promise as a cheap, effective and safe means of lowering blood pressure and improving autonomic-cardiovascular dysfunction in patients who are unwilling or unable to use the standard CPAP therapy.
  • Support.
    • Our work is supported by National Institutes of Health Grants (NIDCD: K23 007597; RO1 009587; Challenge Grant EB 10915) and by UA Gift Fund 560040 and by the American Heart Association (Grant in Aid GRNT 26700007).

Shaowen Bao, PhD. (Neuroscience: Auditory Perception and Learning)

Program Affiliations:  Neuroscience GIDP, Physiology, Physiological Sciences

Website and Publications:  Bao Lab Homepage

Contact Information:  (520) 621-5680, sbao@email.arizona.edu

Research Interests:  Neuroscience: Auditory Perception and Learning

  • Perception is shaped by early experience. For example, exposure to native speech sounds improves our sensitivity to native speech contrasts, but can also reduce our sensitivity to foreign speech contrasts. How does experience alter neural circuits? How do the changes in neural circuits influence our perception? We address these questions in rodent models using a combination of electrophysiological, behavioral, and computational approaches.

  • In certain neurological disorders, learning mechanisms are either impaired or operate under abnormal conditions. For example, while early acoustic exposure alters the auditory brain circuits in normal mice, such experience-dependent brain changes are absent in a mouse model of fragile X syndrome. Another example is homeostatic plasticity, which, under normal physiological conditions, keeps the neuronal firing rate in a range to optimally encode information. However, under the pathological condition of hearing loss, homeostatic plasticity may operate erroneously and cause tinnitus and hyperacusis. What are the cellular and molecular mechanisms underlying these brain disorders? Can we target those mechanisms for treatment of the disorders? We investigate these questions using a multifaceted approach that includes molecular biology, biochemistry, intracellular electrophysiology, ontogenetics, and behavioral techniques.

Carol Barnes, PhD. (Neuroscience: Brain Changes/Functional Consequences on Processing)

Program Affiliations:  Bio5 Institute, Psychology, Physiological Sciences

Website and Publications:  Psychology Faculty Homepage

Contact Information:  (520) 626-2616, carol@nsma.arizona.edu

Research Interests:  Neuroscience: Delineation of brain changes during late ontogeny and functional consequences on information processing

  • Dr. Barnes' research interests involve the delineation of brain changes during late ontogeny (senescence) and the functional consequences of these changes on information processing and memory in older organisms. The major emphasis of the research in her lab has been an examination of the relationship between neurological change in the hippocampal formation of old rats and the accompanying decline of spatial learning-memory performance.

  • The methods used include extra- and intracellular stimulation and recording in the in vitro hippocampal slice preparation and extracellular techniques in both the acute (anesthetized) and chronically prepared (unrestrained) animal.  Some recent experiments have also been conducted using the new multiple single cell recording system developed here at the ARL Division of Neural Systems, Memory and Aging. Behavioral tests of spatial perception and memory (known to require an intact hippocampus for their proper performance) are routinely used in conjunction with the neurophysiological experiments, in order to most effectively assess brain-behavior relationships.

  • The long-term goal of this work is a more complete understanding of the biological basis for the deterioration of cognitive function known to occur in the elderly. Such an understanding will hopefully lead to the development of neuropharmacological manipulations which much alleviate or delay neurophysiological and neuroanatomical changes known to occur normally with age, and which are responsible for the observed cognitive defects.  

Randy Bogan, PhD. (Reproductive Physiology, Animal Sciences)

Program Affiliations:  Animal Sciences, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-9435, boganr@email.arizona.edu

Research Interests:  Reproductive Physiology, Animal Sciences

  • In his position at the University of Arizona Dr. Bogan will be researching reproductive physiology with an emphasis on ovarian biology. Once his research lab has been launched Bogan will begin teaching several classes in reproduction with the exact topics to be determined.

Scott Boitano, PhD. (Asthma, Respiratory Physiology, Lung Epithelia)

Program Affiliations:  Physiology, Cell Biology & Anatomy, Immunobiology, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

Contact Information:  (520) 626-2105, sboitano@email.arizona.edu

Research Interests:  Asthma, Respiratory Physiology, Lung Epithelia

  • We use unique primary tissue culture models of lung epithelial cells to study the cellular and tissue function of the lung epithelium. The conducting airway epithelium is an active cellular layer made up of a variety of cell types that is typified by ciliated airway epithelial cells that contribute to mucociliary clearance. The epithelial layer that lines the alveoli of the distal mammalian lung is made up of two distinct cell types, alveolar type I (AT1) and alveolar type II (AT2) cells. Physiological functions of AT1 cells include the primary site of gas exchange and of AT2 cells include the production of critical secretions that keep the lung from collapsing. Just as importantly, AT2 cells serve as "stem cells" that divide, migrate and differentiate to reform the AT1/AT2 epithelial layer following insult or injury. Also important to studies in our laboratory, lung epithelial cells provide innate immune function via a variety of events. These events include: the establishment of an epithelial "barrier;" the secretion of anti-microbial and inflammatory effector molecules; and direct interaction with non-epithelial cells (e.g. alveolar macrophages) to further immune function.
  • Our current studies include four foci: 1) Host/Pathogen Interactions in the Airway; 2) Intercellular Communication in the Airway Epithelium; 3) Arsenic Effects on Airway Epithelial Signaling and Physiology; and 4) Re-establishment of a Functional Airway Epithelium following insult or injury. In the host/pathogen interaction studies, we are using a ciliated cell culture model to better understand early events in airway infection by primary colonizing bacteria from the Bordetellae. This includes elucidation of bacteria and host proteins that contribute to ciliary binding and the innate host defenses activated by this early host/pathogen interaction. In the intercellular communication studies we are elucidating the molecular mechanisms that allow for second messenger signaling within and between airway epithelial cells in the conducting airway and in the alveoli. In the arsenic studies we are evaluating the effects of environmentally significant amounts of arsenic on airway epithelial physiology. In the epithelial repair foci, we are studying the contributions of extracellular matrix molecules and neighboring cells to the re-establishment of a functional airway epithelium following large-scale wounding or local disruption by toxicants and/or toxins.

Heddwen Brooks, PhD., Program Chair (Hypertension, Menopause, Kidney Disease)

Program Affiliations:  Physiology, Biomedical Engineering, Bio5 Institute, Physiological Sciences

Website and Publications:  Brooks Lab on Arizona Illustrated, KUAT, Brooks Lab in UA News, Physiological Sciences Faculty Page, Physiology Faculty Page

Contact Information:  (520) 626-7702, brooksh@email.arizona.edu

Research Interests:  Hypertension, Kidney Disease, Inflammation and Menopause, Lithium Induced NDI, Polycystic Kidney Disease, Sex differences in disease

  • Our laboratory interests focus on how kidney damage progresses in post-menopausal hypertension, metabolic syndrome, lithium-induced nephrogenic diabetes insipidus and polycystic kidney disease (PKD). 

    Research Projects

    • 1) Sex Differences in Hypertension and the Role of the Immune System We are studying how sex differences impact the onset of hypertension, focusing on the increased risk for high blood pressure that occurs as women age. Specifically we are identifying the role that estrogen plays on the immune system, examining how T cell populations are activated during hypertension and how this influences renal salt and water transport, and the regulation of extracellular fluid balance (blood pressure).

    • 2) Vasopressin and Renal Cell Proliferation:  In Polycystic Kidney Disease (PKD)  and in lithium-induced nephrogenic diabetes insipidus (NDI), epithelial cells of the kidney proliferate and renal function is reduced. Vasopressin receptor pathways have been targeted as pharmacological interventions for PKD and they reduce cyst formation and proliferation. We are interested in the mechanisms that trigger collecting ducts to proliferate. We use in vivo and in vitro models to study renal cell proliferative pathways.

Janis Burt, PhD. (Cardiovascular Disease: Gap Junctions, Growth Control, Vascular Remodeling)

Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

Contact Information:  (520) 626-6833, jburt@u.arizona.edu 

Research Interests:  Cardiovascular Disease: Gap Junctions, Growth Control, Vascular Remodeling

  • Role of gap junctions in vascular function

  • Contribution of gap junctions to growth control, vascular remodeling, and response to injury and disease

  • Mechanisms underlying acute regulation of gap junction function by second messenger signaling cascades

  • Biophysics of gap junction channels

  • Gap Junctions in vascular smooth muscle: Growth control

  • Functional consequences of connexin interactions in blood vessels

Haijiang Cai, PhD (Neuroscience: Neural Circuits of Animal Behaviors)

Program Affiliations:  Neuroscience, Bio 5 Institute, Physiological Sciences

Website and Publications:  Cai Lab Page, Google Scholar Page, Neuroscience Faculty Page

Contact Information:  (520) 621-6654, haijiangcai@email.arizona.edu

Research Interests:  As listed on the Lab Page, "We are studying the neural circuits of animal behaviors, with a focus on understanding how the neural circuits regulate feeding and emotional behaviors like fear, anxiety, and depression." 

