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Department of Neurobiology and Anatomy Edward Jekkal Muscular Dystrophy Research Fellowship

About the Fellowship

The Edward Jekkal Muscular Dystrophy Research Fellowship is designed to strengthen the training of senior postdoctoral students or young research faculty members interested in neuromuscular disease research. The fellowship is a one-year award with the possibility of a second year of funding.

The fellowship is funded through the generosity of the Muscular Dystrophy Association and the late Edward Jekkal, an AT&T mechanical designer who lived in Bucks County, Pennsylvania. Mr. Jekkal is remembered for his kindness and generosity and the talent that enabled him to design assistive devices to compensate for disabilities.

Creation of the fellowship was furthered by Leonard S. Jacob, MD, PhD, an MCP alumnus who was a Board of Trustees member and a friend of the Jekkal family. The Jekkal estate and the MDA contributed to establish the fellowship, with a matching contribution from Drexel University.

Drexel University will provide the training environment that will assist the fellow in establishing an independent multidisciplinary research program. Interested applicants will be expected to work with a primary sponsor at Drexel University for the purpose of establishing a host laboratory and developing the proposal. Junior research faculty at Drexel University can submit an independent application with emphasis on a plan for the development of their academic career. The typical postdoctoral applicant will already have completed several years of postdoctoral research training, and will be about to move into a faculty position. Applicants can also be junior faculty. Special consideration will also be given to MDs who have completed their residency training and will be in the position to plan and execute a research program while receiving input and guidance from a core group of faculty, in addition to a primary sponsor.

This core training group will be drawn from faculty having demonstrated strengths in the physiology and pathology of neuromuscular and spinal related disorders, molecular biology of transmitter receptors and ion channels, regulation of contractile activity in muscles, and the structural organization and regenerative capacity of neurons. These faculty members represent the Departments of Neurobiology & Anatomy, Pharmacology & Physiology, Neurology and Biology at Drexel University. The sponsor will be responsible for providing the primary training and the host laboratory.

Jekkal Fellowship Advisory Committee

Itzhak Fischer, PhD, Chair
Leonard Jacob, MD, PhD
Peter Baas, PhD
John Houle, PhD
Marion Murray, PhD
Veronica Tom, PhD

Jekkal Fellowship Training Faculty & Research Descriptions

Peter W. Baas, PhD, Professor, Neurobiology & Anatomy

Peter W. Baas, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8298
215.843.9082 (fax)
pwb22@drexel.edu

Dr. Baas is interested in all aspects of the neuronal cytoskeleton, with particular emphasis on the regulation of microtubules in developing neurons. He has made many important discoveries, such as ascertaining the differences in microtubule polarity orientation between axons and dendrites, and documenting the importance of molecular motors previously believed to be mitosis-specific in the establishment and organization of the axonal and dendritic microtubule arrays. He has studied the centrosome of the neuron, the length distribution of microtubules in developing axons, and the role of microtubule-severing in the formation of axonal branches.

Over the years, Dr. Baas has studied the issue of microtubule transport in the axon, as a highly visible participant when the issue was most controversial, and now he has broadened the topic to study the specific molecular motor proteins that transport microtubules in both axons and dendrites, and how these motors are regulated. Dr. Baas proposed the existence of microtubule severing in neurons before microtubule-severing proteins had been discovered, and has now become a leader in the field of microtubule-severing proteins in neurons. In recent years, Dr. Baas has greatly increased the use of live-cell imaging as well as molecular biology in his research, and is currently focusing on the specific properties and functions of molecular motor proteins and microtubule-severing proteins in the neuron.

Moving forward, Dr. Baas is expanding his studies both conceptually and technically to resolve fundamental questions on how motor proteins usually considered in the context of mitosis work collaboratively to co-regulate the organization of microtubules in axons and dendrites. In addition, he is moving forward aggressively to elucidate the roles played by microtubule-severing proteins in the remodeling of the microtubule array, underlying major morphological changes in the neuron that occur during development. These studies also include work on the organization and regulation of microtubules in migrating neurons during the lamination of the brain.

