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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. Application forms are available in PDF format or MS Word format.

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 be about to move into a faculty position, and 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 their primary sponsor.

This core training group will be drawn from faculty having demonstrated strengths in the physiology and pathology of neuromuscular and spinal disorders, molecular biology of transmitter receptors and ion channels, regulation of contractile activity in muscles, and the structural organization and regenerative capacity of neurons. 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
Simon Giszter, PhD
John Houle, PhD
Veronica Tom, PhD

Jekkal Fellowship Training Faculty & Research Descriptions

Jessica Ausborn, PhD, Assistant Professor, Neurobiology & Anatomy

Jessica Ausborn, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8310
ja696@drexel.edu
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My scientific interests focus on understanding the neurophysiological mechanisms of how neural networks process and encode activity to generate appropriate behaviors. Using a data-driven approach and often in close collaboration with experimental scientists, we develop detailed, cutting-edge models to study mechanisms involved in sensory-motor integration, neural processing and the generation and control of locomotor behaviors and respiratory activity. Our modeling efforts often tackle complex sets of sometimes puzzling or seemingly contradictory experimental results that would be difficult to interpret without a rigorous examination of possible underlying mechanisms and their dynamic interactions. Models also help to identify which results might represent general principles across the animal kingdom and are invaluable tools to help plan experiments. Fundamental biological, mathematical and physics principles are used to interpret experimental data and place hypothesized explanations of results into a consistent framework.

Neural algorithms underlying diversity in visual feature integration

Animals can select diverse behaviors in response to highly similar visual inputs. The mechanisms that underlie these transformations, however, remain primarily unknown. We use looming feature integration in Drosophila melanogaster as a well-defined model of sensory-motor integration to uncover neuronal algorithms that transform visual features into multiple distinct, behaviorally relevant outputs. Our models investigate novel algorithms and encoded sensory features, and identify how different algorithms play together or contrast each other to achieve output diversity across different descending pathways. We integrate modern machine learning and data science techniques with biophysically realistic computational models and develop formal descriptive mathematical models to directly derive and verify sensorimotor integration algorithms computed in the neuronal pathways that transform visual information into motor programs. In doing so we also illuminate many general problems that every neuron or neural network has to solve, including the precise timing of output patterns, dealing with more or less precise inputs, and how computations can be accomplished at the subcellular level. Our work provides insight into how behavioral diversity is generated in sensory evoked behaviors across species, and across sensorimotor transformations.

Control strategies of descending command systems for the generation of context-specific locomotor behaviors

Locomotion needs to be continuously adapted to the task at hand. Brainstem centers transform inputs from higher motor regions into meaningful commands to control speed and gait, stop or freeze locomotion, direct turning maneuvers, and orchestrate the transitions between them. In addition to their role in initiating, driving and terminating different behaviors, these brainstem areas have also been implicated in recovery after spinal cord injury and represent promising targets for deep brain stimulation in patients with Parkinson’s disease. However, the logic of the processing in these centers and the transformation of their output into locomotor activity is still unclear. We therefore develop detailed data-based computational models to systematically structure, integrate and probe current knowledge on the organization and function of subpopulations of brainstem-spinal pathways controlling locomotion. Our models identify key strategies in locomotor control and provide a theoretical framework for the future investigation of motor control strategies and restoration of function after disease or injury.

Selected relevant publications:

  • “Multiple Rhythm-Generating Circuits Act in Tandem with Pacemaker Properties to Control the Start and Speed of Locomotion”
    Song J#, Pallucchi I#, Ausborn J#, Ampatzis K#, Bertuzzi M, Fontanel P, Picton LD, El Manira A
    Neuron 105, 1048-1061.e4., #equal contributions (2020)
  • “Computational modeling of brainstem circuits controlling locomotor frequency and gait”
    Ausborn J#, Shevtsova NA#, Caggiano V, Danner SM, Rybak IA
    eLife 8:e43587. #equal contributions (2019)
  • “Organization of the core respiratory network: Insights from optogenetic and modeling studies”
    Ausborn J#, Koizumi H#, Barnett WH, John TT, Zhang R, Molkov Y Smith JC, Rybak IA
    PLoS Computational Biology; 14(4) #equal contributions (2018)
  • “State-dependent rhythmogenesis and frequency control in a half-center locomotor CPG”
    Ausborn J, Snyder AC, Shevtsova NA, Rybak IA and Rubin JE
    Journal of Neurophysiology, 119(1), 96–117 (2018)
  • “A Hardwired Circuit Supplemented with Endocannabinoids Encodes Behavioral Choice in Zebrafish”
    Song J, Ampatzis K, Ausborn J, El Manira A
    Current Biology, 25; 20:2610-20 (2015)
  • “Decoding the rules of recruitment of excitatory interneurons in the adult zebrafish locomotor network”
    Ausborn J, Mahmood R, El Manira A
    Proceedings of the National Academy of Sciences 109; 52 E3631-9 (2012)
  • “Principles governing recruitment of motoneurons during swimming in zebrafish”
    Gabriel JP#, Ausborn J#, Ampatzis K, Mahmood R, Eklöf Ljunggren E, El Manira A
    Nature Neuroscience, 14; 1 93-9; #equal contributions (2011)
  • “The interaction of positive and negative sensory feedback loops in dynamic regulation of a motor pattern”
    Ausborn J, Wolf H, Stein W
    Journal of Computational Neuroscience, 27:245-257. (2009)
  • “Frequency Control of Motor Patterning by Negative Sensory Feedback”
    Ausborn J, Stein W and Wolf H
    The Journal of Neuroscience, 27(35): 9319-9328 (2007)
  • “Motor pattern selection by combinatorial code of interneuronal pathways”
    Stein W, Straub O, Ausborn J, Mader W, Wolf H
    Journal of Computational Neuroscience, 25:543-561 (2008)

See my website for additional information.

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

Peter W. Baas, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8298
215.843.9082 (fax)
pwb22@drexel.edu
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Dr. Baas studies the underlying mechanisms of neurodegeneration and dysfunction of the nervous system, resulting from degenerative diseases, developmental disorders and injury, with the goal of developing therapies for prevention, treatment and repair. Rather than focusing on just one type of disease, disorder or injury, he focuses on a common downstream target that goes awry across almost all of them. By focusing downstream, he believes mechanistic insights can be gained and that therapies can be developed that can broadly apply across maladies. Specifically, the downstream target he studies is the microtubule – a cytoskeletal structure that is critically important for all aspects of the architecture, intracellular transport and mobility of neurons and other cells of the nervous system.

Project 1. Neurodevelopmental Disorders

As neurons develop from mitotic precursors, they undergo a migratory journey to their final locations in the brain or elsewhere in the body. Axons develop with growth cones heralding their journey to their targets, and dendrites form as well. Both axons and dendrites undergo extensive branching, pruning and remodeling. All of these events are microtubule-based, with the relevant proteins and pathways vulnerable to disorders such as autism. For over 30 years, Dr. Baas has worked to elucidate the mechanisms, proteins and pathways of neurodevelopment to foster unique insights into such neurodevelopmental disorders.

Project 2. Hereditary Spastic Paraplegia (HSP)

HSP is (usually) an adult-onset disease that most often arises due to autosomal dominant mutations of the SPAST gene, which encodes for a microtubule-severing protein called spastin. The patients have a pronounced gait deficiency and eventually become confined to a wheelchair, due to corticospinal degeneration. Dr. Baas’ focus on microtubules has fostered unique insights into the etiology of the disease, which he is studying with various experimental models. In the past he has used cultured rodent neurons and Drosophila, but now he is using a mouse model for HSP that he has developed that displays the hallmark characteristics of the disease. He is conducting behavioral, anatomical and histochemical studies, pursuing molecular mechanisms, and is now poised to begin testing therapies.

Watch a lecture from Dr. Baas for patients and their caregivers.

Project 3. Disease of Tau

Tau is a microtubule-associated protein that goes awry in Alzheimer’s disease, coming off the microtubules to form neurofibrillary tangles. Many other diseases also involve abnormalities to tau including frontotemporal dementia, supranuclear palsy, and Parkinson’s disease, as well as injuries such as traumatic brain injury. Most researchers in the field believe that microtubules become destabilized in tau diseases, but Dr. Baas’ hypothesis is different: He posits that tau is important for keeping much of the microtubule content of the axon labile and dynamic and that tau diseases cause the loss of the labile/dynamic component of the microtubule array. He also posits that microtubules become disorganized in the axon as a result of toxic properties of the abnormal tau. He is using mouse models and hiPSC lines from human patients to test these hypotheses and pursue novel therapies.