Yin Chen, PhD. (Lung Disease: Mucin Genes in Asthma Pathogenesis, Asthma Exacerbation)

Program Affiliations:  Pharmacology and Toxicology, College of Pharmacy, Southwest Environmental Health Sciences Center, Bio 5 Institute, Arizona Respiratory Center, Physiological Sciences

Website and Publications:  College of Pharmacy Faculty Page

Contact Information:  (520) 626-2823, ychen@pharmacy.arizona.edu

Research Interests:  Mucin Genes in Asthma Pathogenesis, Asthma Exacerbation

  • Airway epithelial differentiation and mucous cell metaplasia in chronic airway diseases
    • Mucous cell metaplasia and mucus over-production are hallmarks of almost all chronic airway diseases (e.g. asthma, chronic obstructive pulmonary diseases, cystic fibrosis, etc.) and significantly increase the morbidity and mortality. No therapy is available besides the mechanical suction. We are now investigating the function and regulation of mucin genes in asthma pathogenesis using both in vivo (gene targeting model, induced mouse model of asthma, as well as tissues and secretions from asthmatic patients) and in vitro (differentiated epithelial culture and cell line) models.
  • A new paradigm in virus-induced asthma exacerbation
    • Airway rhinovirus (RV) infection is the major cause of asthma exacerbation, a severe precipitation of the symptom in otherwise stable asthmatics who are often still under the routine medication. Thus, asthma exacerbation may have a different pathogenic mechanism that is largely unknown at present. Among different asthma-inducing allergens, Alternaria (Alt) is a fungal species that causes asthma in arid and semi-arid areas. In collaboration with the researchers in Arizona Respiratory Center, we have found the shift of airway response to viral infection during Alt exposure, which promotes inflammation and depresses antiviral response. This shift causes further increase of viral production and inflammation, similar to what would happen in the airways of asthma exacerbation. We are currently investigating the potential underlying mechanisms using both in vivo and in vitro models.  (College of Pharmacy: http://www.pharmacy.arizona.edu/directory/yin-chen-phd

Dawn Coletta, Ph.D. (Molecular and Physiological Basis of Insulin Resistance)

Program Affiliations:  Department of Medicine, Division of Endocrinology, Department of Physiology, Physiological Sciences

Website and Publications:  Department of Medicine Page, Physiology Faculty Page

Contact Information:  (520) 626-9412, dcoletta@email.arizona.edu

Research Interests:  Molecular and physiological basis of insulin resistance, which is a characteristic feature of a number of common metabolic diseases including type 2 diabetes mellitus, obesity and the insulin resistance syndrome. My laboratory combines state of the art techniques and in vivo clinical methods to identify and characterize genes/loci that influence this complex phenotype.

Robert J. Collier, PhD. (Environmental Physiology)

Program Affiliations:  Animal and Biomedical Sciences, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-7622, rcollier@ag.arizona.edu

Research Interests:  Environmental Physiology

  • The focus of this laboratory is in studying environmental effects on gene expression in domestic animals. Research program utilizes both practical management models as well as controlled environmental facilities to modify environments around animals. Environmental effects on gene expression are then evaluated using gene expression microarrays, real time PCR and northern blots. Domestic animals of interest include dairy and beef cattle, horses, sheep and goats.

Brett Colson, PhD. (Cardiovascular Physiology)

Program Affiliations:  Arizona Biological and Biomedical Sciences, Biomedical Engineering, Biochemistry and Cellular & Molecular Biology, Physiological Sciences

Website and Publications:  NCBI MyBibliography, The Colson Laboratory, Sarver Heart Center Profile,

Contact Information:  (520) 621-1950, bcolson@email.arizona.edu

Research Interests:  Cardiovascular Physiology: Deciphering the structural basis for cardiac muscle contraction and genetic heart disease at the molecular level

  • Dr. Colson’s research interests include understanding the molecular motions of muscle proteins that finely-tune and regulate the heart’s contractile performance.

  • The primary goal of his current research is to understand the relationship between the structural, biochemical, and physiological states in the mechanisms underlying cardiovascular dysfunction in genetic heart disease. These insights from the mechanistic studies in his lab are then used to design novel molecular therapies for heart failure and cardiovascular disease.

  • Recent work in the Colson lab has focused on how genetic mutations and changes in post-translational modifications in myosin binding protein-C can cause the development of hypertrophic cardiomyopathy, the most common cause of sudden cardiac death in young people.

  • Using site-directed spectroscopy, with high resolution in both space and time, Dr. Colson and his research team decipher the molecular dynamics in these muscle proteins, which are involved with controlling the strength and speed of cardiac muscle contraction. For these biophysical experiments, they attach fluorescent probes to track protein motions, orientation, and functional characteristics including protein binding and force development in the muscle cell. Similar state-of-the-art approaches are also used in his lab’s efforts for drug and small molecule discovery as novel heart failure therapies.

Stephen Cowen, PhD. (Neuroscience: Psychology)

Program Affiliations:  Psychology, Physiological Sciences

Website and Publications:  Psychology Faculty Homepage 

Contact Information:  (520) 626-2615, scowen@email.arizona.edu

Research Interests:  Neuroscience: Psychology

Zelieann Craig, PhD. (Reproduction and Infertility in Animals and Humans)

Program Affiliations:  Animal and Biomedical Sciences, Bio5 Institute, Southwest Environmental Health Sciences Center, Arizona Cancer Center, Physiological Sciences

Website and Publications:  ACBS Faculty Homepage, NCBI MyBibliography, Lab Website  

Contact Information:  (520) 621-9965, zr.craig@arizona.edu

Research Interests:  Reproduction and infertility in animals and humans

  • Dr. Craig's work focuses on understanding how phthalates affect the function of the ovary, the major reproductive organ in females.  Thus, work in her laboratory is focused on using animal models to help us understand the mechanisms by which phthalates exert their effects on the ovary, determine whether phthalates cause female infertility, and examine whether the effects of phthalates on female reproduction can be prevented or reversed.  Using this knowledge she hopes to develop additional models to evaluate other chemicals and environmental factors that could influence both human and animal reproduction.

Thomas P. Davis, PhD. (Stroke, Drug Transport, Blood-Brain Barrier)

Program Affiliations:  Medical Pharmacology, Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-7643, davistp@U.arizona.edu

Research Interests:  Stroke, Drug Transport, Blood-Brain Barrier

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

Nicholas Delamere, PhD. (Glaucoma, Na,K-ATPase)

Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications:  NCBI MyBibliography, Physiology Faculty Page

Contact Information:  (520) 626-6425, delamere@arizona.edu

Research Interests:  Glaucoma, Na,K-ATPase

  • Na,K-ATPase regulation
  • Aqueous humor secretion
  • Na,K-ATPase-Src kinase interaction in lens epithelium
  • Role of Na,K-ATPase alpha 2 in astrocytes

Ankit Desai, M.D. (Post-Translational Mechanisms of Pulmonary Vascular Disease)

Program Affiliations:  Department of Medicine, Department of Cellular and Molecular Medicine, Physiological Sciences

Website and Publications:  Laboratory of Ankit Desai, NCBI MyBibliography

Contact Information:  (520) 626-6867, adesai@shc.arizona.edu

Research Interests:  Understanding post-translational mechanisms of pulmonary vascular disease involving ubiquitination and glycosylation 

  • The Desai lab focuses on two projects both converging on investigating post-translational mechanisms of pulmonary vascular disease. Project one goals will dissect the role of candidate genes within the ubiquitination pathway; project two will characterize the role of o-glycosylation and relevant candidate genes in the development of pulmonary vascular disease.  The lab leverages genome-wide studies (GWAS and expression profiling) in patients with pulmonary hypertension (PH) to prioritize and functionally elucidate target genes and variants in vitro and in vivo. The lab utilizes cell culture work with pulmonary artery endothelial and smooth muscle cells from healthy controls and patients with PH as well as murine and rodent animal models of PH. Base don these mechanisms, we are testing novel pharmacological and molecular therapeutics in PH animal models.

Erika Eggers, PhD. (Diabetic Retinopathy, Neurophyisiology, Visual Physiology, Inhibition)

Program Affiliations:  Physiology, Biomedical Engineering, Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications:  Eggers Laboratory, NCBI MyBibliography, Physiology Faculty Page

Contact Information:  (520) 626-7137, eeggers@u.arizona.edu

Research Interests:  Diabetic Retinopathy, Neurophysiology, Visual Physiology, Inhibition

  • The broad goal of research in our laboratory is to understand how inhibitory inputs influence neuronal signaling and sensory signal processing in the healthy and diabetic retina.  Neurons in the brain receive inputs that are both excitatory, increasing neural activity, and inhibitory, decreasing neural activity.  Inhibitory and excitatory inputs to neurons must be properly balanced and timed for correct neural signaling to occur.

  • To study sensory inhibition we use the retina, a unique preparation which can be removed intact and can be activated physiologically, with light, in vitro.  Thus using the retina as a model system, we can study how inhibitory synaptic physiology influences inhibition in visual processing. This intact system also allows us to determine the mechanisms of retinal damage in early diabetes.

