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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. 

Admitted Ph.D. and M.S. students are encouraged to contact faculty directly to inquire about arranging a laboratory rotation. Rotations and laboratory placements are at the disgression of faculty and should be determined based on discussion of research interests and the goals of both the laboratory and the graduate student.  

* indicates availability for 2021-2022 Ph.D. rotations and research placements

^ indicates availability for 2021-2022 M.S. research placements

Gene Alexander, Ph.D. (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, Ph.D. (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, Ph.D. (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).

Christopher Banek, Ph.D. (Hypertension; Neurogenic Inflammation; Renal Physiology)

Program Affiliations: Physiology, Physiological Sciences GIDP

Website and Publications: Physiology Faculty Page, PubMed CT Banek,

Contact Information: Location: AHSC 4130; Office: 520-621-6068; Email: cbanek@email.arizona.edu

Research Interests: Hypertension, Renal Disease, Sympathetic Nervous System, Peripheral Sensory Nerves, Neurogenic Inflammation

Throughout my career, I have focused on the physiological underpinnings of high blood pressure (i.e. hypertension). While hypertension is a multi-faceted disease, our research focuses primarily on neural (brain) and renal (kidney) contributions to the development and maintenance of hypertension. This was driven, in part, by recent reports that it is now possible to perform targeted nerve ablation of renal nerves in humans, which mitigates or even reverses drug-resistant hypertension. Unfortunately, the mechanisms mediating these beneficial effects are unclear. Thus, our studies aim to elucidate the detailed mechanisms of renal nerves in hypertension and related renal inflammation and disease to provide a translational platform for development and refinement of emerging therapies.

A longstanding research interest we are currently addressing is the role - and cause of - elevated renal nerve activity in hypertension. We employ a myriad of integrative experimental approaches to dissect the changes in sympathetic (efferent) and sensory (afferent) activity in tandem with changes in blood pressure and renal inflammation. These studies are currently funded by the NIH (R00HL141650).

In general, students should expect rigorous, hands-on training in small animal recovery surgery, telemetry-based physiological measurements, large data set processing and analysis, acute multiunit peripheral nerve recording, in vivo assessment of sympathetic tone and glomerular filtration rate, and many more.

Shaowen Bao, Ph.D. (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, Ph.D. (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.  

Scott Boitano, Ph.D. (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, Ph.D. (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.

Haijiang Cai, Ph.D. (Neuroscience: Neural Circuits of Animal Behaviors) * ^

Program Affiliations:  Neuroscience, Bio 5 Institute, Physiological Sciences

Website and Publications: 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." 

Qin Chen, Ph.D. (Pharmacogenomics) * ^

Program Affiliations:  Pharmacogenomics, Pharmacology & Toxicology, Applied Biosciences, Cancer Biology, Pharmacology, Genetics

Website and Publications: Pharmacy Faculty Page

Contact Information:  (520) 626-9126, qchen1@pharmacy.arizona.edu

Research Interests: 

  • Dr. Chen's laboratory has been focused on studying the molecular biology of oxidative stress. Ongoing research projects in her laboratory include 1) stress induced de novo protein synthesis for organ protection; 2) role of Nrf2 transcription factor in protection against cardiac injury; 3) function of Glucocorticoid Induced Leucine Zipper in the myocardium; 4) pharmacological agents that protect the heart from ischemic and chemotherapeutic injuries; and 5) biomarker discovery for predicting tissue injury due to oxidative stress.

Floyd “Ski” Chilton, (Gene-Diet Interactions: Inflammation and Health Disparities)

Program Affiliations:  Department of Nutrition, The Bio5 Institute, Physiological Sciences GIDP

Website and Publications: https://nutrition.cals.arizona.edu/, https://www.ncbi.nlm.nih.gov/pubmed/?term=Chilton+FH

Contact Information:  (520) 621-5327, fchilton@email.arizona.edu

Research Interests: 

Dr. Chilton is widely recognized in academia and industry for his work on nutrition in the context of variation in the human genome and has been a pioneer in the areas of personalized or precision nutrition and wellness. He currently is the Director of the Precision Nutrition and Wellness Initiative. Specifically, his lab examines how genetic and epigenetic variations interact with human diets (especially the modern Western diet) to drive inflammation and inflammatory disorders (including cardiovascular disease and cancer), as well as psychiatric/developmental disorders (ADHD, autism spectrum disorder, and depression). These precision-, individualized- and population-based research approaches provide a wide range of opportunities to benefit human health and enhance wellness and disease prevention throughout the life span. Dr. Chilton currently has research grants, on-going studies, and collaborations in four major areas including: 1) Gene-diet interactions that drive racial/ethnic disparities; 2) Lifestyles and related molecular mechanisms that augment disease prevention and enhance wellness; and 3) Metabolomic and lipidomic analysis for the identification of molecular networks and related circulating and tissue biomarkers associated with human disease and aging.

