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Won-Kyu Ju

Researcher at University of California, San Diego

Publications -  70
Citations -  5543

Won-Kyu Ju is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Retina & Retinal ganglion. The author has an hindex of 37, co-authored 67 publications receiving 5066 citations. Previous affiliations of Won-Kyu Ju include Catholic University of Korea & Washington University in St. Louis.

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Diffusion tensor imaging detects and differentiates axon and myelin degeneration in mouse optic nerve after retinal ischemia.

TL;DR: The hypothesis that lambdaparallel and lambdaperpendicular hold promise as specific markers of axonal and myelin injury, respectively, and, further, that the coexistence of axon andMyelin degeneration does not confound this utility, are supported.
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Correction: Corrigendum: Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration

TL;DR: This Article contains an error in panel C of Figure 4, where “WT” was incorrectly written as “E50K−tg” and the correct Figure 4 appears below as Figure 1.
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Recharacterization of the RGC-5 Retinal Ganglion Cell Line

TL;DR: Investigators using cells designated as RGC-5 should confirm the species to be of rat origin and retinal-specific marker expression before considering their use as retinal ganglion-like cells.
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A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics.

TL;DR: It is demonstrated that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress, and a new vicious cycle involved in neurodegeneration is proposed that includes glutamate excitement, oxidative Stress, and mitochondrial dynamics.
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Oxidative Stress Is an Early Event in Hydrostatic Pressure–Induced Retinal Ganglion Cell Damage

TL;DR: It is demonstrated that oxidative stress is an early event in hydrostatic pressure/IOP-induced neuronal damage and this findings support the view that oxidative damage contributes early to glaucomatous optic neuropathy.