Dr. Baas is interested in how flaws in microtubule-related proteins and mechanisms give rise to neurological diseases, and how the expanding base of knowledge from his basic science experiments can be used to develop strategies for treating patients with neurological diseases and injuries. He has been studying diseases such as hereditary spastic paraplegia and Alzheimer’s disease, and has been working to develop novel microtubule-based strategies for augmenting nerve regeneration after injury to the brain and/or the spinal cord.

Visit the Baas Lab website for additional information.

Marie-Pascale Côté, PhD, Assistant Professor, Neurobiology & Anatomy

Marie-Pascale Côté, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8598
215.843.9082 (fax)
mc849@drexel.edu

Dr. Côté’s research focuses on activity-dependent neuroplasticity in spinal networks after a spinal cord injury (SCI). Activity-dependent neuroplasticity refers to the remarkable ability of neuronal cells and networks to form and reorganize synaptic connections in response to learning and experience provided by repetitive activation in order to adapt to a new context such as an injury.

With this in mind, Dr Côté is primarily interested in identifying the physiological and anatomical modifications in the spinal cord that lead to the impairment of motor function following SCI, with a particular emphasis on the benefits and optimization of rehabilitative strategies. Over the years, she has investigated the beneficial effect of locomotor and bicycle training on spinal networks after SCI in several research models ranging from rat to human, so the challenges of translational research are at the forefront of her research program.

Activity-based therapies are routinely integrated in SCI rehabilitation programs in the clinic and oftentimes result in improvement in sensorimotor recovery. Among the beneficial effects of exercise is a reduction of hyperreflexia in proprioceptive and nociceptive pathways that would otherwise lead to spasticity and neuropathic pain. However, exercise-dependent functional improvement is ultimately limited and eventually reaches a plateau. The objective is to understand the mechanisms underlying activity-dependent plasticity of the nervous system by tapping into the spinal circuitry to facilitate sensorimotor recovery. Unraveling the mechanisms at play is crucial for the design of optimized rehabilitation strategies.

Research in the Côté Lab is designed to examine multiple aspects of rehabilitative strategies after SCI, including, but not limited to, the effect of SCI and activity-dependent plasticity on the 1) excitability of lumbar motoneurons 2) modulation of associated reflex responses 3) deficits/recovery of locomotor movements. Our work also focuses on identifying the molecular pathways responsible for differences in functional recovery. Activity-based therapies used in the laboratory include passive bicycle training, treadmill locomotor training and transcutaneous stimulation.

We use a multidisciplinary approach that includes in vivo electrophysiology (intramotoneuronal recordings in the spinal cord, electromyograms, eletroneurograms, etc.), magnetic stimulation, transpinal stimulation, immunohistochemistry, laser capture, western blotting and PCR analysis to evaluate synaptic and functional changes occurring in the spinal cord in response to exercise (i.e., step and bicycle-training) after SCI.

Our research has direct relevance to the design and implementation of future treatment and rehabilitation programs for SCI. Defining the involvement of specific molecular pathways in both the impairment and recovery of spinal excitability and locomotion after SCI is critical to identify possible new targets to enhance pharmacological management of SCI and improve locomotor function when combined with rehabilitation programs.

Visit Dr. Côté's faculty profile for additional information or visit the Côté Lab website.

Kimberly Dougherty, PhD, Assistant Professor, Neurobiology & Anatomy

Kimberly Dougherty, PhD,
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8407
215.843.9082 (fax)
kjd86@drexel.edu

The long-term interest of Dr. Dougherty’s lab is to reveal the functional connectivity of spinal circuits and to determine how these circuits go awry in injury and disease states. Current projects are particularly focused on the spinal circuits involved in orchestrating locomotion. Locomotor rhythm and pattern are controlled by neuronal networks in the spinal cord called central pattern generators. Central pattern generators are capable of operating in the absence of descending inputs from the brain. As these locomotor networks are located in the lumbar spinal cord, they are below the level of most spinal cord injuries and therefore relatively intact for therapeutic targeting; however, a tremendous amount of plasticity occurs below the level of the injury. The identification of circuit elements, function, neuronal properties, connectivity and cell-specific injury-induced plasticity is of particular interest in our research.

