S
Swapan K. Ray
Researcher at University of South Carolina
Publications - 226
Citations - 22587
Swapan K. Ray is an academic researcher from University of South Carolina. The author has contributed to research in topics: Apoptosis & Calpain. The author has an hindex of 55, co-authored 221 publications receiving 18632 citations. Previous affiliations of Swapan K. Ray include Brookhaven National Laboratory & Medical University of South Carolina.
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Journal ArticleDOI
Spinal cord injury: a review of current therapy, future treatments, and basic science frontiers.
Abhay K. Varma,Arabinda Das,Gerald C. Wallace,John Barry,Alexey Vertegel,Swapan K. Ray,Naren L. Banik +6 more
TL;DR: This review gives an overview of current basic research and clinical studies for the treatment of SCI and suggests that early treatment may improve neurological recovery.
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Oxidative stress and Ca2+ influx upregulate calpain and induce apoptosis in PC12 cells.
TL;DR: A role for calpain in PCD of PC12 cells due to oxidative stress and Ca2+ influx is suggested and western analysis indicated degradation of 68 kDa neurofilament protein (NFP), a calpain substrate.
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Hippocampal tissue of patients with refractory temporal lobe epilepsy is associated with astrocyte activation, inflammation, and altered expression of channels and receptors
Arabinda Das,Gerald C. Wallace,Casey O. Holmes,Misty L. McDowell,Joshua A. Smith,Jennifer D Marshall,Leonardo Bonilha,Jonathan C. Edwards,Steven S. Glazier,Swapan K. Ray,Naren L. Banik +10 more
TL;DR: In this article, the authors examined resected human hippocampus tissue for a variety of changes including gliosis that might contribute to the development and presentation of temporal lobe epilepsy (TLE) and found that activation of astrocytes was significantly increased in epileptic tissue as compared to corresponding regions of the control group.
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Calpain in the pathophysiology of spinal cord injury: neuroprotection with calpain inhibitors.
TL;DR: Aberrant Ca(2+) homeostasis following SCI inevitably activates calpain, which has been shown to play a crucial role in the pathophysiology of SCI and appears to be a potential therapeutic target in SCI.
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Flavonoids activated caspases for apoptosis in human glioblastoma T98G and U87MG cells but not in human normal astrocytes.
TL;DR: The authors induced apoptosis in human glioblastoma T98G and U87MG cells after treatment with apigenin, (−)‐epigallocatechin, (−]‐epigenin‐3‐gallate (EGCG), and genistein, which did not induce apoptotic in human normal astrocytes.