Torsten Falk, PhD. (Neuroscience: Parkinsons)

Program Affiliations:  Neurology, Pharmacology, Physiological Sciences

Website and Publications:  Neurology Faculty Homepage, NCBI MyBibliography

Contact Information:  (520) 626-3927, tfalk@u.arizona.edu

Research Interests:  Neuroscience: Parkinsons 

Jean-Marc Fellous, PhD. (Processes Involved in Learning and Memory Consolidation)

Program Affiliations:  Psychology, Physiological Sciences

Website and Publications:  Psychology Faculty Homepage, Fellous Homepage

Contact Information:  (520) 621-7447, fellous@email.arizona.edu

Research Interests:  The processes involved in learning and memory consolidation depend on sleep and emotions, the neural substrates of PTSD and the neural substrate of empathy

  • My research and academic interests focus on the study of brain-behavior relationships in the Computational Neuroscience. Neural substrate of emotion, learning and memory in rats and humans, PTSD, empathy.

Ralph Fregosi, PhD. (Neuroscience: Sleep Apnea, Neurophysiology, Regulation of Breathing)

Program Affiliations:  Physiology, Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

Contact Information:  (520) 621-2203, fregosi@u.arizona.edu

Research Interests:  Neuroscience: Sleep Apnea, Neurophysiology, Regulation of Breathing

  • We are interested in the development of inhibitory and excitatory synaptic transmission in brainstem respiratory neurons, and how normal development is disrupted by in utero nicotine exposure.  We use hypoglossal motoneurons and preBotzinger complex inspiratory neurons as our model.   Studies are done using neonatal rat or mouse brainstem slices that retain rhythmic respiratory-related motor output in vitro.  We also use the in vitro brain stem spinal cord preparation of neonatal rats and mice, and conduct parallel in vivo studies of breathing behavior in awake neonatal rodents.Techniques include whole cell patch clamp electrophysiology (both voltage and current clamp), extracellular recording, immunohistochemistry, Western blot analysis, and in vivo measures of neonatal breathing using plethysmography.

Randall Freise, M.D. (Surgery)

Program Affiliations:  Surgery, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-0478, rfriese@surgery.arizona.edu

Research Interests:  Surgery 

Andrew Fuglevand, PhD. (Neuroscience: Neurophysiology, Motor Control, Motor Neurons, Skeletal Muscles)

Program Affiliations:  Physiology, Neuroscience, Biomedical Engineering, Bio5 Institute, Physiological Sciences

Website and Publications:  Fuglevand Lab, Physiology Faculty Page

Contact Information:  (520) 621-6983, fuglevan@u.arizona.edu

Research Interests:  Neuroscience: Neurophysiology, Motor Control, Motor Neurons, Skeletal Muscles

  • The broad goal of the work carried out in our laboratory is to understand how the mammalian nervous system controls the action of skeletal muscles to produce coordinated movements. We use a variety of experimental approaches, including computer modeling and simulation, single motor unit recording, and microneurographic methods to record and stimulate single sensory and motor axons. Our experiments address a range of topics from those related to how individual neurons integrate synaptic information to those associated with the development of new methods to restore movement and sensation in paralyzed individuals. Of particular emphasis at present are studies designed to characterize the functional organization of the corticospinal pathways that underlie the control of hand and finger movements.

Janet Funk, M.D. (Osteoporosis, Arthritis, Cardiovascular, Botanicals)

Program Affiliations:  Department of Medicine, Bio5 Institute, Arizona Cancer Center, Sarver Heart Center, Physiological Sciences

Website and Publications:  Cancer Center Profile 

Contact Information:  (520) 626-3242, jfunk@u.arizona.edu

Research Interests:  Osteoporosis, Arthritis, Cardiovascular, Botanicals

  • Current Research projects include:

  • Exploring the efficacy and mechanism of action of medicinal botanicals in the treatment of common bone disorders, including osteoporosis and arthritis.

  • Targeting PTHrP for breast cancer bone metastases prevention.

  • Use of botanical dietary supplements as anti-inflammatory agents in the treatment of cardiovascular disease and diabetes.

Fayez K. Ghishan, M.D. (Pediatrics: Gastroenterology and Nutrition)

Program Affiliations:  Department of Pediatrics, Arizona Cancer Center, Institute for Clinical and Translational Science, Steele Children's Research Center, Diamond Children's Center, Horace W. Steele Endowed Chair in Pediatric Research, Physiological Sciences

Website and Publications:  NCBI MyBibliography, Publications on PubMed, Faculty Home Page

Contact Information:  (520) 626-5170, meckler@peds.arizona.edu

Research Interests:  Pediatrics: Gastroenterology and Nutrition - Interests on Faculty Homepage:

  • Autoimmune disorders (Inflammatory Bowel Disease (IBD), Crohn's disease, ulcerative colitis, eosinophilic esophagitis, eosinophilic gastroenteritis), the role curcumin plays in treating autoimmune disorders; intestinal ion transport of phosphate across the gastrointestinal tract;  intestinal ion transport; regulation of digestive vesicular glutamate transporter
  • Clinical Interests:
    • Inflammatory Bowel Disease (IBD), Crohn's disease, ulcerative colitis, eosinophilic esophagitis, eosinophilic gastroenteritis, nutrition, autoimmune disorders 

Scott B. Going, PhD. (Diabetes/Obesity: Body Composition, Growth and Aging)

Program Affiliations:  Nutritional Sciences, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-4705, going@u.arizona.edu

Research Interests:  Diabetes/Obesity: Body Composition, Growth and Aging

  • Current projects include:

    • The Bone, Estrogen and Strength Training (BEST) study, a randomized prospective study of the effects of hormone replacement therapy on bone mineral density, soft tissue composition, and muscle strength in postmenopausal women (National Institutes of Health).

    • The Profile-based Internet-linked Obesity Treatment study (PILOT), a randomized study of internet support for weight maintenance after weight loss in peri-menopausal women (National Institutes of Health).

    • The Trial of Activity for Adolescent Girls (TAAG) study, a multi-center, school-based activity trial designed to prevent the usual decline in physical activity in adolescent girls (National Institutes of Health).

    • The Adequate Calcium Today (ACT) study, a randomized multi-center study of a behavioral intervention to promote healthy eating, calcium intake and bone development in adolescent girls (United States Department of Agriculture).

    • The Healthy Weight in Adolescents study, a randomized, multi-center study of the effects of a science-based curriculum focused on concepts of energy balance on body weight and composition in adolescent boys and girls (United States Department of Agriculture).

    • The KNEE study, a randomized clinical trial of the effects of resistance exercise on disease progression, pain, and functional capacity in osteoarthritis patients (National Institutes of Health).

    • The STRONG study, a randomized clinical trial of the effects of resistance exercise and Remicaid on disease progression, pain, muscle strength and functional capacity in rheumatoid arthritis patients (Centocor, Inc.).

    • Partners for Healthy Active Children, Campañeros Para Niños Sano y Actives, designed to create and implement research-based physical education and nutrition curricula at YMCA after-school programs and Sunnyside District elementary schools, in alignment with the State of Arizona , Health and Physical Activity standards (Carol M. White Physical Education Program CFDA #84.215F).

    • Longitudinal Changes in Hip Geometry, an observational and experimental cohort study of changes in muscle mass, hip structural parameters and hip bone strength in middle-aged and older women in the Women's Healthy Initiative study (National Institutes of Health).

Steven Goldman, M.D. (Heart Failure, Medicine and Cardiology)

Program Affiliations:  Department of Medicine, Cardiology, Sarver Heart Center, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 629-4624, goldmans@shc.arizona.edu

Katalin Gothard, PhD. (Neuroscience: Emotion, Social Behavior)

Program Affiliations:  Physiology, Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

Contact Information:  (520) 626-1448, kgothard@email.arizona.edu

Research Interests:  Neuroscience: Emotion, Social Behavior

  • The broad goal of the research in our laboratory is to understand the neural basis of emotion. We use non-human primates as a model system for normal and pathological emotions generated in the context of social behavior.  The experiments involve eliciting emotions in freely behaving monkeys while recording neural activity from several brain areas in conjunction with cardiovascular and other autonomic measurements. These experiments reveal the real-time dynamic interaction of multiple systems implicated in emotion regulation and the mechanisms by which emotional responses produce immediate behavioral effects

Michael Grandner, PhD. (Sleep and Sleep-Related Behaviors)

Program Affiliations: Psychiatry, Medicine, Psychiary, Psychology, Sarver Heart Center, Physiological Sciences

Website and Publications:  Michael Grandner, Psychiatry Faculty Page

Contact Information:  (520) 626-6336, grandner@email.arizona.edu  

Research Interests:  Sleep and sleep-related behaviors related to cardiovascular disease, neurobehavioral functioning, mental health, and general well-being.