All current projects in the lab focus on the study of genetically identified populations of spinal interneurons involved in locomotion or projection neurons transmitting locomotor feedback or pain information to the brain in mice. Rhythm-generating neurons identified by the transcription factor Shox2 are central to several projects in the lab. We are using Shox2 neurons to explore cellular and network mechanisms of rhythmogenesis, testing hypotheses we generate based on predictions of computational models of our collaborators in the Rybak lab. Additionally, we are looking at the ways in which locomotion is modified by various sensory afferent and motor efferent feedback mechanisms, both globally and at the level of specific rhythm- and pattern-generating populations.

In addition to Shox2 neurons, other current projects include the study of specific neuronal populations involved in the gating of sensory input to the central pattern generator and ascending tract neurons mediating affective components of pain. We are using a variety of techniques including whole cell patch clamp, optogenetics, chemogenetics, extracellular recordings, mouse genetics, immunohistochemistry, and confocal microscopy to examine the above neuronal populations in order to determine their connectivity within their respective spinal circuits, the roles they play in locomotor/pain network function, plastic changes that occur after spinal cord injury, and effects of potential therapeutic strategies. Most of our experiments are performed ex vivo, both in full spinal cords isolated from neonatal mice and in our recently established adult mouse slice preparation. In addition to shifting to more mature or adult preparations ex vivo, our most recent projects are incorporating adult in vivo experiments. This allows for the association of changes in functional abilities and/or behaviors with changes in underlying circuitry. Near future experiments will take advantage of cell-specific manipulation techniques, currently well-established in our ex vivo preparations, to acutely activate or silence specific populations of spinal interneurons in behaving mice. Overall, our experiments will provide insights into the functioning of various spinal circuitries during normal conditions and potential mechanistic targets for therapeutics aimed at restoring function after injury or disease.

Visit Dr. Dougherty's faculty profile for additional information.

Itzhak Fischer, PhD, Professor and Chair, Neurobiology & Anatomy

Itzhak Fischer, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8400
215.843.9082 (fax)
if24@drexel.edu

My research is designed to promote regeneration and recovery of function after spinal cord injury by identifying the best strategies for cellular transplantation, to apply gene therapy methods to introduce therapeutic genes into the injured spinal cord and to utilize multifunctional scaffolds to facilitate therapy. We are currently studying the efficacy of neural stem cells derived from rodent and human cells and use injury models prepared for both sensory and motor systems. Our long-term goal is to prepare effective protocols for clinical trials.

Transplantation of neural stem cells to reconnect the injured spinal cord. Our lab has developed transplantation methods that support neuronal cell replacement and neural repair using mixed populations of neuronal and glial restricted precursors (NRP/GRP). The experiments are designed to build neuronal relays with active synapses in a lesion of sensory and motor systems. The project is addressing critical issues related to application of stem cell biology to CNS injury including generation of graft-derived neurons, directional axon growth, overcoming the inhibitory environment of the injury and most importantly how to generate functional synaptic connections with denervated targets.

We transplanted a combination of NRP/GRP into a dorsal column lesion, and used a lentivirus vector to generate a neurotrophin gradient and guide axons to their target. We showed that host sensory axons regenerated into the graft, while graft-derived axons grew into the dorsal column nucleus (DCN) target. We demonstrated the formation of synaptic connections at the structural and functional levels including electrophysiological recording. Ongoing experiments are designed to build neuronal relays with active synapses in lesions of motor systems, and to apply these strategies to human cells and to chronic injuries.

Using permissive astrocytes to promote regeneration and functional recovery. This project is focused on therapeutic potential of glial restricted progenitors (GRP) isolated from the embryonic CNS and astrocytes derived from the GRP. The in vitro studies defined differentiation protocols to generate permissive astrocytes that support axonal growth over the inhibitory scar molecules. The in vivo studies demonstrated the ability of GRP and derived astrocytes to promote regeneration and recovery of function. Recent work has been carried out with human cells that were prepared in a GMP process for FDA approval in collaboration with Q-therapeutics.

The use of gene therapy for delivering therapeutic factors into the injured. We developed viral vectors (e.g., lentivirus) for ex vivo gene therapy (genetic modification of cells) and in vivo gene therapy (direct injection into the CNS). Therapeutic genes of interest include neurotrophic factors, enzymes that degrade the gliotic scar and factors that increase the regenerative capacity of CNS neurons. For example, few studies have addressed chronic SCI due to the experimental complexities and the daunting challenges associated with axonal growth through a chronic scar. We developed a recombinant form of chondroitinase (Chase) that can be secreted and effectively digest the CSPG component of the scar. Delivery of Chase by a lentivirus vector into the spinal cord allowed sustained secretion of the enzyme accompanied by digestion of the scar, thus improving the potential for axon regeneration and repair in chronic SCI.