Read about his work in Science Daily.

Project 4. Gulf War Illness (GWI)

A substantial portion of the veterans who served in the 1991 Gulf War suffer from a disease called GWI. The symptoms are mainly of the CNS (central nervous system), including memory deficits, sleep disorders, headache and fatigue. Dr. Baas is part of the Gulf War Illness Consortium, a group of researchers and physicians from around the country who work collaboratively to understand the etiology of this mysterious disease and develop therapies. The disease seems to have arisen from a combination of stress of the battlefield together with various toxicants such as the neurotoxin sarin as well as pesticides. Dr. Baas is using rodent models and hiPSC lines (that he developed) in 2-dimensional culture and 3-dimensional cerebral organoids to test his hypothesis that microtubule abnormalities underlie the neurodegeneration and develop novel therapies accordingly.

Read about his work in the College of Medicine Alumni Magazine and Science Daily.

Project 5. Spinal Cord Injury (SCI)

The Baas laboratory is part of the Marion Murray Spinal Cord Research Center, which is a multidisciplinary group of labs at Drexel University aimed at developing novel approaches for improving the lives of people suffering from spinal cord injuries. Mostly in collaboration with partner labs, he is striving to use his knowledge of microtubule-based pathways to prompt injured nerves in the spinal cord to regenerate in ways that lead to functional recovery.

Visit the Baas Lab website for additional information.

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

Marie-Pascale Côté, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8598
215.843.9082 (fax)
mc849@drexel.edu
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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 exercise-based and/or spinal cord stimulation-based rehabilitation programs on the 1) excitability of lumbar motoneurons, 2) modulation of associated reflex responses, and 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 and treadmill locomotor training, while stimulation-based therapies include transcutaneous and epidural stimulation.

The lab uses a multidisciplinary approach that includes in vivo electrophysiology (intramotoneuronal recordings in the spinal cord, electromyograms, eletroneurograms, etc.), magnetic stimulation, transcutaneous stimulation, immunohistochemistry, laser capture, western blotting and PCR analysis to evaluate synaptic and functional changes occurring in the spinal cord in response to exercise and/or stimulation after SCI.

This 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.

Publications:

  • “Rehabilitation Decreases Spasticity by Restoring Chloride Homeostasis through the Brain-Derived Neurotrophic Factor-KCC2 Pathway after Spinal Cord Injury”
    Beverungen H, Klaszky SC, Klaszky M, Côté MP
    J Neurotrauma, 37:846-859 (2020)
  • “Enhancing KCC2 activity decreases hyperreflexia and spasticity after chronic spinal cord injury”
    Bilchak J, Yeakle K, Caron G, Malloy D, Côté MP
    Exp Neurol:113605 (2021)
  • “Direct evidence for decreased presynaptic inhibition evoked by PBSt group I muscle afferents after chronic SCI and recovery with step-training in rats”
    Caron G, Bilchak JN, Côté MP
    J Physiol 598:4621-4642 (2020)
  • “Role of chloride cotransporters in the development of spasticity and neuropathic pain after Spinal Cord Injury”
    Côté MP
    In: Neuronal Chloride Transporters in Health and Disease (Tang X, ed), p 650: Elsevier (2020)

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

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Megan Detloff, PhD, Assistant Professor, Department of Neurobiology & Anatomy

Megan Detloff, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8986
215.843.9082 (Fax)
mrd64@drexel.edu
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My research is focused on understanding the molecular underpinnings that contribute to the development of chronic, debilitating neuropathic pain after spinal cord injury. There are two active lines of research ongoing in the lab.

1. Neuroimmune interactions associated with pain development after injury

Traumatic injury to the spinal cord induces a robust immune and inflammatory response at the site of primary injury. Recent evidence from our lab and others suggests that these responses are not limited to the site of injury, but rather extend to remote regions of the spinal cord, brain and dorsal root ganglia. We are focused on understanding how a specific type of immune cells called macrophages interact with pain-sensing neurons after injury to result in their dysfunction.

