A5044037694- Traumatic Brain Injury and Neurovascular Disturbances
- Herpesvirus Infections and Treatments
- Cytomegalovirus and herpesvirus research
- Traumatic Brain Injury Research
- Anesthesia and Neurotoxicity Research
- RNA regulation and disease
- Virus-based gene therapy research
- Poxvirus research and outbreaks
- Healthcare Systems and Public Health
- Primary Care and Health Outcomes
- Electrolyte and hormonal disorders
- Neonatal and fetal brain pathology
- Tryptophan and brain disorders
- Cerebrospinal fluid and hydrocephalus
- Functional Brain Connectivity Studies
- Monoclonal and Polyclonal Antibodies Research
Queen's University
2018-2024
Dalhousie University
2023-2024
Traumatic brain injury (TBI) involves an acute (primary damage), which may evolve in the hours to days after impact (secondary damage). Seizures and cortical spreading depolarization (CSD) are metabolically demanding processes that worsen secondary injury. Metabolic stress has been associated with mitochondrial dysfunction, including impaired calcium homeostasis, reduced ATP production, elevated ROS production. However, association between impairment vascular function TBI is poorly...
Cortical spreading depolarization (CSD) is a promising target for neuroprotective therapy in traumatic brain injury (TBI). We explored the effect of NMDA receptor antagonism on electrically triggered CSDs healthy and brain-injured animals. Rats received either one moderate or four daily repetitive mild closed head impacts (rmTBI). Ninety-three animals underwent craniectomy with electrocorticographic (ECoG) local blood flow monitoring. In animals, ketamine memantine inhibited 44 to 88% 50 67%...
It is well established that the herpesvirus nuclear egress complex (NEC) has an intrinsic ability to deform membranes. During viral infection, membrane-deformation activity of NEC must be precisely regulated ensure efficient capsids. One protein known regulate herpes simplex virus type 2 (HSV-2) tegument pUL21. Cells infected with HSV-2 mutant lacking pUL21 (ΔUL21) produced a slower migrating species serine/threonine kinase pUs3 was shown hyperphosphorylated form enzyme. Investigation...
Abstract The multifunctional tegument protein pUL21 of HSV-2 is phosphorylated in infected cells. We have identified two residues the unstructured linker region pUL21, serine 251 and 253, as sites phosphorylation. Both phosphorylation are absent HSV-1 which likely explains why was not detected cells with HSV-1. Cells strain 186 viruses deficient exhibited reductions both cell-cell spread virus infection replication. Defects secondary envelopment cytoplasmic nucleocapsids were also observed...
The multifunctional tegument protein pUL21 of HSV-2 is phosphorylated in infected cells. We have identified two residues the unstructured linker region pUL21, serine 251 and 253, as phosphorylation sites. Both sites are absent HSV-1 which likely explains why was not detected cells with HSV-1. Cells strain 186 viruses deficient exhibited reductions both cell-cell spread virus infection replication. Defects secondary envelopment cytoplasmic nucleocapsids were also observed well multiple...
Abstract It is well established that the herpesvirus nuclear egress complex (NEC) has an intrinsic ability to deform membranes. During viral infection, membrane-deformation activity of NEC must be precisely regulated ensure efficient capsids. One protein known regulate herpes simplex virus type 2 (HSV-2) tegument pUL21. Cells infected with HSV-2 mutant lacking pUL21 (ΔUL21) produced a slower migrating species serine/threonine kinase pUs3 was shown hyperphosphorylated form enzyme....
The following are abstracts from the research competition at 14th annual Canadian Undergraduate Conference on Healthcare. conference was entitled “The Future of Healthcare: A Multidisciplinary Approach,” held Novem-ber 9th-11th, 2018 Queen’s University. Abstracts grouped under categories oral and poster presentations, with sub-categories based general field in which abstract is found. For more information about confer-ence, please go to https://www.cucoh.com/.
INTRODUCTION: Cortical spreading depolarization (CSD) represents a pathomechanistic target for neuroprotective therapy given the association with lesion development and poor outcomes following traumatic brain injury (TBI). METHODS: Experiments were conducted using 9-week-old Sprague Dawley rats. Daily neurobehavioral scores recorded by trained, blinded observers. Using an established weight-drop model, animals received either single moderate (modTBI; n = 23) or four daily mild (rmTBI; 30)...
Abstract Traumatic brain injury (TBI) involves an acute (primary damage), which may evolve in the hours to days after impact (secondary damage). Seizures and cortical spreading depolarization (CSD) are metabolically demanding processes that worsen secondary injury. Metabolic stress has been associated with mitochondrial dysfunction, including impaired calcium homeostasis, reduced ATP production, elevated ROS production. However, association between impairment vascular function TBI is poorly...