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Full-Text Articles in Neurosciences
The Effects Of Vagus Nerve Stimulation On Neuroinflammation In Epilepsy, Elizabeth A. St. Clair, Gabriel O Albors, Pedro Irazoqui Dr., Amy Brewster
The Effects Of Vagus Nerve Stimulation On Neuroinflammation In Epilepsy, Elizabeth A. St. Clair, Gabriel O Albors, Pedro Irazoqui Dr., Amy Brewster
The Summer Undergraduate Research Fellowship (SURF) Symposium
Epilepsy is a neurological disorder characterized by chronic, unexplainable seizures. Recurring epileptic seizures are associated with long-term structural damage and cognitive deficits, and can even lead to sudden, unexplainable death. Approximately 30% of epilepsy cases are not responsive to medication. Epileptic seizures often induce inflammation in the brain and may increase the frequency of future seizures, resulting in a detrimental cycle. Vagus nerve stimulation (VNS) is a non-pharmaceutical treatment method for epilepsy that has been shown to reduce inflammation in peripheral pathways. The role of VNS in the modulation of neuroinflammation has yet to be demonstrated experimentally. To explore this, …
Mitochondria-Associated Micrornas In Rat Hippocampus Following Traumatic Brain Injury, Wang-Xia Wang, Nishant P. Visavadiya, Jignesh D. Pandya, Peter T. Nelson, Patrick G. Sullivan, Joe E. Springer
Mitochondria-Associated Micrornas In Rat Hippocampus Following Traumatic Brain Injury, Wang-Xia Wang, Nishant P. Visavadiya, Jignesh D. Pandya, Peter T. Nelson, Patrick G. Sullivan, Joe E. Springer
Sanders-Brown Center on Aging Faculty Publications
Traumatic brain injury (TBI) is a major cause of death and disability. However, the molecular events contributing to the pathogenesis are not well understood. Mitochondria serve as the powerhouse of cells, respond to cellular demands and stressors, and play an essential role in cell signaling, differentiation, and survival. There is clear evidence of compromised mitochondrial function following TBI; however, the underlying mechanisms and consequences are not clear. MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression post-transcriptionally, and function as important mediators of neuronal development, synaptic plasticity, and neurodegeneration. Several miRNAs show altered expression following TBI; however, the …
Neuroinflammatory Alterations Via Cd-36 In Traumatic Brain Injury, Diana G. Hernandez-Ontiveros
Neuroinflammatory Alterations Via Cd-36 In Traumatic Brain Injury, Diana G. Hernandez-Ontiveros
USF Tampa Graduate Theses and Dissertations
Traumatic brain injury (TBI) has become an increasingly unmet clinical need due to intense military conflicts worldwide. Directly impacted brain cells suffer massive death, with neighboring cells succumbing to progressive neurodegeneration accompanied by inflammatory and other secondary cell death events. Subsequent neurodegenerative events may extend to normal areas beyond the core of injury, thereby exacerbating the central nervous system’s inflammatory response to TBI. Recently CD-36 (cluster of differentiation 36/fatty acid translocase (FAT), a class B scavenger receptor of modified low-density lipoproteins (mLDLs) in macrophages, has been implicated in lipid metabolism, atherosclerosis, oxidative stress, and tissue injury in cerebral ischemia, and …