Virginia Commonwealth University

Postdoctoral Fellow

Department of Neurology, laboratory of Dr. Laxmikant Deshpande

Senior researcher on DoD funded project investigating Gulf War Illness(GWI)

Virginia Commonwealth University

Research Scientist

Neurotoxicology of nerve gas

Senior scientist investigating molecular mechanisms underlying psychiatric morbidities associated with Gulf War Illness

Virginia Commonwealth University

Research assistant

Laboratory of Dr. Imad Damaj, Department of Pharmacology and Toxicology

Studied effects of nicotine and amphetamines on nicotinic receptors and motor activity in mice

Virginia Commonwealth University

Postdoctoral Research Fellow

Department of Neurology, laboratory of Dr. Robert J. DeLorenzo

Senior member of a multi-disciplinary research team developing a model of organophosphate (OP) exposure that realistically models the acute toxicity and long term effects of nerve gas exposure. The model can be used to rapidly screen newer agents and interventions to improve medical countermeasures against OP exposure and aid in studying the long term toxicity and neurological aspects of such exposure.

Virginia Tech

Assistant Professor and Director of Undergraduate Programs

Kristin worked at Virginia Tech as a Assistant Professor and Director of Undergraduate Programs

Virginia Tech

Behavioral mentor

Virginia Tech Department of Psychology, Dr. Angela Scarpa

Performed cognitive behavioral therapies with a toddler diagnosed with Autism Spectrum Disorder

Virginia Tech

Research assistant, VT Autism Research Team

Lead researcher on a team of undergraduates studying the services needs for autism in the New River Valley region

Responsible for creating a survey that assesses the service needs for Autism Spectrum Disorders in the NRV and administering the survey to family physicians, pediatricians, educators, and parents of children with autism within the NRV

Analyzed the responses and used the information to develop the Virginia Tech Autism Clinic and specialized training within the Clinical Psychology Program

Performed literature reviews and assisted in writing newletters

J Sargeant Reynolds Community College

Adjunct Associate Professor

Teach Anatomy and Physiology I and II (BIO 141, BIO 142) lecture and lab in face-to-face and distance learning settings

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Repeated low-dose organophosphate DFP exposure leads to the development of depression and cognitive impairment in a rat model of Gulf War Illness

Neurotoxicology

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Repeated low-dose organophosphate DFP exposure leads to the development of depression and cognitive impairment in a rat model of Gulf War Illness

Neurotoxicology

Pharmacological blockade of the calcium plateau provides neuroprotection following organophosphate paraoxon induced status epilepticus in rats

Neurotoxicol Tertol

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Repeated low-dose organophosphate DFP exposure leads to the development of depression and cognitive impairment in a rat model of Gulf War Illness

Neurotoxicology

Pharmacological blockade of the calcium plateau provides neuroprotection following organophosphate paraoxon induced status epilepticus in rats

Neurotoxicol Tertol

Hypothermia reduces calcium entry via the N-methyl-D-aspartate and ryanodine receptors in cultured hippocampal neurons

European Journal of Pharmacology

Hypothermia is a powerful neuroprotective method when induced following cardiac arrest, stroke, and traumatic brain injury. The physiological effects of hypothermia are multifaceted and therefore a better knowledge of its therapeutic targets will be central to developing innovative combination therapies to augment the protective benefits of hypothermia. Altered neuronal calcium dynamics have been implicated following stroke, status epilepticus and traumatic brain injury. This study was therefore initiated to evaluate the effect of hypothermia on various modes of calcium entry into a neuron. Here, we utilized various pharmacological agents to stimulate major routes of calcium entry in primary cultured hippocampal neurons. Fluorescent calcium indicator Fura-2AM was used to compare calcium ratio under normothermic (37 °C) and hypothermic (31 °C) conditions. The results of this study indicate that hypothermia preferentially reduces calcium entry through N-methyl-D-aspartate receptors and ryanodine receptors. Hypothermia, on the other hand, did not have a significant effect on calcium entry through the voltage-dependent calcium channels or the inositol tri-phosphate receptors. The ability of hypothermia to selectively affect both N-methyl-D-aspartate receptors and ryanodine receptors-mediated calcium systems makes it an attractive intervention for alleviating calcium elevations that are present following many neurological injuries.