2. Rehabilitative strategies to prevent or reduce chronic neuropathic pain after injury

Physical therapy and rehabilitation are the standard of care for individuals who have sustained a spinal cord injury. In the lab, we use animal models of both injury and rehabilitation to understand how aerobic, resistance or range-of-motion exercises can induce plasticity or alterations in the anatomical and functional properties of pain sensing neurons.

Visit my website for additional information.

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Kimberly Dougherty, PhD, Associate Professor, Neurobiology & Anatomy

Kimberly Dougherty, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8407
215.843.9082 (fax)
kjd86@drexel.edu
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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 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 by 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 inhibitory interneuronal 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 adult mouse slice preparations. 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.

Recent publications:

  • “Neural interactions within developing rhythmogenic spinal network: Insights from computational modeling”
    Shevtsova NA, Ha NT, Rybak IA, and Dougherty KJ
    Front in Neural Circuits. 14:614615 (2020)
  • “Flexor and extensor ankle afferents broadly innervate locomotor spinal Shox2 neurons and induce similar effects in neonatal mice”
    Li EZ, Garcia-Ramirez DL and Dougherty KJ
    Front Cell Neurosci. 13:452. (2019)
  • “The rhythm section: An update on spinal interneurons setting the beat for mammalian locomotion”
    Dougherty KJ and Ha NT
    Curr Op Physiol. 8:84-93 (2019)
  • “Spinal Shox2 interneuron interconnectivity related to function and development”
    Ha NT and Dougherty KJ
    Elife. 7, pii:e42519 (2018)
  • “Delineating the diversity of spinal interneurons in locomotor circuits”
    Gosgnach S, Bikoff J, Dougherty KJ, El Manira A, Lanuza G and Zhang Y
    J Neurosci. 37(45):10835-10841 (2017)
  • “Anatomical Recruitment of Spinal V2a Interneurons into Phrenic Motor Circuitry after High Cervical Spinal Cord Injury”
    Zholudeva LV, Karliner JS, Dougherty KJ and Lane MA
    J Neurotrauma. 34(21):3058-3065 (2017)
  • “Spinal Hb9::Cre-derived excitatory interneurons contribute to rhythm generation in the mouse”
    Caldeira V, Dougherty KJ#, Borgius L and Kiehn O#
    Sci Rep. 7:41369. #Co-Corresponding authors (2017)
  • “Organization of the mammalian locomotor CPG: Review of computation model and circuit architectures based on genetically identified spinal interneurons”
    Rybak IA, Dougherty KJ, and Shevtsova NA
    eNeuro. 2(5): pii: ENEURO.0069-15.2015 (2015)
  • “Peeling back the layers of locomotor control in the spinal cord”
    McLean DL and Dougherty KJ
    Curr Opin Neurobiol. 33, 63-70 (2015)
  • “Locomotor rhythm generation linked to the output of spinal Shox2 excitatory interneurons”
    Dougherty KJ, Zagoraiou L, Satoh D, Rozani I, Doobar S, Arber S, Jessell TM and Kiehn O
    Neuron. 80, 920-933 (2013)

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

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

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

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Simon Giszter, PhD, Professor, Neurobiology & Anatomy

Simon Giszter, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8412
215.843.9082 (fax)
sg33@drexel.edu
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The lab is focused on motor control, neuroengineering, neurorobotic and neuroprosthetic approaches to understanding spinal and cortical function and recovery of function, especially after SCI. The lab specializes in the study of modularity and biological motor primitives (muscle synergies) in movement control and learning.

Modularity of representation in biological motor control is an important feature of movement, likely representing evolutionary timescale tuning of the neural networks in the CNS and especially the spinal cord. Understanding biological motor modularity may thus supplement information on movement control networks that arises from the theoretical or simulation work, e.g., with deep learning in robotics systems. The biological modularity shows the effects of 'big data' accumulated on geologic timescales, through evolution.

We seek to understand and modulate these systems after injury and in intact conditions using spinal microelectrode systems for neural interfaces. These are customized and designed in-house. We are using braided constructions to build ultrafine and flexible neuroprosthetics. As such, our textile and braid inspired designs link conceptually to the efforts in Advanced Functional Fabrics of America and the Center for Functional Fabrics at Drexel. Our lab has developed tools to construct our electrodes that are completely novel, and has gained and licensed patents for these construction tools and methods. We believe these may help in next-generation prosthetics and neural interfaces. In particular, in addition to spinal recording and stimulation applications, we are exploring applications to single motor unit recordings in electromyography for both research and clinical electrodiagnostic and therapeutic applications.