Jared Churko, Ph.D. (Cardiovascular disease and stem cell biology) * ^

Program Affiliations: Cellular and Molecular Medicine, Physiological Sciences, Director, iPS Cell Core

Website and Publications: Cellular & Molecular Medicine Faculty

Contact Information: Office: (520) 626-2347, Lab: (520) 626-3942, jchurko@email.arizona.edu

Research Interests: His lab is located within the Sarver Heart Center, where he studies heart development and cardiovascular disease. Specifically, his lab combines systems biology, stem cell biology, cardiac biology, genetic engineering, and bioinformatics to understand the mechanisms leading to heart disease.

 

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.

Brett Colson, Ph.D. (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, Ph.D. (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, Ph.D. (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.

Zhiyu Dai, Ph.D. (Pulmonary Vascular Biology) *

Program Affiliations: Department of Internal Medicine, Clinical Translational Sciences, Physiological Sciences GIDP

 

Website and Publications: lab website, publications

 

Contact Information: zhiyudai@email.arizona.edu

Research Interests: My laboratory focuses on studying signaling pathways and molecular mechanism of pulmonary vascular diseases including pulmonary arterial hypertension. The lab employs the state-of-the art technologies including genetic lineage tracing, genetic depletion, genetic reporter, and CRISPR-mediated genomic editing, AAV, single cell RNA-sequencing as well as patient samples to study the molecular mechanisms of vascular disorder including pulmonary arterial hypertension and identify novel therapeutics for these devastating diseases.

Thomas P. Davis, Ph.D. (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, Ph.D. (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

Frank Duca, Ph.D. (Diabetes, Obesity, Microbiome, Gut-Brain Axis)

Affiliations: School of Animal & Comparative Biomedical Sciences, Microbiology, Physiolgical Sciences GIDP

Website and Publications: Faculty Homepage

Contact Information: 520-626-9532, faduca@email.arizona.edu

Research Interests:

An overwhelming obesogenic environment, the backdrop to a globally-expanding western lifestyle, has led to a ‘diabesity’ pandemic that represents a costly and urgent global health crisis.  The success of gastric bypass surgery and gut-derived diabetes/obesity treatments highlight the major role of the gastrointestinal (GI) tract in metabolic diseases.  My research aims to better understand the complex intestinal signaling mechanisms involved in the regulation of energy and glucose homeostasis in physiological and pathophysiological states.  My work to date has focused on elucidating how nutrients are sensed by the gut, and how changes in these mechanisms lead to a reduction in food intake and/or a reduction in endogenous hepatic glucose production via a gut-brain neuronal axis.  More specifically, my work focused on alterations in intestinal detection of fats and carbohydrates and paracrine gut peptide signaling (CCK and GLP-1) during high-fat feeding, the influence of the gut microbiota on these pathways, and how these contribute to the development of obesity and diabetes.  As such, I plan to continue to decipher this complex interaction between gut-sensing mechanisms and the gut microbiota, as a better understanding of these pathways are crucial for the development of successful, gut-targeted therapeutic options in the treatment of metabolic diseases.

Given the rapid rise of obesity/diabetes in only several generations, obesity cannot be attributed to genomic alterations, but more likely results from a complex set of interactions between genetic risk factors and environmental changes. Importantly, studies suggest the development of adult phenotypes (obesity and diabetes) results from early, transient environmental interactions, coined ‘early life programming,’ which has been partly attributed to epigenetic changes. Gut microbiota development is also crucial during this time, and differing modes of development (i.e. maternal microbiota, type of delivery, breastfeeding vs. formula feeding, etc.) can lead to later metabolic dysfunctions. Therefore, using animals models prone to the development of obesity and/or diabetes from polygenetic inheritance and transgenerational, epigenetic, changes in gene activity, I am studying how varying environmental factors (diet, housing, exercise, pre/post-natal environment, etc.) result in differential effects on the gut microbiota, intestinal nutrient sensing, and whole body energy and glucose homeostasis. A better understanding of how early changes in the gut microbiota can impact the development of metabolic regulation, and vice versa, is vital for developing successful strategies to curb diabetes and obesity.