Visit Dr. Fischer's profile for additional information.

Simon Giszter, PhD, Professor, Neurobiology & Anatomy

Simon Giszter, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8412
215.843.9082 (fax)
sg33@drexel.edu

The emphasis of my laboratory is on understanding how some spinal systems can function effectively but independently of the brain in muscle controls, and how to leverage this to rehabilitate after spinal cord injury (SCI) or stroke. We focus on the modular organization of spinal cord and how it helps the brain solve the degrees of freedom problem faced in motor control as a key feature of independent motor operations in the spinal cord. These are issues of fundamental importance in understanding motor learning, motor development and the evolution of action systems.

We use a basic science and comparative strategy, using both rats and frogs, and we also examine the impact of spinal modularity on corticospinal organization in the rodent. We examine the neural and biomechanical modularity of motor output in spinal cord systems separated from brain control, and in spinalized rats that can still walk (neonatal spinalized rats). In rats, our focus is an examination of how spinal modularity affects both the development and recovery of locomotor function after SCI. We have extended this approach to the development of brain-machine-interface (BMI) and to novel neurorobotic rehabilitation strategies. The goal is to use BMIs and neurorobotics, combined with our understanding of modularity, to assist recovery of function after SCI and to further our understanding of corticospinal and spinal bases of motor actions and adaptations.

Modularity in Spinal Cord
We are able to identify modular elements by examining the statistical decomposition of motor patterns, the modular addition and deletion of muscle groups and force-patterns in reflex behaviors, and the neural clustering observed in neural recordings. Our data suggest that the behavioral and reflex repertoire of frogs may rest on the use of linear combinations of a small number of motor elements or primitives recruited by voluntary and pattern generator systems. My lab was the first to demonstrate modular primitive-based trajectory corrections. In cats and humans, similar modular locomotor pattern results seem to hold. Our work in rodent locomotion also supports such modularity in the hindlimb controls.

Neural basis of modularity. To address this, we record in the spinal cord of frogs using multi-electrode probes and use information-based clustering and conventional physiology to relate activity to modular primitives in the motor pattern. Using these techniques, our lab is the first to establish the neural support of primitives. Our data support a number of dedicated distribution interneurons for organizing and controlling the action sequences of different spinal motor primitives seen in the motor pattern. 

Modularity, Adaptation and Rehab/Recovery of Function After Spinal Injury in Rats
About 20% of rats that are spinal transected on postnatal day 1 or 2 somehow succeed in developing a quadruped weight-supported locomotion as adults, despite the complete separation of the lumbar spinal cord from the brain. These rats master the integration of actions generated by this autonomously operating piece of CNS into a coherent body support behavior. This ability of the neonate may be a sign-post to the mechanisms of recovery that could be engaged in adult injury in rats and then translated to clinically relevant interventions.

Cortical organization and role in recovery in thoracic spinalized rats. We used intracranial microstimulation (ICMS) of motor cortex to establish that all rats with weight-supported locomotion after neonatal injury had mid to low trunk representations in motor cortex. "Failed" rats did not. Lesion of the trunk region in weight-supporting rats reduced the quality of their stepping measures by 40-50% and caused greatly increased pelvic roll. The cortex in these rats seems intimately engaged in locomotor control, significantly more so than observed in intact rats. Our data in this area is very novel and suggests that (1) the trunk could be a very important rehabilitation target, and that (2) cortical signals from trunk regions might be engaged in brain machine interface and neurorobotic strategies to improve locomotion.