Using our methods and tools we have made substantial contributions to understanding and assisting recovery of function after SCI in animal model systems, including enhancing both cortical and spinal function and motor contributions. Currently, through a collaboration with the laboratory of Dr. Kim Dougherty we are exploring the interactions of viral treatments to deliver brain-derived neurotrophic factor to the injured spinal cord with epidural stimulation to activate the injured spinal cord. These effects are being jointly examined in the mouse and rat models. We have found important interactions of impact on our understanding of post-injury plasticity and the rehabilitation of the injured spinal cord systems. Finally, we are also examining the effects of optogenetically enhancing motor cortical function in the spinal cord injured rat, again with substantial outcome effects. The cortical changes associated with successful rehabilitation and with optogenetic enhancements are being investigated in different rehabilitation regimes and associated with the outcomes.

Training opportunities exist in all these research areas, spanning from basic motor control to recovery of function and corticospinal plasticity in the context of regeneration.

Example laboratory literature:

  • “Highly Flexible Precisely Braided Multielectrode Probes and Combinatorics for Future Neuroprostheses”
    Kim T, Schmidt K, Deemie C, Wycech J, Liang H, Giszter SF
    Front Neurosci. 2019 Jun 18;13:613. doi: 10.3389/fnins.2019.00613. eCollection 2019. (2019)
  • “Motor primitives are determined in early development and are then robustly conserved into adulthood”
    Yang Q, Logan D, Giszter SF
    Proc Natl Acad Sci U S A. 2019 Jun 11;116(24):12025-12034. doi: 10.1073/pnas.1821455116. Epub 2019 May 28. (2019)
  • “Precise Tubular Braid Structures of Ultrafine Microwires as Neural Probes: Significantly Reduced Chronic Immune Response and Greater Local Neural Survival in Rat Cortex”
    Kim T, Zhong Y, Giszter SF
    IEEE Trans Neural Syst Rehabil Eng. 2019 May;27(5):846-856. doi: 10.1109/TNSRE.2019.2911912. Epub 2019 Apr 18. (2019)
  • “Teaching Adult Rats Spinalized as Neonates to Walk Using Trunk Robotic Rehabilitation: Elements of Success, Failure, and Dependence”
    Udoekwere UI, Oza CS, Giszter SF
    J Neurosci. 2016 Aug 10;36(32):8341-55. doi: 10.1523/JNEUROSCI.2435-14.2016. (2016)
  • “Motor primitives--new data and future questions”
    Giszter SF
    Curr Opin Neurobiol. 2015 Aug;33:156-65. doi: 10.1016/j.conb.2015.04.004. Epub 2015 Apr 22. Review. (2015)
  • US Patent US8639311B2: Sensing probe comprising multiple, spatially separate, sensing sites. Jan 28, 2014
  • US Patent US8534176B2: Method and Apparatus for braiding microstrands. Sept 17, 2013

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Michael Lane, PhD, Associate Professor, Neurobiology & Anatomy

Michael Lane, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8892
215.843.9082 (fax)
mal395@drexel.edu
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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 University College of Medicine 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 on 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.’ They are 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 exploring 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.

Publications:

  • “Spinal interneurons as gatekeepers to neuroplasticity after injury or disease”
    Zholudeva LV, Abraira V, Satkunendrarajah K, McDevitt TC, Goulding MD, Magnuson DK, Lane MA
    Journal of Neuroscience (invited). [PMID: XXXX] Citations: XX; Impact Factor: 6.074 (present) (2021)
  • “Transplanting neural progenitor cells to restore connectivity after spinal cord injury”
    Fischer I, Dulin J, Lane MA
    Nature Reviews Neuroscience (invited), 21(7): 366-383 [PMID: 30520996] Citations: 1; Impact Factor: 33.162 (present) (2020)
  • “Forelimb muscle plasticity following unilateral cervical spinal cord injury”
    Gonzalez-Rothi EJ, Armstrong GT, Cerreta AJ, Fitzpatrick GM, Reier PJ, Lane MA, Judge AR, Fuller DD
    Muscle Nerve, 53(3): 475-478 [PMID: 26662579] Citations: 2; Impact Factor: 2.605 (publication date) / 2.605 (present) (2016)
  • “Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury”
    Lee K-Z, Dougherty BJ, Sandhu MS, Lane MA, Reier PJ, Fuller DD
    Experimental Neurology, 249: 20-32 [PMID: 23954215] Citations: 27; Impact Factor: 4.617 (publication date) / 4.562 (present) (2013)
  • “Spinal respiratory motoneuron anatomy”
    Lane MA
    Respiratory Physiology and Neurobiology, 179: 3-13 – Invited Review [PMID: 21782981] Citations: 62; Impact Factor 2.382 (publication date) / 1.582 (present) (2011)