Erika Eggers, Ph.D. (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, Ph.D. (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, Ph.D. (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, Ph.D. (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.

Andrew Fuglevand, Ph.D. (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. (Endocrinology, Bone Biology, Cancer Biology, Nutrition, Pharmacology, Whole Systems Physiology) ^

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 

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, Ph.D. (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

Ravi Goyal, M.D. Ph.D. (Animal & Biomedical Sciences)

Program Affiliations:  Animal & Biomedical Sciences - Research, Bio5 Institute, Physiological Sciences

Website and Publications: BIO5 Profile

Contact Information:  (520) 626-5573, goyalr@email.arizona.edu

Research Interests: 

  • My major interests include epigenetic regulation of angiogenesis and vascular development. Angiogenesis plays a critical role in both physiological and pathological conditions. I am investigating various mechanisms involved in angiogenesis with development and aging of organisms and its role in organ development as well as cancers. My other area of investigation is involving adipose-derived stem cells and their usefulness in treating osteoarthritis, diabetes, stroke, traumatic brain injury, myocardial infarction, and spinal cord injuries following road traffic accidents. 

Michael Grandner, Ph.D. (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, Ph.D. (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, Ph.D. (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, Ph.D. (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 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 dysfunction, chest compression - only BLS CPR, blood flow during CPR, pharmacological and mechanical adjuncts for CPR

Pawel Kiela, Ph.D. (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, Ph.D. (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, Ph.D., Program Chair (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

  • Gut microbiome and cardiac remodeling. Our lab has a long-standing interest in the ability of environmental factors, like diet, to impact cardiac disease. Advances in sequencing and bioinformatic technologies have allowed unprecedented characterization of the gut microbiome. We have discovered novel modifiers of the gut microbiome that protect against cardiac injury following ischemia.
  • Sarcomere dynamics and crossbridge kinetics. Contractile perturbations downstream of Ca2+ binding to troponin C, the so-called sarcomere-controlled mechanisms, represent the earliest indicators of cardiovascular disease. We can now state the dynamics of cardiac contraction and relaxation during CVD are governed by downstream mechanisms, particularly the kinetics and energetics of the cross-bridge cycle. Our lab focuses on the contractile properties of the cardiomyocyte and how this changes with CVD.
  • Sex dimorphisms in cardiac adaptation. Sex/gender differences exist in human cardiac disease resulting from many disease etoilogies including hypertension, myocardial infarction, and cardiomyopathies (HCM). We have adapted a novel model of menopause to uniquely address HCM and CVD, in general. As part of these studies, we became interested in a specific, energy-dependent signaling pathway, adenosine monophosphate-activated kinase (AMPK) demonstrating that AMPK regulates contractile function and energy cost of contraction.
  • Predicting and mitigating postoperative surgical outcomes. (1) Cognitive impairment resulting from cardiac bypass surgery. Although treatment strategies for cardiovascular disease (CVD) are improving, coronary revascularization remains one of the most common interventional procedures. Following CABG surgery, cognitive impairment is reported in 50-75% of patients at discharge, 20-50% at 6 weeks and up to 40% at five years. Exciting new preclinical data from our group shows that systemic administration of Ang-(1-7) attenuates and even reverses CHF-induced cognitive impairment in mice. Our work has resulted in 2 patent applications (UA13-120 UA 14-167) and an IND application for the for Ang-(1-7) as a protective agent against CABG-induced cognitive impairment. (2) Predicting and mitigating postoperative new onset atrial fibrillation and cardiac remodeling. We have discovered a potential use for Human Amniotic Membranes for the prevention of postoperative (bypass surgery) outcomes. In human subjects, membrane placement during CABG preventative new onset postoperative atrial fibrillation. In mice, we prevented wall thinning post-myocardial infarction.