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Repeated low-dose organophosphate DFP exposure leads to the development of depression and cognitive impairment in a rat model of Gulf War Illness

Neurotoxicology

Pharmacological blockade of the calcium plateau provides neuroprotection following organophosphate paraoxon induced status epilepticus in rats

Neurotoxicol Tertol

Hypothermia reduces calcium entry via the N-methyl-D-aspartate and ryanodine receptors in cultured hippocampal neurons

European Journal of Pharmacology

Hypothermia is a powerful neuroprotective method when induced following cardiac arrest, stroke, and traumatic brain injury. The physiological effects of hypothermia are multifaceted and therefore a better knowledge of its therapeutic targets will be central to developing innovative combination therapies to augment the protective benefits of hypothermia. Altered neuronal calcium dynamics have been implicated following stroke, status epilepticus and traumatic brain injury. This study was therefore initiated to evaluate the effect of hypothermia on various modes of calcium entry into a neuron. Here, we utilized various pharmacological agents to stimulate major routes of calcium entry in primary cultured hippocampal neurons. Fluorescent calcium indicator Fura-2AM was used to compare calcium ratio under normothermic (37 °C) and hypothermic (31 °C) conditions. The results of this study indicate that hypothermia preferentially reduces calcium entry through N-methyl-D-aspartate receptors and ryanodine receptors. Hypothermia, on the other hand, did not have a significant effect on calcium entry through the voltage-dependent calcium channels or the inositol tri-phosphate receptors. The ability of hypothermia to selectively affect both N-methyl-D-aspartate receptors and ryanodine receptors-mediated calcium systems makes it an attractive intervention for alleviating calcium elevations that are present following many neurological injuries.

Development of status epilepticus, sustained calcium elevations and neuronal injury in a rat survival model of lethal paraoxon intoxication

Neurotoxicology

Role of the calcium plateau in neuronal injury and behavioral morbidities following organophosphate intoxication

Ann NY Acad Sci

Repeated low-dose organophosphate DFP exposure leads to the development of depression and cognitive impairment in a rat model of Gulf War Illness

Neurotoxicology

Pharmacological blockade of the calcium plateau provides neuroprotection following organophosphate paraoxon induced status epilepticus in rats

Neurotoxicol Tertol

Hypothermia reduces calcium entry via the N-methyl-D-aspartate and ryanodine receptors in cultured hippocampal neurons

European Journal of Pharmacology

Hypothermia is a powerful neuroprotective method when induced following cardiac arrest, stroke, and traumatic brain injury. The physiological effects of hypothermia are multifaceted and therefore a better knowledge of its therapeutic targets will be central to developing innovative combination therapies to augment the protective benefits of hypothermia. Altered neuronal calcium dynamics have been implicated following stroke, status epilepticus and traumatic brain injury. This study was therefore initiated to evaluate the effect of hypothermia on various modes of calcium entry into a neuron. Here, we utilized various pharmacological agents to stimulate major routes of calcium entry in primary cultured hippocampal neurons. Fluorescent calcium indicator Fura-2AM was used to compare calcium ratio under normothermic (37 °C) and hypothermic (31 °C) conditions. The results of this study indicate that hypothermia preferentially reduces calcium entry through N-methyl-D-aspartate receptors and ryanodine receptors. Hypothermia, on the other hand, did not have a significant effect on calcium entry through the voltage-dependent calcium channels or the inositol tri-phosphate receptors. The ability of hypothermia to selectively affect both N-methyl-D-aspartate receptors and ryanodine receptors-mediated calcium systems makes it an attractive intervention for alleviating calcium elevations that are present following many neurological injuries.

Development of status epilepticus, sustained calcium elevations and neuronal injury in a rat survival model of lethal paraoxon intoxication

Neurotoxicology

Chronic behavioral and cognitive deficits in a rat survival model of paraoxon toxicity

Neurotoxicology