Trunk-based rehabilitation and brain-machine-interface designs. We have developed a system that allows real-time BMI control of a robot for experiments in rats and frogs. We also developed an orthosis that can be implanted in the pelvis of rats. The robots we use can be attached to the orthosis to interact directly with the skeleton of the rat. In this way extrinsic (external world) or intrinsic (within body) force effects can be generated. Forces delivered in this way can be used for rehabilitative assistance following the control designs of the MIT-manus from the Hogan Lab. They can be used to examine adaptation to altered external or internal mechanical conditions during locomotion. They can be used "closed loop," being driven by recorded brain activity, so as to form a BMI. Our published experiments with this system support the efficacy of such a BMI design, and this rehabilitation strategy. Robust adaptations with after effects can be examined in intact rats.   Further, rats are capable of the rapid incorporation of BMI-driven force effects into their adaptive strategies during locomotion. This is a powerful new paradigm for examining adaptation, BMI and rehabilitation. Recent studies have extended these results to exploring epidural stimulation driven through a robot system for more optimal interactions of stimulation, robot and functional rehabilitation processes.

We are now exploring combinations of viral, bridging, and epidural and robot rehabilitation therapies in these frameworks.

Visit Dr. Giszter's faculty profile for additional information.

Michael Lane, PhD, Assistant Professor, Neurobiology & Anatomy

Michael Lane, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8892
215.843.9082 (fax)
michael.lane@drexelmed.edu

Dr. Lane received his PhD at the University of Melbourne in Australia. After completing postdoctoral training at the Universities of Melbourne and Florida, he accepted a tenure-track position with the Spinal Cord Research Center at Drexel to continue his ongoing research in spinal cord injury, neuroplasticity and strategies to optimize lasting functional recovery. Dr. Lane’s research team is investigating cervical spinal cord injury (SCI) and how recovery can be optimized. A primary focus of this work is the functional consequences of cervical SCI (in particular how breathing and upper extremity/arm function is impaired) and what potential there is for progressive, spontaneous functional recovery – or functional "plasticity." The team is also developing and testing strategies for promoting beneficial plasticity and recovery following cervical SCI.

Using a range of neuroanatomical (histological, immunohistochemical, neural tracing), neurophysiological (electrophysiological recording from muscle, nerve or neurons directly) and behavioral approaches (e.g., assessment of forelimb use or patterns of breathing), Dr. Lane’s research has helped to define the respiratory and upper extremity circuitries in the normal (uninjured) spinal cord, how this circuitry is affected by SCI and how treatments can be used to promote repair. A particular focus of our research has been on the role of spinal interneurons in mediating normal motor function, and spontaneous or therapeutically enhanced functional plasticity following SCI. Several studies have shown that spinal interneurons are involved with spontaneous reorganization of neuronal circuitry, which can provide new anatomical pathways capable of facilitating functional recovery. These interneurons – interspersed throughout the spinal cord – can receive input from neurons in the brain and then themselves make contact with neurons below the SCI. Thus, they can relay information from the brain, around the injury, to neurons below the injury that control the muscles. While this remodeling of connections can occur spontaneously, it may also be enhanced by some developing therapeutic strategies. While there is a growing appreciation among scientists and clinicians that spinal interneurons may be essential to plasticity and recovery after SCI, little is known about their distribution or how they aid functional improvement. Dr. Lane’s research team believes that treatments capable of harnessing and enhancing this natural plasticity may circumvent the need for long-range axonal growth. Accordingly, they believe that spinal interneurons are a key therapeutic target for optimizing anatomical repair and functional recovery following SCI.

With a focus on respiratory function and breathing after cervical SCI, Dr. Lane’s research program is exploring two key therapeutic strategies. The first is a cellular therapy capable of promoting spinal cord repair. This approach has been used extensively in the past 30 years in a wide range of SCI models, and other neurological disorders. The work being pursued by Dr. Lane’s research team now builds upon this extensive research foundation to assess whether transplantation of neural precursor cells can repair respiratory pathways after cervical SCI and promote recovery of respiratory function. Their primary focus is on promoting recovery of phrenic motor function, as the diaphragm (controlled by the phrenic motor system) is an essential component of breathing. Impaired breathing is a devastating consequence of cervical level SCI and remains the leading cause of morbidity and mortality following injuries at this level. A second goal of the research program is to explore the therapeutic benefits of rehabilitation on respiratory function after SCI. The use of "activity"-based therapies following SCI has been explored extensively as a means of driving plasticity and recovery of locomotor function. Experimental studies have been translated to clinical studies, which have led to some functional improvements in injured individuals. Activity-based therapies are also useful at promoting recovery of non-locomotor function, such as breathing. Dr. Lane’s research is now exploring how such strategies can be used to drive plasticity and recovery of breathing following cervical spinal cord injury.