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 – Quantitative Proteomics Laboratory, University of Arizona, College of Medicine, Department of Medicine, Endocrinology Division; Center for Disparities in Diabetes, Obesity & Metabolism; Physiological Sciences GIDP

Website and Publications: Langlais Lab, Quantitative Proteomics Laboratory, 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, Ph.D. (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, Ph.D. (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, Ph.D. (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, Ph.D. (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., Ph.D. (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.

Patrick Mantyh, Ph.D., 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

Juanita Merchant,M.D., Ph.D. (Gastroenterology, Hepatology and Cancer Biology) ^

Program Affiliations:  Medicine, Chief, Division of Gastroenterology, Physiological Sciences GIDP

Website and Publications: Dr. Merchant's Banner Health profile, UA Cancer Center profile, Publications

Contact Information:  (520) 626-6453 , jmerchant@email.arizona.edu

Research Interests:  Gastroenterology

Sonic Hedgehog and Gastric Cancer. Studies from my lab focus on the role of bacterial colonization and the development of type B chronic atrophic gastritis in a mouse model. Chronic atrophic gastritis is a precursor lesion in the development of intestinal metaplasia and gastric cancer. We found that the gastrin-deficient mice, which are hypochlorhydric, develop antral gastric tumors within 9 –12 months of age. The tumors appear to be dependent on the microflora. Gastric atrophy exemplified by loss of the acid-secreting parietal cell precedes tumor development as observed in human subjects. We found that Helicobacter infection coincides with acute secretion of Shh from the parietal cells then eventually reduced Shh expression prior to parietal cell atrophy. Apparently pro-inflammatory cytokines, e.g., IL-1b, are sufficient to suppress parietal cell acid secretion and Shh gene expression (Waghray, M et al, Gastroenterology 2010). We showed that gastric acid stimulates Shh gene expression through calcium-mediated PKC activation (El-Zataari, M, Gastroenterology, 2010). During infection by Helicobacter, Gli1+immune cells are recruited to the stomach and over time change their phenotype from pro-inflammatory to immune-suppressive by becoming myeloid derived suppressor cells (MDSCs). The switch to an immune-suppressive phenotype triggers the epithelium to become metaplastic (El-Zaatari et al., PloS One, 2013; Ding L et al. J Clinical Invest., 2016; Merchant, JL and Ding L, CMGH 2017).

Regulation of GI Growth and Homeostasis by ZBP-89. We are also actively investigating the role of a zinc finger transcription factor in the regulation of cell growth. The factor is named ZBP-89 and was expression cloned in my lab using a DNA element from the gastrin promoter that mediates EGF regulation. The conditional knock-out of this transcription factor reduces serotonin gene expression and circulating serotonin levels. Current studies are focused on how ZBP-89 regulates the serotonin-producing enterochromaffin cells. Studies completed last year that are under review demonstrate that a conditional knock-out of the ZBP-89 locus in mice reduces expression of tryptophan hydroxylase 1, the rate-limiting enzyme in serotonin biosynthesis. As a result, mice missing ZBP-89 in the gastrointestinal tract are unable to mount an effective mucosal defense against invading pathogens such as Salmonella typhimurium(Essien et al., Gastroenterology, 2013). Our studies have important implications with respect to understanding the role of serotonin in the innate immune response. In parallel studies, we find that ZBP-89 plays a role through its ability to interact with bcatenin. Deletion ofZBP-89 on an APC mutant background suppresses polyp formation (Essien B et al,Cancer Res, 2016). We have now demonstrated that ZBP-89 is required for butyrate-induced senescence (Ocadiz et al., Oncotarget, 2017).

Mechanism of Gastrinoma Development. We have developed a mouse model of gastrinoma by crossing the villin-Cre mouse to the floxed menin mouse. Gastrinomas are the most malignant tumor that develops as a result of menin deletion. Menin is the protein product of the MEN I (multiple endocrine neoplasia) locus. Human subjects with MENIlocus mutations develop tumors in neuroendocrine cells of the duodenum that secrete gastrin. We have found that mice conditionally heterozygous for the menin allele develop hypergastrinemiaand G cell hyperplasia but not gastrinomas (tumors). We are now able to generate type II gastric carcinoids when Men1 is deleted and placed on a Sst-/-genetic background. The development of ECL cell hyperplasia is accelerated in the presence of acid suppression with a proton pump inhibitor (Sundaresan S, Gut, 2016). Moreover, gastrin-expressing cells appear in the lamina propria of the duodenum, which we hypothesize are the precursors of duodenal gastrinomas. Surprisingly, these gastrin+ cells are enteric glial cells suggesting that they express gastrin under conditions that decrease the nuclear expression of menin through a PKA-dependent pathway (Sundaresan S, Gastroenterology 2017).

