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Victor Y. L. Leung

Researcher at University of Hong Kong

Publications -  58
Citations -  3154

Victor Y. L. Leung is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Intervertebral disc & Mesenchymal stem cell. The author has an hindex of 25, co-authored 51 publications receiving 2542 citations. Previous affiliations of Victor Y. L. Leung include Li Ka Shing Faculty of Medicine, University of Hong Kong & Hospital Authority.

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Concise review: the surface markers and identity of human mesenchymal stem cells.

TL;DR: The reported expression of surface molecules in MSCs from various sources are revisited, aiming to assess their potential as MSC markers and define the critical panel for future investigation.
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Regeneration of intervertebral disc by mesenchymal stem cells: potentials, limitations, and future direction

TL;DR: The state-of-the-art in the field of stem cell regeneration of the intervertebral disc is examined, and critically discusses, with scientific support, the issues involved, before stem cells could be used in human subjects.
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SOX9 governs differentiation stage-specific gene expression in growth plate chondrocytes via direct concomitant transactivation and repression.

TL;DR: A regulatory paradigm whereby direct concomitant positive and negative transcriptional control by SOX9 ensures differentiation phase-specific gene expression in chondrocytes is proposed.
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The effects of microenvironment in mesenchymal stem cell–based regeneration of intervertebral disc

TL;DR: This review majorly examines how resident disc cells, hypoxia, low nutrition, acidic pH, mechanical loading, endogenous proteinases, and cytokines regulate the behavior of the exogenous MSCs in the hostile microenvironment of the degenerated IVD.
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Mesenchymal Stem Cells Arrest Intervertebral Disc Degeneration Through Chondrocytic Differentiation and Stimulation of Endogenous Cells

TL;DR: It is shown that the BMSC could arrest the degeneration of the murine notochordal NP and contribute to the augmentation of the ECM in the NP by both autonomous differentiation and stimulatory action on endogenous cells.