S. Scott Panter
University of California, San Francisco
44 Papers
633 Citations
S. Scott Panter is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Heme oxygenase & Traumatic brain injury. The author has an hindex of 29, co-authored 44 publications. Previous affiliations of S. Scott Panter include University of California, Los Angeles & United States Department of Veterans Affairs.
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Papers
The role of excitatory amino acids and NMDA receptors in traumatic brain injury.
TL;DR: Brain injury induced by fluid percussion in rats caused a marked elevation in extracellular glutamate and aspartate adjacent to the trauma site, which contributes to delayed tissue damage after brain trauma.
1.5K
Alteration in extracellular amino acids after traumatic spinal cord injury.
TL;DR: The hypothesis that excitatory amino acids may contribute to delayed tissue injury after central nervous system trauma is consistent with the hypothesis that they limit tissue damage after spinal cord trauma.
296
Intranasal deferoxamine provides increased brain exposure and significant protection in rat ischemic stroke.
Leah R. Hanson,Annina Roeytenberg,Paula M. Martinez,Valerie G. Coppes,Donald C. Sweet,Reshma J. Rao,Dianne L. Marti,John D. Hoekman,Rachel B. Matthews,William H. Frey,S. Scott Panter +10 more
TL;DR: These experiments suggest that intranasally administered DFO may be a useful treatment for stroke, and a prophylactic for patients at high risk for stroke.
217
Neurotoxicity of hemoglobin in cortical cell culture.
Raymond F. Regan,S. Scott Panter +1 more
TL;DR: The results of these experiments suggest that, in this system, Hb is a potent neurotoxin, and that Hb neurotoxicity may contribute to secondary injury processes after trauma and intracranial hemorrhage.
186
Heme-oxygenase-1 induction in glia throughout rat brain following experimental subarachnoid hemorrhage.
Paul G. Matz,Christopher P. Turner,Philip Weinstein,Stephen M. Massa,S. Scott Panter,Frank R. Sharp +5 more
TL;DR: The results suggest that HO-1 is induced in microglia throughout rat brain as a general, parenchymal response to the presence of oxyhemoglobin in the subarachnoid space and not as a stress response, which could be protective against the lipid peroxidation and vasospasm induced by hemoglobin.
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