 

Klearchos Papas, Ph.D. (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.

Paulo W. Pires, Ph.D. (Cardiovascular Disease, Alzheimer’s Disease, Neurovascular Physiology, Cell Physiology) * ^

Program Affiliations: Physiology, Physiological Sciences

Website and Publications: Faculty website, Faculty Publications

Contact Information: (520) 626-8632, ppires@email.arizona.edu, AHSC Room 4224

Research Interests:

Research in the Pires lab focuses on understanding the regulation of blood flow to the brain under normal and disease states. We are particularly interested in the communication between neurons, astrocytes (a type of glial cells) and endothelial cells that control blood flow to discrete regions of the cerebral cortex, a process called neurovascular coupling. Disease states, such as Alzheimer’s disease and hypertension, are known to alter neurovascular coupling in the brain, leading to improper blood flow delivery to neurons and, consequently, loss of brain cells and cognitive decline. Our lab studies particular receptors in endothelial cells that have their function diminished by Alzheimer’s disease and hypertension, and possible therapies that can improve their function. 

Another interest of the lab is to investigate how chronic disease states alter intracellular signaling pathways that regulate influx and release of calcium (Ca2+) in vascular cells. Ca2+ is an important second messenger within vascular cells with opposing effects on the cell types that form the blood vessel wall: in smooth muscle cells, increases in intracellular Ca2+ are linked to contractility, or the ability of the cell to contract and, thus, reduce the diameter of the blood vessel; on the other hand, increases in intracellular Ca2+ in endothelial cells are connected to pathways that will culminate in vasodilation and increases in blood vessel diameter.  Many of these different pathways are known to be altered by chronic diseases, and projects in the laboratory focus on studying how intracellular Ca2+ handling is altered in disease conditions.

Keywords: neurovascular coupling, cerebral blood flow regulation, cardiovascular diseases, neurological diseases, vascular function.

Olga Rafikova, M.D., Ph.D. (Pulmonary Hypertenstion, Gender Studies) * ^

Program Affiliations: Department of Medicine, Physiological Sciences GIDP

Website and Publications: https://cddom.uahs.arizona.edu/profile/olga-rafikova-md-phd, College of Medicine Faculty Page, Research News, NIH Grant News, Publications,

Contact Information: (520) 626-0313, orafikova@deptofmed.arizona.edu

Research Interests:

  • Redox biology and protein post-translational modifications, which compromise the function of critical cell enzymes and lead to the development or exacerbation of vascular disease.
  • The manifestation of sexual dimorphism in pulmonary hypertension. In particular, Dr. Rafikova investigates the gender difference in the way cells respond to stress and damage.
  • Gender-specific signaling in the development of “male” and “female” phenotypes of pulmonary hypertension.
  • Role of mitochondrial dysfunction in pulmonary hypertension
  • Development and testing of gender-specific therapeutics
  • In her work, Dr. Rafikova utilizes an integrative manner of research and addresses the problem on multiple levels including protein level, cell signaling, animal models of disease, and finally studies in humans. Such an approach allows her to understand, in depth, the particular molecular mechanisms contributing to the disease and their pathophysiological consequences.

Benjamin Renquist, Ph.D. (Fatty Liver, Obesity, Diabetes, and Hypertension: The Role of the Peripheral Nervous System)

Program Affiliations: Animal Sciences, Physiological Sciences

Website and Publications:  ACBS Faculty Homepage 

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

Research Interests:

Fatty Liver, Obesity, Diabetes, and Hypertension: The Role of the Peripheral Nervous System

 

Research in the Renquist Lab is focused on understanding how the liver communicates nutritional status to the rest of the body to affect glucose homeostasis, blood pressure, energy intake, and energy expenditure.  Additional projects are focused on improving the efficacy of cancer therapeutics and understanding the regulation of food intake by mesenteric blood flow.

Patrick Ronaldson, Ph.D. (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.

Rick G. Schnellmann, Ph.D. (Identifying and Developing Drugs to Treat Injury and Disease; Renal Physiology & Drug Discovery)

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.(renal physiology, renal pharmacology, drug discovery, mitochondrial biology, & molecular-whole animal)

Timothy W. Secomb, Ph.D. (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.