Visit Dr. Lane's laboratory website for additional information.

Ramesh Raghupathi, PhD, Professor, Laboratories for Head Injury Research, Neurobiology & Anatomy

Ramesh Raghupathi, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8405
215.843.9082 (fax)
mal395@drexel.edu

The spectrum of traumatic brain injuries ranges from mild concussions that are treated in the emergency room to severe head injuries that require acute critical and neurosurgical care. Improved critical and advanced radiological and neurosurgical techniques have led to decreases in mortality rates over the past two decades. However, survivors of brain injuries suffer long-term behavioral problems such as learning deficits, memory dysfunction, psychological and emotional disturbances – functional aspects that affect the quality of life and currently have no therapies. The economic costs of traumatic brain injuries, which include hospitalization, health care and lost work hours, is estimated at almost $35 billion. This problem has become particularly relevant in the past four years, with Iraq War veterans returning home having suffered blast-related concussions, an injury that is poorly understood. It is estimated that over 2,500 soldiers have suffered head injuries since March 2003. The ongoing research efforts, funded in part by the National Institutes of Health and the Division of Veteran’s Affairs, are aimed at addressing the feasibility of cellular and pharmacologic strategies to attenuate and reverse TBI pathology. Brain injury research at Drexel offers some unique capabilities such as:

  1. Comparisons of acute and chronic pharmacologic treatments in multiple models of TBI, in both mice and rats.
  2. A strong neuroengineering program that focuses on neurorobotics and prosthetics.
  3. Behavioral modifications such as enriched environments, treadmill stepping, to improve cognitive and motor function.
  4. Combination treatment strategies that encompass acute pharmacologic treatments with chronic phase behavioral modifications and/or stem cell transplants.

The mission of the Brain Injury Laboratories is to develop pharmacological treatment and behaviorally therapeutic strategies to, respectively, reduce acute post-traumatic neural damage and augment behavioral recovery in the chronic phase.

The studies of traumatic brain injury at Drexel University College of Medicine have led to the following accomplishments:

  • Documenting programmed cell death after brain injury in rats and in humans
  • Demonstrating that strategies aimed at reduced the extent of programmed cell death can attenuate cognitive and motor deficits
  • Development of injury-specific and clinically-relevant animal models of TBI (concussive to repetitive to severe brain injuries)
  • Identification of specific intracellular pathways that underlie grey matter injuries (neuronal death) and white matter injuries (axonal damage).

We currently use models of focal or diffuse brain trauma in rodents. Behavioral measures include: cognitive function using the Morris water maze, motor function using the Schallert Cylinder test of limb placement, and the Feeney beam walk test. In addition, standard outcome measures include measurement of compound action potentials in the corpus callosum using ex vivo preparations of uninjured and injured coronal brain slices. Histological techniques include gross alterations using Nissl-Luxol Fast Blue stained sections followed by quantification of lesions; microscopic evidence of cell survival using unbiased stereology with the optical fractionator; stereologic approaches to counting double-labeled axonal profiles with confocal microscopy; optical imaging in live animals; and cryoplane microscopy for imaging from the micro- to the macro-scale.

Image illustrating the research of Ramesh Raghupathi, PhD

Visit Dr. Raghupathi's faculty profile for additional information.

Ilya Rybak, PhD, Professor, Neurobiology & Anatomy

Ilya Rybak, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8596
215.843.9082 (fax)
iar22@drexel.edu

Research interests of Dr. Rybak include the organization of brainstem and spinal cord circuits, and neural control of respiration and locomotion. The long-term goal of Dr. Rybak’s studies is to investigate and understand the key issue of neural control of movement: how different cellular, network and systems neural mechanisms are integrated across multiple levels of organization to produce motor behavior and to adapt this behavior to various external and internal conditions. Investigations of the brainstem neural mechanisms responsible for neural control of breathing, as well as neural circuits in the spinal cord involved in control of locomotion, provide a unique and attractive opportunity to develop and investigate comprehensive computational models that can bring into a uniform framework the existing experimental data and current hypotheses related to different levels of systems organization and behavior. These theoretical and computational studies, and computational models of spinal and brainstem circuits developed in these studies, have direct implications for the recovery from spinal cord injury (SCI). The developed model provide important information about the functional relationships and neural coupling that need to be considered in the development of therapeutic strategies following SCI. In addition, these models can serve as test beds for direct simulation and comprehensive analysis of the consequences of SCI and applied medical treatments.