  • Current research projects are funded by the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Environmental Health Sciences (NIEHS).  One study focuses on sleep patterns and how they relate to cardiometabolic disease risk and neurocognitive function. The other study is on social, environmental and behavioral factors and how they impact sleep. His methodologies include population-level surveys, computer-based geospatial analyses, home-based assessments of sleep and health, and in-laboratory studies. (Faculty Page)

Henk L. Granzier, PhD. (Cardiovascular Disease: Muscle, Cardiac, Cells, Mechanics, Titin, Contractility)

Program Affiliations:  Cellular and Molecular Biology, Physiology, Biomedical Engineering, Biological Physics, Physiological Sciences

Website and Publications:  NCBI MyBibliography, Physiology Faculty Page

Contact Information:  (520) 626-3641, granzier@email.arizona.edu

Research Interests:  Cardiovascular Disease: Muscle, Cardiac, Cells, Mechanics, Titin, Contractility

  • Muscle structure and function

Samantha Harris, PhD. (Cardiovascular Disease: Cellular and Molecular Medicine)

Program Affiliations:  Cellular and Molecular Medicine, Physiological Sciences

Website and Publications:  Department of Medicine Faculty Homepage

Contact Information:  (520) 621-0291, samharris@email.arizona.edu

Research Interests:  Cardiovascular Disease: Cellular and Molecular Medicine

Meredith Hay, PhD. (Neuroscience/Hypertension: Neurotransmitter, Peptide and Cellular Mechanisms in Central Brain)

Program Affiliations:  Physiology, The McKnight Brain Institute, Sarver Heart Center, National Institute for Civil Discourse, Physiological Sciences

Website and Publications:  Hay Laboratory, Physiology Faculty Page

Contact Information:  (520) 626-7384, mhay@arizona.edu

Research Interests:  Neuroscience/Hypertension: neurotransmitter, peptide and cellular mechanisms in central brain

  • The primary focus of our laboratory is the understanding of how the brain regulates blood pressure.
  • We study the neurotransmitter, peptide and cellular mechanisms in central brain nuclei that regulate sympathetic outflow and ultimately arterial blood pressure.
  • Our ultimate goal is to identify potential new phamacotherapies that will improve the lives of individuals who suffer from cardiovascular disease.

Karl B. Kern, M.D. (CPR Research, Cardiology)

Program Affiliations:  Department of Medicine, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-2477, kernk@u.arizona.edu

Research Interests:  CPR Research, Cardiology

  • CPR research including: post resuscitation myocardial dysfunction, chest compression-only BLS CPR, blood flow during CPR, pharmacological and mechanical adjuncts for CPR

Zain Khalpey, M.D., PhD. (Surgery)

Program Affiliations:  Surgery, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-0120, zkhalpey@surgery.arizona.edu

Research Interests:  Surgery

Pawel Kiela, PhD. (Pediatrics)

Program Affiliations:  Pediatrics, Bio5 Institute, Physiological Sciences

Website and Publications:  Pediatrics Faculty Page

Contact Information:  (520) 626-9687, pkiela@peds.arizona.edu

Research Interests:  Pediatrics

  • Therapeutic and pathophysiological aspects of Inflammatory Bowel Diseases.Crohn's disease (CD) and ulcerative colitis (UC) are two spontaneously relapsing, immunologically mediated disorders of the gastrointestinal tract which are characterized by intestinal inflammation and mucosal damage. These chronic, debilitating conditions characterized by abnormal and persistent immune response to intestinal commensal flora have multifactorial etiology with genetic predispositions and environmental factors contributing to the ultimate clinical manifestation. Despite recent advances in understanding the pathophysiology of IBD and development of new biological agents to treat active inflammation and to maintain remission, our knowledge and therapeutic options are still limited.Our laboratory, funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH, studies three aspects of IBD:
    • Pre-clinical studies on the effectiveness and mechanism of action of curcumin (a natural non-specific inhibitor of NF-kappa-B) in mouse models of CD and UC (chemically induced colitis and spontaneous colitis in IL-10 or TCR-alpha knockout mice).
    • The role of NHE3. the major intestinal Na+/H+ exchanger in the maintenance of epithelial integrity of the gut. and in modulation of the immune response in Inflammatory Bowel Diseases.
    • The effects of acute and chronic colitis and inflammatory mediators on key players of systemic inorganic phosphate homeostasis and its contribution to osteopenia and osteoporosis frequently associated with IBD.

Kwang Chul Kim, PhD. (Otolaryngology: Cell Biology of Mucus Lining the Airway Lumen)

Program Affiliations:  Department of Otolaryngology - Head and Neck Surgery, Respiratory Mucus Research Program, Physiological Sciences

Website and Publications:  Faculty Home Page

Contact Information:  (520) 626-6673, kckim@email.arizona.edu

Research Interests:  Cell Biology of Mucus Lining the Airway Lumen - interests from Faculty Homepage:

  • To further elucidate the molecular interaction between MUC1 and TLRs in the presence of EGFR (Kato K. et al, J Immunol 188:2014, 2012).
  • To understand the role of MUC1 in other cell types in the lung, including type II pneumocytes and alveolar macrophages (Yen JH et al, Brain Behav Immun 29:70, 2013).
  • To determine whether MUC1/Muc1 is involved in the genesis of COPD (Umehara T. et al, Inflamm Res 61:1013, 2012).

John Konhilas, PhD. (Cardiovascular Disease: Heart Disease, Impact of Diet, Exercise, Sex)

Program Affiliations:  Physiology, Bio5 Institute, Biomedical Engineering, Molecular Cardiovascular Research Program, Physiological Sciences

Website and Publications:  Physiology Faculty Page

Contact Information:  (520) 626-6578, konhilas@arizona.edu

Research Interests:  Cardiovascular Disease: Heart Disease, Impact of Diet, Exercise, Sex

  • We are very interested in how the molecular and cellular biology of the heart cell impacts the contractile properties of the intact heart. We know that a number of factors influence gene expression and cell signaling in the cardiac myocyte including diet, exercise, disease and sex/gender. The changes induced by these factors will ultimately affect cardiac contractile function. It is this functional relationship that we are studying using a variety of molecular, cellular, and physiological techniques. We focus on the intermediates responsible for substrate utilization and presentation to the contractile apparatus. We hope to understand how the physiological factors of diet, exercise, disease and sex/gender impact substrates in the cell and how the presentation of these substrates affects contractile function. We believe that the interplay between contractile function and energy use is critical to health and disease.

  • We are also interested in how cardiac disease can influence peripheral organ systems including skeletal muscle. We know that humans with cardiac disease also experience severe skeletal muscle weakness and fatigue. This cannot be attributed entirely to poor circulation caused by reduced contractile function. Instead, we believe that is the specific alteration of specific muscle factors responsible for substrate metabolism and delivery to the muscle cell.

Paul Langlais, Ph.D. (Proteins Involved in Insulin Signal Transduction and Insulin Resistance))

Program Affiliations:  Associate Professor, College of Medicine, Department of Medicine, Division of Endocrinology; Director – Proteomics Lab, University of Arizona, College of Medicine, Department of Medicine, Endocrinology Division, Physiological Sciences 

Website and Publications:  List of Publications

Contact Information:  (520) 626-5909, langlais@email.arizona.edu

Research Interests:  From UA Vitae:

  • The role of insulin is to lower blood glucose levels by stimulating glucose uptake into muscle and adipose tissue. Resistance to insulin, a phenomenon directly involved in the pathogenesis of type 2 diabetes, remains to be understood. Basic research has yet to fully discover how insulin action is elicited. Research in the laboratory of Paul R. Langlais, Ph.D., focuses on the identification and characterization of proteins involved in insulin signal transduction and also tests whether the dysfunction of these proteins is involved in the pathogenesis of insulin resistance and type 2 diabetes.Dr. Langlais specializes in the use of mass spectrometry to perform proteomics, a technique that allows for large-scale quantitative analysis of protein abundances between different treatments. This approach led him to the discovery that CLIP-associating protein 2 (CLASP2) is responsive to insulin stimulation, and his now-published findings support the involvement of CLASP2 in insulin-stimulated glucose uptake. Current research is aimed at discovering the role of CLASP2 in insulin action, in addition to identifying new proteins previously unknown to function in this system.Dr. Langlais leads the University of Arizona College of Medicine Proteomics Laboratory, a collaborative environment for investigators at the University of Arizona and their colleagues to perform proteomic studies in their respective projects.

Julie Ledford, PhD (Respiratory Disease, Genetics, Immunobiology)

Program Affiliations:  Department of Medicine, Immunobiology, Arizona Respiratory Center, Bio 5 Institute, Physiological Sciences

Website and Publications:  Department Faculty Page

Contact Information:  (520) 626-0276, jledford@email.arizona.edu

Research Interests:  Respiratory disease, genetic and molecular mechanisms of allergic airway diseases in children.

Kirsten H. Limesand, PhD. (Cancer: Apoptosis, Salivary Acinar Cells, Radiation, Signaling)

Program Affiliations:  Nutritional Sciences, Cancer Biology, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-4517, limesank@u.arizona.edu

Research Interests:  Cancer: Apoptosis, Salivary Acinar Cells, Radiation, Signaling

  • Radiation therapy for head and neck cancer causes adverse secondary side effects in the normal salivary gland including xerostomia, oral mucositis, malnutrition, and increased oral infections. Although improvements have been made in targeting radiation treatment to the tumor, the salivary glands are often in close proximity to the treatment site. The significant destruction of the oral cavity following radiation therapy results in diminished quality of life and in some cases interruptions in cancer treatment schedules.