Richard J. Simpson, Ph.D., FACSM (Exercise Immunology; Psychoneuroimmunology; Transplantation Immunology; Space Life Sciences)

Program Affiliations: Department of Nutritional Sciences; Department of Pediatrics, Department of Immunobiology; Arizona Cancer Center (Therapeutic Development Program); Steele Children's Research Center; Collaboratory for Metabolic Disease Prevention and Treatment; Physiological Sciences GIDP; Cancer Biology GIDP

 

Website and Publications: NCBI Bibliography; Faculty Homepage

 

Contact Information: (520) 621-4108,  rjsimpson@email.arizona.edu 

 

Research Interests:

Dr. Simpson is an Associate Professor in the department of Nutritional Sciences (College of Agriculture and Life Sciences) at the University of Arizona and holds joint appointments in Pediatrics (College of Medicine) and Immunobiology (College of Medicine). He is also part of the mentoring team for the Physiological Sciences and Cancer Biology Graduate Interdisciplinary Programs, which recruit students who are continuing in education.  His research interests are concerned with the effects of aging, stress and exercise on the immune system, and the role of adrenergic receptor signaling on immune cell redistribution and activation. Major focus areas include understanding:

 

(1) how exercise and other behavioral interventions can offset age-related decrements in the normal functioning of the immune system (immunosenescence)

(2) how adrenergic receptor signaling can be used to improve cellular products for hematopoietic stem cell transplantation and immunotherapy, 

(3) the interplay between the immune and neuroendocrine system during high level human performance and extreme isolation (i.e. space travel), (4) how persistent virus infections such as cytomegalovirus (CMV) can alter the phenotype and function of T-cells and NK-cells to protect the host from certain hematological malignancies, and 

(5) how physical exercise can improve immunological outcomes and reduce graft-versus-host disease in recipients of allogeneic hematopoietic stem cell transplantation (allo-HCT). 

 

Dr. Simpson is a Fellow of the American College of Sports Medicine and an honorary board member of the International Society of Exercise Immunology (ISEI). He is an Associate Editor of Exercise Immunology Review and sits on the editorial board of Brain, Behavior and Immunity. His current research is supported by NASA, the NIH (National Cancer Institute) and industry. 

Ann Skulas-Ray, Ph.D. (Nutritional Strategies for Reducing Chronic Inflammation and Cardiovascular Disease Risk)

Program Affiliations:  Nutritional Sciences, Physiological Sciences

Website and Publications:  https://nutrition.cals.arizona.edu/people/ann-skulas-ray-phd

Contact Information:  (520) 621-2084, skulasray@email.arizona.edu

Research Interests:  My research focuses on exploring and refining the following questions: How can we improve nutritional strategies for reducing chronic inflammation and cardiovascular disease risk? And how can we best evaluate the efficacy of these potential therapies in human participants? Developing clinical research models that can more effectively study these dietary and supplement interventions is the overarching theme of my projects.

Research Areas

  • Clinical studies of omega-3 fatty acids and plant-derived bioactives on markers of metabolism, oxidative stress, central blood pressure, and indices of arterial stiffness using the SphygmoCor System
  • Clinical studies of inflammatory and oxidative stress responses using a human model of induced inflammation (intravenous endotoxin challenge)

Research Overview – Human Model of Induced Inflammation

Translating pre-clinical research findings into evidence-based recommendations that optimize human health has been a long standing challenge in nutrition research—largely due to the absence of consistent clinical trial evidence. My research attempts to overcome the barriers of pre-clinical to clinical translation by utilizing a human low dose (0.6 ng/kg) intravenous endotoxin (lipopolysaccharide, LPS) challenge model. This model safely produces an acute, controlled inflammatory response in healthy participants, with consistently-timed increases in pro-inflammatory cytokines (IL-6 and TNF-α) and the acute phase reactant C-reactive protein (CRP), which peak at 2-3 hrs. and 24 hrs. post-injection, respectively. This type of model allows for a clinical research design in which omega-3 concentrations can be increased prior to the inflammatory insult and thereby modulate resulting signaling pathway cascades. We have also begun to identify inter-individual factors that may modulate the inflammatory response, including subjective sleep quality and gender, to further improve our sensitivity in detecting the effects of nutritional interventions. In our preliminary work, dietary doses of omega-3 fatty acids demonstrated the potential to reduce the inflammatory and oxidative stress response to this LPS challenge. My current and planned research projects build on this finding.