See my website for additional information.

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

Ramesh Raghupathi, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8405
215.843.9082 (fax)
rr79@drexel.edu
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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 quality of life and currently have no therapies. The economic costs of traumatic brain injuries, which include hospitalization, health care and lost work hours, are estimated at almost $35 billion. This problem has become particularly relevant in the past four years, with the 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. behavioral modifications such as enriched environments and treadmill stepping, to improve cognitive and motor function;
  3. 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 TBI 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; cryoplane microscopy for imaging from the micro- to the macro-scale.

See my website for additional information.

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Ilya Rybak, PhD, Professor, Neurobiology & Anatomy

Ilya Rybak, PhD
Department of Neurobiology & Anatomy
Drexel University
2900 W. Queen Lane
Philadelphia, PA 19129
215.991.8596
215.843.9082 (fax)
iar22@drexel.edu
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I have a broad background in neuroscience, computational and mathematical modeling of biological neurons, neural networks and neural systems. The goal of my 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, and how these mechanisms change following different motor disorders and injuries and during recovery. I perform these studies in close interactive collaboration with leading researchers conducting complementary experimental investigations. For the past 20 years, my studies focused on the investigation and computational modeling of neural circuits in the mammalian brainstem and spinal cord responsible for neural control of respiration and locomotion. Working in collaboration with leading respiratory physiologists (Jeffrey Smith, NINDS; Julian Paton, Bristol University, U.K.; Diethelm Richter, University of Göttengen, Germany; Thomas Dick, CWRU, and others), I developed the most complicated and realistic computational models describing the respiratory CPG and neural control of respiration from cellular to systems levels. Similarly, in collaboration with several leading physiologists, experts in spinal cord physiology (David McCrea, University of Manitoba, Canada; Ronald Harris Warrick, Cornell University; Frederic Brocard, Marseille University, France; Ole Kiehn, Karolinska Institute, Sweden; Michel Lemay, Drexel University; Boris Prilutsky, Georgia Tech, and others), I developed a series of well-known models of the mammalian spinal circuits, locomotor CPG, and neural control of locomotion.

Representative publications:

  • “Modelling spinal circuitry involved in locomotor pattern generation: insights from deletions during fictive locomotion”
    Rybak IA, Shevtsova NA, Lafreniere-Roula M, McCrea DA
    Journal of Physiology 577:617-639. PMCID: PMC1890439 (2006)
  • “Modelling spinal circuitry involved in locomotor pattern generation: insights from the effects of afferent stimulation”
    Rybak IA, Stecina K, Shevtsova NA, McCrea DA
    Journal of Physiology 577:641-658. PMCID: PMC1890432 (2006)
  • “Spatial organization and state-dependent mechanisms for respiratory rhythm and pattern generation”
    Rybak IA, Abdala APL, Markin SN, Paton JFR, Smith JC
    Progress in Brain Research. 165:201-220. PMCID: PMC2408750 (2007)
  • “Spatial and functional architecture of the mammalian brainstem respiratory network: a hierarchy of three oscillatory mechanisms”
    Smith JC, Abdala APL, Koizumi H, Rybak IA, Paton JFR Journal of Neurophysiology 98: 3370-3387. PMCID: PMC2225347 (2007)
  • “Organization of mammalian locomotor rhythm and pattern generation”
    McCrea DA and Rybak IA
    Brain Research Reviews 57: 134-146. PMCID: PMC2214837 (2008)
  • “Modelling genetic reorganizations in the mouse spinal cord affecting left-right coordination during locomotion”
    Rybak IA, Shevtsova NA, Kiehn O
    Journal of Physiology 591: 5491-5508. PMCID: PMC3853491 (2013)
  • “eNeuro Organization of the mammalian locomotor CPG: review of computational model and circuit architectures based on genetically identified spinal interneurons”
    Rybak IA, Dougherty KJ, Shevtsova NA
    eNeuro 2(5). pii: ENEURO.0069-15.2015. PMCID: PMC4603253. Free PMC Article. (2015)
  • “Organization of left-right coordination of neuronal activity in the mammalian spinal cord: insights from computational modelling”
    Shevtsova NA, Talpalar AE, Markin SN, Harris-Warrick RM, Kiehn O, Rybak IA
    Journal of Physiology 593:2403-2426. PMCID: PMC4461406 (2015)
  • “Computational modeling of spinal circuits controlling limb coordination and gaits in quadrupeds”
    Danner SM, Shevtsova NA, Frigon A, Rybak IA
    Elife. 6. pii: e31050. PMCID: PMC5726855. Free PMC Article (2017)
  • “Computational modeling of brainstem circuits controlling locomotor frequency and gait”
    Ausborn J, Shevtsova NA, Caggiano V, Danner SM, Rybak IA
    Elife. 8: e43587. Free Article (2019)

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Veronica J. Tom, PhD, 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
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Injury to the spinal cord interrupts input to and from the brain. Because adult central nervous system axons fail to fully regenerate following injury, severed axons are permanently disconnected from their target neurons. This results in deficits in voluntary (e.g., walking) and involuntary (e.g., diaphragmatic activity for respiration) motor function, autonomic function (e.g., cardiovascular regulation, bladder function, immunity), and sensation.

The overall goals of the lab are to understand acute and long-term sequelae of spinal cord injury and to build upon these findings to identify potential therapeutic targets that will ultimately help restore function in people living with spinal cord injury.

We study two broad research areas:

1. Promoting axon regeneration

There are several obstacles that impede successful regeneration after a spinal cord injury. Firstly, adult axons have a diminished intrinsic capacity for regenerating. Secondly, a glial scar forms at the injury site. The scar is rich in growth inhibitory molecules that act as chemical barriers to 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 immune suppression, are leading causes of morbidity and mortality for chronically injured individuals. We believe that one of the primary drivers of morbidity and mortality after an SCI is a dysregulated sympathetic nervous system. Neurons that modulate the sympathetic nervous system reside in the spinal cord.

After a severe SCI, there is:

  1. the loss of descending input onto sympathetic preganglionic neurons that regulate autonomic control, and
  2. maladaptive plasticity within the spinal sympathetic reflex circuit.

These injury-induced changes, in toto, have been implicated in secondary complications of SCI, e.g., cardiovascular and immune dysfunction.

We are currently determining:

  1. the mechanisms that drive this maladaptive plasticity of the spinal sympathetic reflex circuit, and
  2. if targeting these mechanisms post-SCI mitigates life-threatening, “secondary” complications of SCI.

Visit my website for additional information.

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The Edward Jekkal Muscular Dystrophy Association Fellowship Application Procedures

Purpose

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 research project should be in an area consistent with the objectives of the Muscular Dystrophy Association, including muscle and motoneuron disorders, muscle structure and physiology, motor control, injury and paralysis.

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 1, 2021. No late submissions or submissions sent by facsimile will be accepted.

Download the application form:

Review Considerations

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

  • 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

Section I

Face Page

Self explanatory. If there will be multiple sponsors, list the primary one here. The earliest possible start date for the fellowship is July 1, 2021.

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.

  1. Specific Aims – State the specific purposes of the research proposal and the hypothesis to be tested.
  2. 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.
  3. 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.
  4. 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.

Instructions for Submission of References

Applications will not be reviewed unless at least two references are received with the application, either as sealed letters 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 materials by May 1, 2021:

  • A PDF version submitted to: kg35@drexel.edu. Note that the pages must be assembled in the order specified in the table of contents.
  • At least two letters of reference in sealed envelopes or as PDF files with electronic signatures submitted to kg35@drexel.edu.

 
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Enlarged neuronet, glassy texture.