  • My research program has its foundation in radiation-induced salivary gland dysfunction; mechanisms of damage, clinical prevention measures, and restoration therapies. Evidence suggests that salivary acinar function is compromised due to apoptosis induced by these treatments and temporary suppression of apoptotic events in salivary glands would have significant benefits to oral health. We utilize a number of techniques in my laboratory including: genetically engineered mouse models, real-time RT/PCR, immunoblotting, immunohistochemistry, primary cultures, siRNA transfections, irradiation, and procedures to quantitate salivary gland physiology.

Sean W. Limesand, PhD. (Diabetes: Pancreas Formation and Function, Fetal Nutrition, Type 2 Diabetes)

Program Affiliations:  Animal Sciences, Bio5 Institute, Physiological Sciences

Website and Publications:  Sarver Heart Center Profile

Contact Information:  (520) 6262-7623, limesand@ag.arizona.edu

Research Interests:  Diabetes: Pancreas Formation and Function, Fetal Nutrition, Type 2 Diabetes

  • Some of the most debilitating diseases affecting public health and those that impose an extreme monetary impact on health care costs in the United States are metabolic diseases and endocrine disorders such as Type 2 Diabetes. The prevalence of these diseases in the USA has been growing faster than Mendelian inheritance rates suggesting that environmental cues are influencing the prevalence of adulthood metabolic disorders. Inappropriate fetal growth and development due to inadequate fetal nutrition has been associated with several adult onset diseases including diabetes (Barker Hypothesis). Pancreatic b-cells secrete the anabolic hormone, insulin, in response to nutrient changes during the second half of gestation, likely coordinating fetal growth rate with fetal nutrient supply, making the fetal b-cell a potential target for nutritional adaptation in utero.

  • To understand nutrient regulation of fetal pancreas development, I am studying how poor fetal nutrition reduces pancreas formation and function. Environmental stress during pregnancy in sheep causes placental insufficiency; thus, creating an inadequate fetal nutrient supply that leads to fetal growth restriction and impaired insulin secretion due to decreased b-cell number and function. Current research aims are designed to determine mechanism that reduced b-cell responsiveness in intrauterine growth restricted fetuses. The first aim is to determine stages of pancreatic development and endocrine cell replication in this large animal model to understand how b-cell numbers are reduced. In addition to a lower number of b-cells, their stimulus secretion coupling is impaired due to reduced insulin production. Therefore, the second aim is to determine deficits in insulin biosynthesis. If these inadequacies shown in the growth restricted fetus are not compensated for after birth, they might persist into adulthood and contribute to failure of insulin secretion to predispose offspring to Type 2 Diabetes.

Ron Lynch, PhD. (Diabetes and Cancer: Second Messenger Signalling, Diabetes and its Complications)

Program Affiliations:  Physiology, Biomedical Engineering, Biomedical Imaging and Spectroscopy, Bio5 Institute, Physiological Sciences

Website and Publications:  Lynch Lab, Physiology Faculty Page

Contact Information:  (520) 626-2472, rlynch@u.arizona.edu

Research Interests:  Diabetes and Cancer: Second Messenger Signalling, Diabetes and its Complications

  • Research in the Lynch lab primarily focuses on second messenger signaling in vascular smooth muscle cells and nutrient sensing hypothalamic neurons with emphasis on alterations in signaling that occur during development of diabetes. Alterations in Ca2+ homeostasis and contractility are observed in vascular cells in association with the elevated levels of glucose and insulin that occur during development of type II diabetes. To study these issues, cells isolated from transgenic animals in which specific genes for Ca2+ handling are ablated or over-expressed are utilized as model systems. Analysis of subcellular protein distributions and second messenger signaling is performed in our lab using state of the art image acquisition and analysis approaches which is our second area of expertise. Over the past decade, our lab has been involved in the development of unique microscopic imaging and spectroscopy approaches to study cell and tissue function. As part of this effort, we have developed, with collaborators, methods for targeting specific cell types in mice for in situ identification and rapid isolation. Using this approach, analysis of cell-type specific gene expression and function can be performed.

Lalitha Madhavan, M.D., PhD. (Neuroscience: Parkinsons, Stem Cell Biology and Regenerative Medicine)

Program Affiliations:  Neuroscience, Bio5 Institute, Arizona Cancer Center, Evelyn F McKnight Brain Institute, Molecular and Cellular Biology, Physiological Sciences

Website and Publications:  Neurology Faculty Homepage, Madhavan Lab, NIH MyBibliography   

Contact Information:  (520) 626-2330, lmadhavan@email.arizona.edu

Research Interests:  Neuroscience: Parkinsons, Stem Cell Biology and Regenerative Medicine

  • Research in the Madhavan lab centers on understanding the basic biology and therapeutic potential of a variety of stem cell types with the goal of developing novel preventative and treatment strategies for neurodegenerative disorders, especially Parkinson’s disease (PD).  Through recent efforts the lab has identified important mechanisms dictating neural stem cell function during aging, which need to be considered if effective treatments for neurodegenerative disorders are to be developed.  In addition, the lab has also generated human fibroblasts and induced pluripotent stem cells (iPSCs), from individuals diagnosed with PD, and established methods to efficiently generate midbrain dopamine neurons (the specific cell type that degenerates in PD) from the iPSCs.  These patient-derived cell lines are currently being used to investigate molecular processes that may underlie PD, and also create a robust platform for future drug testing as well as cell-based therapeutic approaches for PD.

Ayako Makino, PhD. (The Modulation of Endothelial Function in Pathological State)

Program Affiliations:  Department of Medicine, Physiology, Physiological Sciences

Website and Publications:  Physiology Faculty Page, NIH MyBibliography

Contact Information:  (520) 621-0511, aymakino@email.arizona.edu 

Research Interests:  The modulation of endothelial function in pathological state.

  • Current Main Focus:  Coronary endothelial dysfunction in diabetes.
  • Ongoing Research Projects:
    • 1) Mitochondrial autophagy (mitophagy) in endothelial cells
    • 2) Ca2+ homeostasis in endothelial cells
    • 3) GAP junction intercellular communication (GJIC) between endothelial cells

Patrick Mantyh, PhD., J.D. (Neuroscience: Pharmacology/Pain Research)

Program Affiliations:  Pharmacology, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-0742, pmantyh@email.arizona.edu

Research Interests:  Neuroscience: Pharmacology/Pain Research

  • Develop clinically relevant models of malignant and non-malignant skeletal pain
  • Mechanism-based understanding of the factors driving skeletal pain
  • Evaluation of the effects that therapies have on pain and disease progression
  • Regulation of bone remodeling by nervous system
  • Stem cells and bone health

Thomas Pannabecker, PhD. (Renal Physiology, Membrane Transport)

Program Affiliations:  Physiology, Physiological Sciences

Website and Publications:  Physiology Faculty Page

  • Pannabecker TL, Dantzler WH, Layton HE, Layton AT. 2008. Role of three
    dimensional architecture in the urine concentrating mechanism of the rat renal
    inner medulla. American Journal of Physiology Renal Physiology, 295:F1271-
    F1285.

  • Layton AT, Layton HE, Dantzler WH, Pannabecker TL. 2009. The mammalian
    urine concentrating mechanism: Hypotheses and Uncertainties. Physiology, 24:
    250-256.

  • Pannabecker TL. 2012. Structure and Function of the Thin Limbs of the Loop of
    Henle. Comprehensive Physiology. 2:2063–2086.

  • Pannabecker TL. 2013. Comparative physiology and architecture associated with
    the mammalian urine concentrating mechanism. American Journal of Physiology
    Regulatory Integrative and Comparative Physiology, 304:R488-R503.
    http://ajpregu.physiology.org/cgi/content/full/ajpregu.00456.2012?ijkey=KEkty6wXNBqis&keytype=ref&siteid=physiology”>text (link is external)

Contact Information:  (520) 626-6481, pannabec@email.arizona.edu  

Research Interests:  Renal Physiology, Membrane Transport

  • The goal of the research conducted in my laboratory is to better understand
    kidney structure and function in health and disease. To achieve this goal we
    currently focus both on identifying and characterizing transepithelial fluid and
    solute transport pathways within renal tubules and on characterizing fluid and
    solute flows that occur between nephron segments and blood vessels. This is
    accomplished using isolated tubule perfusion techniques and by constructing
    three-dimensional digital models of the renal medulla. The animal models used
    in the lab include the common laboratory rat and the desert-dwelling kangaroo
    rat. Information from these studies has contributed to development of new and
    revealing mathematical models that attempt to better understand the urine
    concentrating mechanism.