Ashley J Snider, Ph.D. (Diet, Sphingolipids, Intestinal Inflammation and Cancer) * ^

Program Affiliations: Nutritional Sciences, Physiological Sciences

 

Website and Publications: https://nutrition.cals.arizona.edu/person/ashley-j-snider-phd

 

Contact Information: (520) 621-8093, ashleysnider@arizona.edu

 

Research Interests: 

The long-term research goals of my lab are to define the roles of lipid metabolic pathways centered on bioactive sphingolipids in intestinal biology and pathobiology and determine the mechanisms involved. 

Sphingolipids, long thought to be only structural components of cell membranes, have emerged over the last two decades as bioactive lipids with distinct and important biological functions. Fatty acids are incorporated into ceramide, the central lipid in sphingolipid metabolism, via two enzymatic reactions: through de novo synthesis initiated by serine palmitoyl transferase (SPT) into the sphingoid backbone of sphingolipids, and via incorporation by ceramide synthases (CerS) into the fatty-acyl chain of ceramide. Ceramide in turn serves as a metabolic hub for the synthesis of several classes of sphingolipids, including sphingomyelin, ceramide 1-phosphate (C1P), glycosphingolipids and sphingosine-1-phosphate (S1P). We have previously demonstrated the importance of serval sphingolipids and their metabolic enzymes as key regulators in inflammatory bowel disease, as well as colon cancer and colitis-associated colon cancer. In addition, we have demonstrated that specific dietary FAs increase inflammation in the intestinal epithelium in cells and in vivo

Our current research focus builds on this foundation.   

The three main projects in my lab examine:

  1. Effects of dietary fatty acids on sphingolipid metabolism in ER stress and inflammation.  
  2. Roles of dietary fatty acids and sphingolipids in animal models of inflammation and colitis-associated   cancer.
  3. Roles for sphingolipids and their metabolizing enzymes in intestinal biology and pathobiology. 

In our pursuits, we utilize cell lines, intestinal organoids (murine and human), mouse models, patient derived xenografts, and biobanked samples from patients with IBD and colorectal cancer to determine the effects of high fat diets and dietary fatty acids on sphingolipid metabolism and intestinal pathobiology.  Moreover, we utilize unbiased “Omics” approaches in our research efforts, specifically lipidomics, proteomics and phospho-proteomics, in order to define novel mechanisms, interventions, therapeutic targets and biomarkers for intestinal pathobiologies.

Nicholas J Strausfeld, Ph.D. (Neuroscience, Visual Perception, Allocentric Memory, and Action Selection)

Program Affiliations: Neuroscience, Director of Center for Insect Science, Ecology and Evolutionary Biology, Entomology/Insect Science, Physiological Sciences

Website and Publications: Neuroscience Profile, Publications

Contact information: (520) 621-8382  flybrain@email.arizona.edu

Interests:

Research

Brain organization in invertebrates - brain evolution - identification of arthropod-vertebrate brain homologies - neuropalaeontology - vision research - animal behavior.

Teaching

Teaching courses in neurobiology, emphasizing the value of cross-taxonomic comparisons, the avoidance of narrow-minded "model-systems" research, and the crucial integration of evolutionary considerations with respect to every facet of the neurosciences.

Jennifer H. Stern, Ph.D. (Diabetes, Obesity and Aging) * ^

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

Website and Publications: Faculty website

Contact Information: (520) 626-5842, jhstern@deptofmed.arizona.edu, UAHS 6112, Lab – UAHS 5130

Research Interests: Obesity/Diabetes: Glucogon Signaling, Aging and Exercise; Obesity-Associated Cancer

Dr. Stern’s research aims to understand the role of glucoregulatory hormone signaling in the pathogenesis of obesity, type II diabetes mellitus, and aging.  The Stern lab investigates mechanisms in mouse and cell culture models and translates these findings through our collaborations with clinicians with the goal of applying our findings to improve the prevention and treatment of diabetes and age-related metabolic disorders.

