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V. Wee Yong

Researcher at University of Calgary

Publications -  276
Citations -  21024

V. Wee Yong is an academic researcher from University of Calgary. The author has contributed to research in topics: Multiple sclerosis & Microglia. The author has an hindex of 73, co-authored 233 publications receiving 17556 citations. Previous affiliations of V. Wee Yong include Allen Institute for Brain Science & Foothills Medical Centre.

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Vulnerability of Human Neurons to T Cell-Mediated Cytotoxicity

TL;DR: It is reported that polyclonally activated T cells align along axons and soma of cultured human neurons leading to substantial neuronal death, demonstrating for the first time the high and selective vulnerability of human neurons to T cells, and suggesting that when enoughactivated T cells accumulate in the CNS, neuronal cytotoxicity can result through Ag-independent non-MHC class I mechanisms.
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Central Nervous System-Initiated Inflammation and Neurotrophism in Trauma: IL-1β Is Required for the Production of Ciliary Neurotrophic Factor

TL;DR: These findings provide the first evidence of the requirement for IL-1β in the production of CNTF following CNS trauma, and suggest that inflammation can have a beneficial impact on the regenerative capacity of the CNS.
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The Benefits and Detriments of Macrophages/Microglia in Models of Multiple Sclerosis

TL;DR: The evidence supporting the detrimental and beneficial aspects of macrophages/microglia in models of MS are discussed, a discussion of the mechanisms underlying the dichotomous roles are provided, and a few therapies in clinical use in MS are described that impinge on the activity of macophages/ microglia.
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Interleukin-1 is a key regulator of matrix metalloproteinase-9 expression in human neurons in culture and following mouse brain trauma in vivo

TL;DR: The results implicate IL‐1β as a key regulator of neuronal M MP‐9 in culture and of the elevation of MMP‐9 that occurs following mouse CNS trauma.
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Remyelination therapies: a new direction and challenge in multiple sclerosis

TL;DR: New strategies to improve remyelination in preclinical models are addressed, the therapies that are currently undergoing clinical trials are highlighted and the challenges of objectively measuring remyELination in trials of repair in multiple sclerosis are discussed.