Klearchos Papas, PhD. (Diabetes: Organ Transplant, Hypoxia/Oxygenation, Surgery)

Program Affiliations:  Surgery, Physiological Sciences

Website and Publications:  Surgery Faculty Homepage

Contact Information:  (520) 626-4494, kkpapas@surgery.arizona.edu

Research Interests:  Diabetes: Organ Transplant, Hypoxia/Oxygenation, Surgery

  • He has spent the past 21 years of his research career studying the properties of insulin-secreting tissue and their relationship to viability and function. He has worked on the development and validation of assays (especially ones based on mitochondrial function such as oxygen consumption rate) for the real-time, objective assessment of islet quality prior to transplantation. In particular the assay based on oxygen consumption rate has been recently validated based on its ability to predict diabetes reversal in mice and clinical human islet auto transplants in patients with chronic pancreatitis. He has used these assays along with engineering principles to optimize the islet transplantation process from pancreas procurement to islet infusion to the recipient. His group has also developed tools for the real time non-invasive assessment of pancreases and other organs during preservation, and is actively involved in research for improvements in organ preservation technology aiming at extending the allowable time window from procurement to transplantation and the utilization of organs from expanded criteria donors without compromising clinical outcomes. He has had continuous NIH funding for the past 7 years in the area of pancreas preservation and he has spearheaded the effort for the development of humidified oxygen gas perfusion (persufflation) of the pancreas using novel technology for portable in situ oxygen generation from water via electrochemistry. He is also actively collaborating with leaders in the liquid perfusion field on NIH sponsored projects aiming at improving oxygenation. His research in this area has the potential to have a profound impact on reducing overall costs, increasing availability, and improving short-and long-term outcomes in solid organ transplantation.

Naomi E. Rance, M.D., PhD. (Neuroscience: Neuroendocrine Regulation, Estrogen, Hypothalamus)

Program Affiliations:  Department of Pathology, Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-6099, nrance@email.arizona.edu

Research Interests:  Neuroscience: Neuroendocrine Regulation, Estrogen, Hypothalamus

  • My overall research objective is to characterize and understand the events that occur in the human central nervous system in response to menopause. An equally important goal is to contribute to our understanding of the neuroendocrine mechanisms that regulate reproduction. Although complex, the neural basis of reproductive function is amenable to experimentation because of the known feedback circuits. Control mechanisms can be studied at many different levels, ranging from plasma hormone levels, to gene expression in subsets of hypothalamic neurons.

  • Menopause provides a unique opportunity to correlate physiology and neuroanatomy in the human brain because ovarian and pituitary hormones change dramatically and consistently. In the last decade, our laboratory has made considerable progress in characterizing changes in neuronal morphology and neuropeptide gene expression in the hypothalamus of postmenopausal women. We have found a number of changes that correlate with the ovarian failure of menopause. Neurokinin B and substance P gene expression is markedly increased in the infundibular nucleus of postmenopausal women, along with hypertrophy of these neurons. In addition, the gene expression of a separate subpopulation of LHRH neurons is increased in the medial basal hypothalamus of postmenopausal women. In contrast, POMC gene expression in the infundibular nucleus is decreased.

  • These observations have provided the direction of our studies using animal models. For example, the rat was used to test the hypothesis that increased neurokinin B gene expression in the hypothalamus of postmenopausal women is secondary to gonadal failure. These studies showed that that long-term gonadectomy results in increased numbers of arcuate (infundibular) neurons expressing NKB gene transcripts in both males and females. We have also found that long-term orchidectomy results in significant dendritic growth in neuroendocrine neurons in the arcuate nucleus of adult male rats. These data suggested that the withdrawal of gonadal steroids ultimately results in a substantial remodeling of hypothalamic neuronal circuits. We have hypothesized that the hypertrophied NKB neurons participate in the hypothalamic control of LH secretion. Our recent studies using both pharmacological and physiological methods provide strong support for this hypothesis.

  • Because menopause affects a well-characterized system and has consistent and substantial changes in hormone levels, our research program has been able to correlate alterations in hormone secretion with structural and neurochemical changes in the human hypothalamus. Our ability to address basic biological questions in the human CNS is greatly enhanced by the use of animal models to test hypotheses arising from our observations of the human hypothalamus. Characterization of the hypothalamic changes accompanying menopause has the potential not only of shedding light on the regulation of gonadotropin secretion and hypothalamic aging in the human, but may also have practical implications for the health of postmenopausal women.

Benjamin Renquist, PhD. (Neuroscience/Obesity: Neuroendocrine Control of Food Intake and Energy Expenditure)

Program Affiliations: Animal Sciences, Physiological Sciences

Website and Publications:  ACBS Faculty Homepage 

Contact Information:  (520) 626-5793, bjrenquist@email.arizona.edu

Research Interests:  Neuroscience/Obesity: neuroendocrine control of food intake and energy expenditure,  HPA and HPG axis function

  • Dr. Renquist’s research is performed in cell culture, mouse, and fish models to address 4 foci:

    • Understanding the causative role of hepatic lipid accumulation in the development of obesity associated pathophysiologies.  Hepatic lipid accumulation is directly linked to the severity and incidence of both Type II diabetes mellitus and hypertension.  Our research aims to understand the signaling mechanism that links hepatic lipid accumulation to these disease states. 

    • The physiological control of feed intake during heat stress.  Heat stress suppresses food intake.  The Renquist lab is focused on the role of heat induced changes in blood flow and how these may manipulate phagic drive.

    • Development of a single dose injectable sterilant -  This project designed to develop a single dose injectable sterilant, funded by a Michelson Grant in Reproductive Biology, is employing GnRH-toxin conjugates to ablate gonadotropes which produce hormones that stimulate both egg and sperm maturation.  By preventing both egg and sperm maturation we will effectively sterilize the animals.

    • Predicting growth in aquaculturally important species by measuring the metabolic rate of embryonic aquatic organisms (tilapia, oysters, and shrimp).  In fish metabolic rate is tightly coupled to essential functions for growth (e.g. protein and DNA synthesis).  This project will employ an assay that measures metabolic rate of fish, previously designed for drug development by Dr. Renquist, to sort aquaculturally important species (tilapia and trout) by metabolic rate and monitor subsequent growth rate. 

Leslie Ritter, PhD. (Stroke: Community and Systems Health Sciences)

Program Affiliations:  College of Nursing, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-7434, lritter@nursing.arizona.edu

Research Interests:  Stroke: Community and Systems Health Sciences

  • Research focuses on the mechanisms of injury after stroke (cerebral ischemia and reperfusion).

Patrick Ronaldson, PhD. (Neuroscience: Physiology/Pathology of the Blood-Brain Barrier)

Program Affiliations:  Pharmacology, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-2173, pronald@email.arizona.edu

Research Interests:  Neuroscience: Physiology/Pathology of the Blood-Brain Barrier; effect of pathophysiological insult on CNS drug delivery; intracellular signaling systems; nuclear receptor pathways.

  • The blood-brain barrier (BBB) is the principal physical and biochemical barrier that separates the central nervous system (CNS) from the systemic circulation. To this end, the BBB highly restricts flux of circulating substances in an effort to tightly control the CNS microenvironment and maintain cerebral homeostasis. In addition, the BBB is the most significant obstacle to drug delivery to the brain. In fact, many existing drugs have limited or no efficacy in the treatment of neurological diseases primarily due to a limited ability to traverse the BBB and accumulate within the CNS. The BBB has evolved specific transport mechanisms that mediate blood-to-brain xenobiotic permeability (figure 1). Paracellular diffusion between adjacent endothelial cells is restricted by the presence of tight junctions. Tight junctions are an intricate combination of transmembrane and cytoplasmic proteins linked to an actin-based cytoskeleton, which allows the tight junction to form a seal while remaining capable of rapid modulation. Brain uptake of a solute by the paraceullar route generally indicates a perturbation of BBB integrity. In fact, some drugs (i.e., codeine) have been shown to accumulate in the brain via paracellular diffusion. Additionally, uptake into and extrusion from the brain of many therapeutic agents is governed by drug transport proteins. Specifically, endogenous BBB transporters that have been shown to be involved in determining the brain permeation of pharmacological agents include the ATP-binding cassette superfamily of efflux transporters (i.e., P-glycoprotein, Multidrug Resistance Proteins, Breast Cancer Resistance Protein) and Organic Anion Transporting Polypeptides, a group of bidirectional and sodium-independent solute carriers that transport amphipathic substrates (figure 2). Recent evidence has suggested that pathological insult can lead to dramatic changes in expression and/or activity of transport proteins at the BBB and, subsequently, cause significant alterations in CNS drug delivery.
  • The objective of my research is to examine how disease conditions (i.e., pain/inflammation, cerebral ischemia, hypoxia) can affect the uptake and/or efflux of drugs at the BBB. The research involves molecular studies to identify and characterize intracellular signaling systems and nuclear receptor pathways that regulate drug transport mechanisms at the BBB during pathophysiological insult. Signaling pathways may represent cellular targets that can be utilized to optimize CNS drug delivery. We also perform in vivo functional studies to characterize how molecular changes may affect distribution of therapeutic agents in the brain. A thorough identification and characterization of such processes is critical to obtaining an understanding of how disease can affect drug uptake and/or distribution to the CNS. The results of our studies may explain why acute and/or chronic pathophysiological insult may induce clinically significant changes in CNS drug efficacy and development of unexpected drug toxicity. Furthermore, these studies may demonstrate how functional changes in drug transport mechanisms at the BBB may be exploited to effectively deliver novel therapeutic agents to the CNS.

