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J. Travis Parsons,
Ph.D.
Research Associate
Neurology |
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Jonathan Kurz
M.D., Ph.D. Candidate |
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Anh Lee,
Laboratory Specialist
Neurology |
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Matt Ryan, Laboratory
Specialist
Neurology |
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Amanda Winebrenner
Labortory Specialist |
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Bill Holbert, Graduate
Student
Pharmacology and Toxicology |
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Mike Singleton, Graduate
Student
Anatomy and Neurobiology
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Annu Rana,
MS 2002, Physiology
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Kate Fancher
A.D., Williams Scholar, Medical Student |
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Jasmine Awad
Student Worker/Surgeon
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Research
Projects
Ongoing
Grants: |
Molecular
Mechanisms of Receptor Function in SE.
Principal Investigator:
Severn B. Churn, Ph.D.
Agency: National Institutes of Health/NINDS
Type: RO1 (NS39970-01), Project Dates 12-01-2001 to
12-31-2007.
The long term objective of this
research project is to understand the regulation of
neuronal receptors and to understand the long-lasting
alteration of receptor regulation following Status Epilepticus.
Recent studies have focuses on the NMDA receptor-dependent
influx of Ca2+ and alteration of Ca2+ regulated phosphorylation
and systems. |
SE
Duration-dependent Modulation of GABAAR Receptor Function.
Project 4, Medical
College of Virginia Epilepsy Research Center. Robert
J. DeLorenzo, MD, PhD, MPH. Program Director.
Principal Investigator: Severn B. Churn, Ph.D.
Agency: National Institutes of Health/NINDS
Type: PO1 (NS25630, Years 11-15) Period: 1/1/2000 to
12/31/2004.
The long term objective of this
research project is to investigate the mechanisms for
the development of drug resistance in Status Epilepticus.
Recent studies indicate that specific neurotransmitter
receptors are down-regulated or inhibited by continued
Status Epilepticus in the acute phase during the seizures
and acutely following the seizures. This project will
investigate the molecular mechanism underlying these
acute changes due to Status Epilepticus. |
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Pathological
Up-regulation of Neuronal Calcineurin in SE.
Principal Investigator:
Severn B. Churn, Ph.D.
Agency: Jeffries Memorial Trust
Type: Agency Grant-in-Aid.
The overall goal of this research
project is to characterize the increase in calcium-dependent
and calcium-independent calcineurin activity following
SE. |
Status Epiepticus-Induced Alteration of Basal Calcium Homeostatic Mechanisms.
Principal Investigators: Severn B. Churn, Ph.D./ J. Travis Parsons, Ph.D. Agency: Epilepsy Foundation of America Type: Mentored Grant-in-Aid
The overall objective of this project is to characterized the mechanisms, including intracellular sequestration, whereby prolonged Status Epilepticus results in altered intracellular, baseline calcium levels. |
Bilirubin
Toxicity in the Auditory System.
Principal Investigator:
Steven M. Shapiro, MD.
Role on Project: Co-Investigator
Agency: NIH/NIDCD
Type: RO1 (DC000369, Years 1-5) Period: 09/01/98 to
08/31/02
The long-term objective of this
project is to take the molecular approach in understanding
the mechanisms mediating bilirubin toxicity in brain.
The project investigates the effect of bilirubin on
second messenger systems and ion channels in isolated
hippocampal neurons. Sophisticated electrophysiological
and molecular biological techniques are used to probe
the molecular mechanisms involved in this important
brain injury mechanism. |
Traumatic
Brain Injury and GABA Receptor Function.
Principal Investigator:
Robert J. Hamm, Ph.D.
Role on Project: Co-Investigator
Agency: National Institutes of Health/NINDS
Type: RO1
The long-range objectives of this
project are to expand our understanding of ionic dysfunction
that follows brain injury by examining the vital role
of inhibitory processes in the injury pathology. In
addition, this research project will provide important
new information for the potential clinical application
of innovative pharmacological therapies for human head
injury. |
Molecular
Mechanisms of Neuronal Excitability and Epilepsy
Principal Investigator:
Robert J. DeLorenzo, MD, PhD, MPH.
Role on Project: Co-Investigator
Agency: National Institutes of Health/NINDS
Type: RO1 (NS23350, Years 14-19)
Studies in three models of epileptogenesis
are focused on evaluating the effects of NMDA receptor-activated
calcium entry on long-term changes in transcription
factor expression and their relationship to decreased
GABAAR gene expression and function. This research project
was awarded a Jacob Javits Scholar award. RO1- NS 23350. |
Completed
Studies:
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Markel Alzheimer's
Research Award
Principal Investigator:
Robert J. DeLorenzo, MD, PhD, MPH.
Role on Project: Co-Investigator, 1/1/98 to 2002.
Understanding the cellular and
molecular mechanisms which underlie the accelerated
neuronal loss observed in Alzheimer's Disease.
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Medical College of Virginia Epilepsy Research Program Project.
Robert J. DeLorenzo, MD, PhD, MPH. Program Director. Principal Investigator: Robert J. DeLorenzo, MD, PhD, MPH. Role on Project: Co-Investigator, Core D, Clinical Research Section Medical College of Virginia Epilepsy Research Center, 1/1/94 to 12/31/98. |
Molecular Mechanisms of Neurotrauma.
Principal Investigators: Severn B. Churn, Ph.D. Agency: A.D. Williams Internal Research Grant 1996 - 1997 |
Topiramate
restores drug efficacy in refractory status epilepticus.
Principal Investigator:
Severn B. Churn, Ph.D.
Agency: R.W. Johnson Pharmaceutical Research Institute
Type: Extramural Private Funding.
This project grew from the
clinical observation that Topomax may restore the ability
to terminate seizure activity in otherwise refractory patients.
The aim of this project is the characterize the mechanisms
whereby Topomax works to restore drug efficacy in refractory
SE and to establish a new indication for Topomax in treating
refractory SE. 2001-2003.
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