All studies in the laboratory are performed in close interactive collaboration with leading researchers conducting complementary experimental investigations. Working in collaboration with leading respiratory physiologists (Jeffrey Smith, NINDS; Julian Paton, Bristol Univ., U.K.; Diethelm Richter, Univ. of Göttengen, Germany; Thomas Dick, CWRU; and others) we developed the most complicated and realistic computational models describing the respiratory circuits in the brainstem and neural control of respiration from cellular to systems levels. Similarly, in collaboration with several leading physiologists, experts in spinal cord physiology (David McCrea, Univ. of Manitoba, Canada; Ronald Harris Warrick, Cornell Univ.; Frederic Brocard, Marseille Univ., France; Ole Kiehn, Karolinska Institute, Sweden; Michel Lemay, Drexel Univ.; Boris Prilutsky, Georgia Tech; and others) we developed a series of well-known models of the mammalian spinal circuits and neural control of locomotion

Visit the Laboratory for Theoretical and Computational Neuroscience website for more information.

Veronica Tom, PhD, Associate Professor, Neurobiology & Anatomy

Veronica Tom, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
215.991.8590
215.843.9082 (fax)
vjt25@drexel.edu

The overall goal of the projects within my lab is to understand why the adult CNS fails to repair itself, and to develop therapeutic strategies that will help restore function in spinal cord injured patients.

There are two research areas:

1. Promoting axon regeneration
Our strategies are largely based on enhancing the functional regeneration of severed axons. To do this, we concurrently address the two major obstacles to axonal regeneration after injury: 1) the inhibitory environment of the glial scar, and 2) the inability of most adult CNS neurons to mount a robust growth response. We use a combination of growth supportive transplants, modification of the inhibitory environment that is associated with the glial scar, and treating with various agents (e.g., pharmacological and viral vectors) to enhance the intrinsic ability of mature axons to regrow. We assess the extent of axonal regeneration histologically and electrophysiologically. We also use a variety of functional outcome measures to determine whether these regenerated axons successfully and appropriately integrate into neural circuits and mediate behavioral recovery.

2. Promoting recovery of autonomic function
While SCI patients view the regaining of autonomic functions as a high priority to improve their quality of life, promoting recovery of autonomic functions is a vastly understudied area of research. Furthermore, complications due to autonomic function disruption, such as cardiovascular disease and urinary system disorders, are leading causes of morbidity and mortality for chronically injured individuals with a spinal cord injury. One of the primary causes of cardiovascular disease in these patients is autonomic dysreflexia (AD), a life-threatening dysfunction in which some sensory stimulus below the level of SCI triggers extreme hypertension accompanied by bradycardia.  AD is thought to develop from: 1) the loss of tonic input onto sympathetic preganglionic neurons that drive cardiovascular control; 2) aberrant plasticity leading to hyperexcitability of sensory circuitry. We are currently determining: 1) if we can restore sufficient reinnervation sympathetic preganglionic neuron to normalize their activity; 2) if we can dampen hyperexcitability below the injury.

Visit the Tom Lab website for more information.

Edward Jekkal Muscular Dystrophy Association Fellowship Application Process

This program has been established to strengthen the training program for senior postdoctoral fellows about to move into faculty positions or junior research faculty members, including physician scientists, interested in neuromuscular disease research at Drexel University. The fellowship carries an annual award of $53,000, which can be used to cover salary support, fringe benefits and research expenses, with the possibility of a second year of funding.

Applicants are expected to identify a sponsor from within the training faculty at Drexel University and to prepare an application with the sponsor, who will provide the research support and, if appropriate, a salary supplement. Junior faculty at Drexel University can submit an independent application.

The earliest possible start date for the fellowship is July 1, 2018.

Download the Jekkal Fellowship application:

The research project should be in an area consistent with the objectives of the Muscular Dystrophy Association.