Prabir Roy-Chaudhury, PhD (Nephrology, Hemodialysis, Vascular Access, and Kidney Failure Therapies)

Program Affiliations:   Chief of Division of Nephrology in Department of Medicine, American Society of Nephrology, Physiological Sciences

Website and Publications:  Faculty Home Page

Contact Information:  (520) 626-6371, proychaudhury@email.arizona.edu

Research Interests:  Arizona Kidney and Vascular Center and Roy-Chaudhury Laboratory

  • Overview:  We are a translational and patient-centric research program that is focused on uremic vascular biology, both in the context of dialysis vascular access dysfunction and cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD) and end stage renal disease (ESRD; dialysis and transplantation).
  • Vision and Mission:  Our goal is to identify and explore mechanistic pathways that are involved in the pathogenesis of both dialysis vascular access dysfunction and uremic cardiovascular disease in patients with CKD and ESRD, and to then use this information to further a precision medicine approach to this problem (biomarkers; risk stratification and novel therapies). 
    • We aim to achieve this goal through the use of (a) large and small animal models of arteriovenous fistula (AVF), arteriovenous graft (AVG) and tunneled dialysis catheter (TDC) dysfunction (including kidney failure models) (b) human blood and tissue from CKD and ESRD patients undergoing a vascular access or other procedure (c) a robust clinical research program and (d) linkages to clinical care.
  • Ongoing Projects:
    • Elucidation of the mechanistic pathways involved in vascular access dysfunction using a mouse model of AVF stenosis in genetically modified mice
    • Documentation of the interactions between hemodynamic stress and vascular stenosis using pig models of AVF stenosis
    • Analysis of blood and tissue samples from CKD and ESRD patients to better understand the role of uremic vascular biology in both vascular access dysfunction and cardiovascular complications in these patients
    • Development of novel devices and intellectual property to improve the care of patients with vascular access dysfunction
    • Active participation in over 15 NIH, industry sponsored and investigator initiated clinical research projects and clinical trials in the areas of dialysis access dysfunction, cardiovascular morbidity, CKD progression and hemodialysis
  • Academic Community Partnerships:  We have developed strong links with community nephrologists for education, research and clinical care. This is a key aspect of the Arizona Kidney and Vascular Center
  • Academic-Industry Partnerships:  We interact with a number of industry partners to test out novel and innovative technologies.
  • Clinical Correlations:  We have strong relationships with the clinical nephrology enterprise at the University of Arizona (Dr. Roy-Chaudhury is the Division Director of Nephrology) and members of the laboratory and students will have ample opportunities for clinical shadowing and observation of procedures that include dialysis access creation, endovascular interventions, hemodialysis and kidney transplantation.
  • Research Funding:  This research program is funded through the NIH, Veterans Administration, National Science Foundation and Industry grants and contracts.

Raymond Runyan, PhD. (TGF-Beta, Cardiovascular System)

Program Affiliations:  Cellular & Molecular Medicine, Cellular Biology & Anatomy, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-2326, rrunyan@email.arizona.edu

Research Interests:  TGF-Beta, Cardiovascular System

  • In the heart, cells that form the valves are induced to develop by interaction between endothelial cells and adjacent muscle. As a result, cardiac endothelial cells transform into mesenchyme and become the constituents of the valves and walls of the heart. This process is known as an epithelial-mesenchymal transition or EMT. The objective of my research program is to understand the molecular mechanisms that mediate cell transformation in the heart.

  • Using a tissue culture assay, we showed that cardiac endothelia would only transform after stimulation by adjacent muscle. My laboratory has continued to examine the events which take place during this epithelial-mesenchymal cell transformation. Our studies focus upon three basic questions. 1) What is the nature of the signal produced by the muscle? 2) How do the target cells recognize the signal? 3) What events occur in the target cells in response to the stimulus? Answers to these questions will identify potential causes of congenital heart defects.

  • Work in the laboratory initially focused on the observation that the growth factor, Transforming Growth Factor Beta, is a component of the transformation process. As this growth factor is actually a member of a family of related molecules, we used RNase protection assays to show that two isoforms, TGFß2 and TGFß3, were found in the heart. Experiments using antisense DNA oligonucleotides demonstrated that TGFß3 is the critical component. More recently, our work shows that both isoforms are used in complementary roles.

  • Experiments show that this EMT in the heart is blocked by loss of several different classes of TGF-ß receptors, including Alk2, Alk5, TGFß Type II, TGFß Type III and Endoglin. As seen with the two different TGFß isoforms, each receptor component appears to mediate play a distinct role in the EMT process. Other experiments in this laboratory showed that EMT is sensitive to inhibitors of several classes of kinases, Gi proteins, and the phosphoinositide pathway. These pathways are being explored by cloning and targeted degradation of mRNAs of various components in order to track signals from the cell surface to the nucleus.

  • Another approach to the problem is towards the identification of regulatory genes expressed in response to the cardiac signal. Our focus is the immediate early genes which are likely to be transcriptional regulators of other genes required for valve formation. Our most recent efforts have focused on the genes Slug (Snail2), Meox-1, Runx2 and Paraxis. All of these genes appear to be critical transcription factors for the process of cell transformation.

  • A related research program in the lab is focused upon examining the relationship between events which take place during early valve development and the apparent cardio-teratogenicity of the environmental contaminant Trichloroethylene (TCE). In association with members of the Southwestern Environmental Health Sciences Center and the Superfund Program here at Arizona, we are trying to identify genes that are altered in developing hearts by exposure to this chemical.

Rick G. Schnellmann, PhD. (Identifying and Developing Drugs to Treat Injury and Disease)

Program Affiliations:  Pharmacology and Toxicology, Bio5 Institute, Medicine, Nephrology, Sarver Heart Center, Southwest Environmental Health Sciences Center, Physiological Sciences.

Website and Publications:  http://www.pharmacy.arizona.edu/directory/rick-schnellmann-phd, https://www.ncbi.nlm.nih.gov/pubmed/?term=schnellmann+rg

Contact Information: (520) 626-1657, schnell@pharmacy.arizona.edu 

Research Interests:  Research is focused on identifying and developing drugs to treat acute kidney injury, diabetic kidney disease, stroke, spinal cord injury and Parkinson’s disease.

Timothy W. Secomb, PhD. (Theoretical Studies of the Microcirculation)

Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications:  Physiology Faculty Homepage

Contact Information:  (520) 626-4513, secomb@u.arizona.edu

Research Interests:  Theoretical studies of the microcirculation

  • The microcirculation is a network of extremely small blood vessels that supplies oxygen and nutrients to all parts of our tissues. The focus of work in our research group is the use of mathematical and computational approaches to study blood flow and mass transport in the microcirculation. Working in collaboration with experimentalists, we aim to understand quantitatively the processes involved. The main areas of our work are:

  • Mechanics of blood flow in microvessels. We are examining the relationship between red blood cell mechanics and flow resistance in microvessels. Theoretical predictions agree well with observations in glass tubes, but resistance is higher living tissue. We have found that the major cause is the presence of a relatively thick macromolecular lining (endothelial surface layer) on the walls of microvessels.

  • Mass transport to tissue. We are simulating oxygen exchange between networks of microvessels and surrounding tissues in skeletal muscle and tumors. In skeletal muscle, we have shown how oxygen can be exchanged diffusively between arterioles and capillaries, and we are studying the determinants of maximal oxygen consumption. In tumors, we are studying the relationship between network structure and occurrence of local hypoxic (radiation-resistant) regions. Also, we are analyzing the delivery of chemotherapeutic drugs in tumor tissues.

  • Structural adaptation of microvascular networks. We are developing models for the stuctural responses of microvessels to functional demands. We have found that maintenance of a stable, functionally adequate distribution of vessel diameters can be achieved if each vessel responds to changes in wall shear stress, intravascular pressure and local metabolic conditions, and if mechanisms exist for information transfer upstream and downstream along flow pathways.

  • Regulation of blood flow: We are developing models for the active regulation of blood flow by changes in vascular tone, taking into account vascular responses to wall shear stress, pressure and local metabolic state, and including effects of conducted responses along vessel walls.

Scott J. Sherman, M.D., PhD. (Neuroscience: Parkinsons, PD, Basal Ganglia, Potassium Channels, Cell-based Therapy)

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Program Affiliations:  Neuroscience, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-2006, ssherman@u.arizona.edu

Research Interests:  Neuroscience: Parkinsons, PD, Basal Ganglia, Potassium Channels, Cell-based Therapy

  • Our basic research program explores cell-based and gene-based strategies for the treatment of movement disorders including Parkinson’s disease. We are exploring the possibility of using genetic alteration of voltage-gated potassium channels to modify specific pathways in the basal ganglia. Our current project utilizes primary neuronal culture coupled with patch-clamp electrophysiology to measure the electrical activity in isolated basal ganglia neurons. We have developed viral gene-transfer vectors utilizing cell type specific promoters to modify potassium channel expression in these neurons. We are presently studying the effect of these gene-transfer agents on the electrical activity in vitro.
    A second project seeks to develop a cell-based therapy for Parkinson’s disease. We have found that retinal pigment epithelial cells, normally found in the retina, can provide a neuroprotective effect on degenerating neurons that are involved in Parkinson’s disease. These cells could provide an easily transplantable source for a cell-based therapy.