Glucagon Signaling in Obesity and Type II Diabetes:

Insulin resistance and elevated insulin are key to the metabolic disturbances in type II diabetes mellitus (T2DM). Yet, elevated glucagon, common to diabetes, may be equally important in the metabolic abnormalities in T2DM. Dr. Stern has shown that nutritional state differentially affects glucagon secretion in obesity.  In turn, the glucagon:insulin ratio is dysregulated in obesity. Current Stern lab research aims to understand the metabolic consequences of a dysregulated glucagon response to fasting and re-feeding.

Glucagon Signaling and Aging:

More than 25% of the U.S. population greater than 65 years old has Type II diabetes mellitus, representing the highest prevalence of diabetes of any age group. Most research aimed at understanding the consequences of obesity in aging have focused on insulin and downstream signaling cascades, overlooking a potential role for glucagon. Given that many prominent diabetes treatments target glucagon or glucagon signaling pathways, it is essential to understand the role of glucagon in aging. Stern lab research examines 1) the tissue specific effects of glucagon signaling, 2) the role of glucagon signaling in obesity-accelerated aging, and 3) the role of glucagon signaling in healthspan extension promoted by calorie restriction. This work will close a significant gap in our understanding of how glucagon alters aging, while allowing us to assess the potential risks associated with inhibition of glucagon signaling. 

Obesity/Type II Diabetes Cancer Development:

Obesity is the leading cause of multiple solid cancers. In particular, the risk of developing hepatocellular carcinoma (HCC) is more than doubled in obese people with Type II diabetes. To identify new drug targets to treat HCC, the Stern lab applies a chemical model of accelerated hepatocellular carcinoma.  We use this to examine the effects of hepatic lipid accumulation and dysregulated glucoregulatory hormone signaling on HCC development and progression.

Other Stern Lab Research Foci:

  • Sleep disturbance and metabolic dysfunction
  • Obesity related cancer development and progression 

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

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, Ph.D. (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.

Ting Wang, Ph.D. (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

Hua Xu, Ph.D. (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.

Ningning Zhao, Ph.D. (Molecular Nutrition) * ^

Program Affiliations:  Nutritional Sciences, Physiological Sciences

Website and Publications:  Faculty WebsitePublications

Contact Information:  (520) 621-9744, zhaonn@email.arizona.edu

Research Interests:

  • The work in our Lab is focused on advancing molecular mechanisms for the function and regulation of plasma membrane metal transporters. These transporters play fundamental roles in regulating cellular metabolism and cellular function. Mutations and malfunctioning of these transporters are directly pertinent to the initiation and the progression of an increasing number of human diseases, including iron deficiency, hemochromatosis, cancer, and childhood on-set neurodegeneration. We identify and characterize the genes and factors that are involved in determining the structure and function of these metal transporters. We also examine the intracellular trafficking and degradation of these proteins.
  • In our research, we combine cell-line and mouse models, and employ a variety of biochemical and molecular biology techniques. We also utilize the cutting-edge genome engineering technologies, including Adeno-Associated Virus-mediated genomic modification and CRISPR/Cas9-mediated genome editing. We hope that our research will advance the understanding of disease mechanisms, identify therapeutic target genes, and improve the life quality of patients.

 

Chi Zhou, Ph.D. (Reproduction, Vascular/Endothelial Physiology, Fetal Programming)

Program Affiliations:  Animal & Biomedical Sciences – Research, Physiological Sciences

Website and Publications:

Lab website: https://chizhou.lab.arizona.edu/

UA profiles: https://profiles.arizona.edu/person/chizhou

 

Contact Information:  Phone: 520-621-2457, Email: chizhou@email.arizona.edu

Research Interests:  My research aims to reveal the mechanisms controlling the complicated pregnancy-induced fetal sex-specific endothelial dysfunction in female and male fetal endothelial cells. Specifically, I am interested in 1) studying the sexual dimorphisms of complicated pregnancies-associated fetal endothelial dysfunction, 2) exploring the role of microRNAs in complicated pregnancies-induced fetal endothelial dysfunction, and 3) examining the effect of maternal obesity on fetal endothelial function and future cardiovascular risks of the offspring.

Konrad Zinsmaier, Ph.D. (Neuroscience: Molecular Mechanisms, Neurotransmitter Exocytosis) ^

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

Website and Publications: Neuroscience Faculty Page, Automated Analysis of Mitochondrial x-y-t Tracks, 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.