Please submit a PDF version of your application to: kg35@drexel.edu. and two letters of reference in a sealed envelope or as PDF files with electronic signature by May 7, 2018. No late submissions or submissions sent by fax will be accepted.

Review Considerations

Proposals will be judged by the Advisory Committee, with the aid of internal referees. The following criteria will be considered:

Review Criteria:

  • Scientific and research background of the applicant
  • Relevance of the proposed training to the career goals of the applicant
  • Scientific quality of the proposal
  • Appropriateness of the sponsor to the proposed training program and the sponsor’s commitment

Specific instructions for applicant face page:
If there will be multiple sponsors, list the primary one here.

Education information:
Applicant’s education – List all degree programs beginning with baccalaureate or other initial professional education. Include all dates (month and year) of degrees received or expected, in addition to other information requested.

Applicant’s training/employment – List in chronological order all nondegree training, including postdoctoral research training, all employment after college, and military service. Clinicians should include information on internship, residency and specialty board certification (actual and anticipated with dates) in addition to other information requested.

Goals for fellowship training and career – Explain training goals under this fellowship and the relevance to your career goals. Identify the skills, theories, conceptual approaches, etc. that you hope to learn or enhance your understanding of during the fellowship. Describe how the proposed activities, including any research, will contribute to the achievement of these career goals.

Abstract – State the broad, long-term objectives and specific aims of the research proposal, making reference to the health relatedness of the project. Describe concisely the research design and methods for achieving these goals. Do not summarize past accomplishments and avoid the use of the first person. This is meant to serve as a succinct and accurate description of the proposed work when separated from the application.

Table of Contents:
Self-explanatory

Background:
Support – Follow instructions on form.
Academic and professional honors – List any honors that would reflect upon your potential for a fellowship. Include current memberships in professional societies.
Title(s) of thesis/dissertation(s) – Self-explanatory.
Thesis advisor or chief of service – If not submitting a reference from this person, explain why not.
Supplement – List plans, if any, developed with the sponsor to supplement the stipend.

Research:
Summary – Summarize in chronological order your research experience, including the problems studied and conclusions. Specify which problems were theses. If you have no research experience, list other scientific experience. Do not list academic courses here. Do not exceed one page.
Doctoral dissertation – Summarize, not exceeding one page.
Publications – In chronological order, list your entire bibliography, separating abstracts, book chapters, reviews and research papers. For each publication, give the authors in published sequence, full title, journal, volume number, page numbers, and year of publication. Indicate if you have used another name previously. Manuscripts pending publication or in preparation should be included and identified.

Research Training Plan (Sections a-c) not to exceed 5 pages:
Research Training Proposal – This section should be well-formulated and presented in sufficient detail that it can be evaluated for both its research training potential and scientific merit. It is important that it be developed in collaboration with the sponsor. If multiple sponsors are envisioned, describe their individual roles.
Section a., Specific aims – State the specific purposes of the research proposal and the hypothesis to be tested.
Section b., Background and significance – Sketch briefly the background to the proposal. State concisely the importance of the research described in this application by relating the specific aims to broad, long-term objectives.
Section c., Research design and methods. Provide an outline of:

  • Research design and the procedures to be used to accomplish the specific aims
  • Tentative sequence for the investigation
  • Statistical procedures by which the data will be analyzed
  • Any procedures, situations, or materials that may be hazardous to personnel and the precautions to be exercised

Potential experimental difficulties should be discussed together with alternative approaches that could achieve the desired aims.
d. Literature cited – Each citation must include names of all authors, titles, book or journal, volume number, page numbers and year of publication.

Section II: Primary Sponsor

Facilities and Commitment:
Follow instructions on form.

Checklist:
The checklist is the last page of the application.

Submission of References

Applications will not be reviewed unless at least two references are received with the application, either as sealed lettters or as a PDF file with electronic signature. Applicants are responsible for complete applications reaching Drexel University on schedule.

Submitting Your Application

Submit the following material by May 7, 2018:

  1. A PDF version of your application submitted to kg35@drexel.edu. Note that the pages must be assembled in the order specified in the table of contents.
  2. At least two letters of reference in sealed envelopes, or as PDF files with electronic signature submitted to kg35@drexel.edu .
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