Jil Tardiff, M.D., PhD. (Cardiovascular Disease: Heart Failure, Cellular and Molecular Medicine)

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Program Affiliations:  Department of Medicine, Cellular and Molecular Medicine, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-8001, jtardiff@email.arizona.edu

Research Interests:  Cardiovascular Disease: Heart Failure, Cellular and Molecular Medicine

Jennifer Teske, PhD. (Neuroscience/Obesity: Sleep, Feeding, Nutritional Sciences)

Program Affiliations:  Nutritional Sciences, Physiological Sciences

Website and Publications:

Contact Information:  (520) 621-3081, teskeja@email.arizona.edu

Research Interests:  Neuroscience/Obesity: Sleep, Feeding, Nutritional Sciences

  • Neurobiological basis of sleep, physical activity and feeding behavior as they relate to obesity and sleep disorders.

Todd Vanderah, PhD. (Neuroscience: Pharmacology of Acute and Chronic Models of Pain)

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Program Affiliations:  Pharmacology, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-7801, vanderah@email.arizona.edu

Research Interests:  Neuroscience: Pharmacology of acute and chronic models of pain; endogenous opioid systems; sensory neural systems; opioid tolerance; antinociceptive synergy between cannabinoids and opioids

  • Cholecystokinin and receptors as therapeutic targets

    • Recently we have demonstrated both behaviorally and by using microdialysis that the neuropeptide, cholecystokinin (CCK), promotes neuropathic pain by activating descending projection neurons that originate in a region of the brainstem known as the rostral ventromedial medulla (RVM). An increase in the level of release of CCK in the RVM is evident after nerve injury as well as after repeated administration of morphine. This enhanced activity of CCK mediated activation of RVM neurons maintains neuropathic pain, and is also important in the development of analgesic tolerance to spinal morphine after chronic morphine treatment. Thus, CCK antagonism may potentiate morphine antinociception under conditions of neuropathy or chronic morphine. Our collaboration with Dr. Victor Hruby in the Department of Chemistry aims to identify novel molecules that have bifunctional opioid agonist and CCK antagonist actions as prototypes for analgesics for chronic, neuropathic pain.

  • Sensory neuron function and GPCR

    • Sensory nerves that propagate painful signals are highly specialized nerves called nociceptors. The activation of these nociceptors includes noxious stimuli like heat, cold, pressure and chemicals. The excitability of these nociceptors is modulated by a number of G-protein coupled receptors (GPCR) both at their central termini in the spinal cord and in their peripheral nerve endings, which contain one or more specialized cation channels that are activated by specific noxious input. We are interested in how GPCR modulate the activity of these specialized cation channels, in particular the vanilloid receptors that mediate noxious heat, to regulate sensory thresholds in acute and chronic pain conditions

Ting Wang, PhD. (Cardiopulmonary Toxicity of Particulate Matter Air Pollution)

Program Affiliations:  Department of Medicine, Physiological Sciences

Website and Publications:  Department of Medicine Faculty Homepage 

Research Interests: Cardiopulmonary toxicity of particulate matter air pollution, Lung biology of acute lung injury and asthma, Lung genomics and genetics

Stephen H. Wright, PhD. (Membrane Transport, Energetics and Kinetics of Drug Transport)

Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

Contact Information:  (520) 626-4253, shwright@u.arizona.edu

Research Interests:  Membrane Transport, Energetics and Kinetics of Drug Transport

  • Membrane Transport; Energetics and Kinetics of Transport; Molecular Basis of Transporter-Substrate Interaction

  • Our work is focused on understanding the molecular and cellular physiology of organic electrolyte transport in the kidney. The kidney, particularly the proximal tubule, actively secretes a wide array of organic ions, largely derived from dietary or pharmaceutical sources. Many of these compounds are toxic and renal secretion of these xenobiotic compounds plays a critical role in protecting the body from these agents. However, this task also places the kidney in harm's way, and the development of nephrotoxicity is one consequence of the renal secretion of what are typically referred to as organic anions and organic cations.

  • We are currently studying the renal transport of organic anions and cations at several different levels of biological organization.

    • Molecular Level: We clone individual transport proteins for use in studies that gauge the effect of protein and substrate structure on the transport process.

    • Cellular Level: We use cultured cells (including primary renal cells, continuous renal cell lines, and generic cells lines for the expression of cloned transport proteins) in studies of the activity and regulation of transport activity.
      Tissue Level: We use isolated, intact renal proximal tubules, including single non-perfused and perfused tubules, to study the process of organic electrolyte secretion as it occurs in the native renal epithelium.

  • Our studies employ a wide array of methodologies, including

    • Molecular cloning, site-directed mutagenesis, construction of fusion proteins

    • Kinetic assessment of membrane transport in cultured cells, suspensions of isolated renal tubules and in single tubule segments using radiometric and real-time optical approaches

    • Computationally-based assessment of transporter and substrate structure and 3D distribution of cell type distribution along the renal nephron

Hua Xu, PhD. (Gastroenterology and Nutrition)

Program Affiliations:  Pediatrics, Physiological Sciences

Website and Publications:  Pediatrics Faculty Homepage 

Contact Information:  (520) 626-7050, hxu@email.arizona.edu

Research Interests:  Gastroenterology and Nutrition

  • Nutrient transporters--sodium-hydrogen exchangers (NHEs) and sodium-dependent phosphate cotransporters (NaPi) at functional and gene expression levels. My research focuses in mechanisms of sodium and phosphate transport, osteoporosis, male infertility and dry eye disease. These studies help to understand how these proteins response to the normal physiological changes and pathophysiological conditions.

Jason Yuan, M.D., PhD. (Asthma/Lung Disease)

Program Affiliations: Department of Medicine, Transnational Health Sciences, Physiological Sciences

Website and Publications:  NCBI MyBibliography, Physiology Faculty Page

Contact Information:  (520) 626-0787, jasonyuan@email.arizona.edu

Research Interests:  Asthma/Lung Disease: Pulmonary vascular pathophysiology and pathogenic mechanisms of pulmonary vascular disease

  • Pathogenic mechanisms of pulmonary arterial hypertension: Role of ion channels and membrane receptors
  • Cellular mechanisms of hypoxic pulmonary vasoconstriction and chronic hypoxia-induced pulmonary hypertension
  • Electrophysiology of ion channels and transporters in pulmonary vascular smooth muscle and endothelial cells
  • Calcium signaling and regulation: Role in the regulation of smooth muscle cell contraction, migration, and proliferation
  • Molecular mechanisms of smooth muscle and endothelial cell migration, proliferation and apoptosis.
  • Pulmonary vascular physiology, pathophysiology and pharmacology
  • Genetic variations of candidate genes in the development of lung vascular diseases and pulmonary embolism
  • Genetics, genomics, pharmacogenomics and pharmacogenetics
  • Stem cell biology and pathogenic role of adult stem cells in pulmonary vascular disease

Konrad Zinsmaier, PhD. (Neuroscience: Molecular Mechanisms, Neurotransmitter Exocytosis)

Program Affiliations:  Neuroscience, Bio5 Institute, Biochemistry and Molecular & Cellular Biology, Insect Science, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 626-1343, kez4@email.arizona.edu

Research Interests:  Neuroscience: Molecular Mechanisms, Neurotransmitter Exocytosis

  • Our research focuses on the molecular mechanisms that structurally and functionally facilitate excitation-dependent neurotransmitter exocytosis at synapses. A synapse signifies a specialized apposition or junction of two nerve cells, which has the particular property of transmitting information from one cell to the other. This information transfer is called synaptic transmission and is essential for neuronal information processing. Superimposed on growth-associated changes in synapses are adaptive modifications of synaptic efficacy that are accomplished by pre- and postsynaptic modulators conferring upon synapses plasticity, adaptability and individuality. However, many obligatory as well regulatory components of this molecular machinery remain to be identified. A long-term understanding of regulated release will probably only come from a systematic identification of all the protein components and interactions.

  • Over the past decades, we have investigated fundamental molecular mechanisms of presynaptic function and structure by undertaking a multidisciplinary approach, exploiting the neuromuscular junction (NMJ) of genetically modified animals. Specifically, research in my laboratory focuses on molecular mechanism that facilitate and/or control the highly regulated and fast secretion of neurotransmitter, which occurs within less than 200 micro-seconds (0.0002 seconds) after stimulation. We successfully employ the fruit fly Drosophila melanogaster as a genetic model system to illustrate the complex relations between basic mechanisms of neurotransmitter secretion and neurological and/or neurodegenerative disorders.