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Affiliated Faculty

The following faculty members are faculty who may serve on dissertation and thesis committees.  Please click on the name of each member to learn more about them.  

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

Program Affiliations: Physiology, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page

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

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

  • Role of gap junctions in vascular function
  • Contribution of gap junctions to growth control, vascular remodeling, and response to injury and disease
  • Mechanisms underlying acute regulation of gap junction function by second messenger signaling cascades
  • Biophysics of gap junction channels
  • Gap Junctions in vascular smooth muscle: Growth Control
  • Functional consequences of connexin interactions in blood vessels

Zoe Cohen, PhD. (Platelets, Immunobiology)

Program Affiliations:   Physiology, Sarver Heart Center, Physiological Sciences

Website and Publications:  Sarver Heart Center Profile

Contact Information:  (520) 621-5485, zcohen@email.arizona.edu

Research Interests:  Platelets, Immunobiology

Lucinda L. Rankin, PhD. (Physiology/Teaching Workshop)

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Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-3104, crankin@u.arizona.edu

Research Interests:  Physiology/Teaching Workshop

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

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

Website and Publications: 

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

Research Interests:  Stroke: Community and Systems Health Sciences

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

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

Program Affiliations:  Neuroscience, Bio5 Institute, Physiological Sciences

 

Website and Publications: 

 

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

 

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

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

Claudia Stanescu, PhD. (Physiology/Director TA's)

Program Affiliations:  Physiology, Physiological Sciences

Website and Publications: 

Contact Information:  (520) 621-2795, stanescu@email.arizona.edu

Research Interests:  Physiology/Director TA's

John A. Szivek, PhD. (Orthopaedic Surgery)

Program Affiliations:  Orthopaedic Surgery, Bio5 Institute, Physiological Sciences

Website and Publications:  Orthopaedic Faculty Homepage

Contact Information:  (520) 626-6094, szivek@email.arizona.edu

Research Interests:  Orthopaedic Surgery

  • John Szivek, PhD, used to employ a risky process to study new cartilage tissue.  His procedure for studying and growing new cartilage tissue involved removing a small piece of cartilage from the joint to be repaired, extracting cells in the lab, and growing the new tissue on a scaffold, which then was implanted into the joint. Due to the complexity of hyaline cartilage tissue, comprised of several layers of cells that do not divide or reproduce readily, the process was painstakingly slow and unpredictable, and new tissue often did not form at all.
  • Four years ago, however, Dr. Szivek’s team discovered that they could grow cartilage from differentiated (converted) adult stem cells extracted from fat tissue. These cells offer numerous advantages over cartilage cells. Not only can they be changed readily into a range of other cell types, but because of their long, spindly shape – unlike the rounded shapes of cartilage cells – researchers easily can judge whether they are aligning into the highly structured form they must be in to build hyaline cartilage. These cells are abundant and easier to obtain than cartilage cells and, since they are derived from a patient’s own fat tissue, they ensure there is no risk for rejection once they are introduced into the patient.
  • While earlier work in the Szivek lab concentrated on repairing damage to a relatively small area of a joint, the ability to grow cartilage more quickly and easily will make it possible to resurface a larger area of a damaged joint and, as such, will offer an alternative to total joint replacement.
  • Dr. Szivek’s earlier work involved implanting a small, rounded scaffold engineered by mimicking perfectly the normal structure of the injured bone in the joint. Before it is implanted, cartilage tissue growth on the surface is started in the lab. On the inside, these scaffolds are porous with a bone-like structure, allowing new bone growth to anchor them in place. Another novel aspect of Dr. Szivek’s scaffold system is that it is equipped with tiny sensors and a radio transmitter to monitor the patients’ activities and warn them if they risk injury to their new cartilage during exercise.
  • With his newest approach to growing cartilage, the scaffold covers one entire surface of the joint and makes it possible to grow cartilage over this much larger surface area. This scaffold also accommodates sensors and a transmitter that measure the loads passing through the replaced surface and notify the patient when the joint is overloaded.

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

Program Affiliations: Pharmacology, Bio5 Institute, Physiological Sciences

Website and Publications:

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

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

  • Cholecystokinin and receptors as therapeutic targets
    • Recently we have demonstrated both behaviorally and by using microdialysis that the neuropeptide, cholecystokinin (CCK), promotes neuropathic pain by activating descending projection neurons that originate in a region of the brainstem known as the rostral ventromedial medulla (RVM). An increase in the level of release of CCK in the RVM is evident after nerve injury as well as after repeated administration of morphine. This enhanced activity of CCK mediated activation of RVM neurons maintains neuropathic pain, and is also important in the development of analgesic tolerance to spinal morphine after chronic morphine treatment. Thus, CCK antagonism may potentiate morphine antinociception under conditions of neuropathy or chronic morphine. Our collaboration with Dr. Victor Hruby in the Department of Chemistry aims to identify novel molecules that have bifunctional opioid agonist and CCK antagonist actions as prototypes for analgesics for chronic, neuropathic pain.
  • Sensory neuron function and GPCR
    • Sensory nerves that propagate painful signals are highly specialized nerves called nociceptors. The activation of these nociceptors includes noxious stimuli like heat, cold, pressure and chemicals. The excitability of these nociceptors is modulated by a number of G-protein coupled receptors (GPCR) both at their central termini in the spinal cord and in their peripheral nerve endings, which contain one or more specialized cation channels that are activated by specific noxious input. We are interested in how GPCR modulate the activity of these specialized cation channels, in particular the vanilloid receptors that mediate noxious heat, to regulate sensory thresholds in acute and chronic pain conditions

Stephen Wright, Ph.D. (Membrane Transport, Engergetics and Kinetics of Drug Transport)

Program Affiliations:  Physiology, Bio5 Institute, Physiological Sciences

Website and Publications: Physiology Faculty Page(link is external)

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

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

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

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

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

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

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

  • Our studies employ a wide array of methodologies, including

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

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

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