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Youngsook Son

Researcher at Kyung Hee University

Publications -  140
Citations -  2484

Youngsook Son is an academic researcher from Kyung Hee University. The author has contributed to research in topics: Mesenchymal stem cell & Stem cell. The author has an hindex of 25, co-authored 137 publications receiving 2069 citations. Previous affiliations of Youngsook Son include University of Maryland University College & New Generation University College.

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A new role of substance P as an injury-inducible messenger for mobilization of CD29(+) stromal-like cells.

TL;DR: It is shown that substance P is an injury-inducible factor that acts early in the wound healing process to induce CD29+ stromal-like cell mobilization, highlighting a previously undescribed function of substance P as a systemically acting messenger of injury and a mobilizer of CD29-like cells to participate in wound healing.
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Dna damage in the kidneys of diabetic rats exhibiting microalbuminuria

TL;DR: Daily injection of insulin starting on the third day after streptozotocin treatment significantly reduced both urinary albumin excretion and papillary 8-OHdG formation, which suggests that these are associated with the diabetic state induced by streptoocin rather than a direct nephrotoxic effect of the drug.
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Substance P induces M2-type macrophages after spinal cord injury.

TL;DR: Early intervention of the devastating inflammatory response by SP treatment caused the lesion cavity to become filled with robust axonal outgrowth that overlaid the M2 macrophages at 2 weeks and culminated in tissue sparing and improvement in functional recovery from the SCI.
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A neuropeptide, Substance-P, directly induces tissue-repairing M2 like macrophages by activating the PI3K/Akt/mTOR pathway even in the presence of IFNγ

TL;DR: The findings show that Substance-P, a neuropeptide, plays a role as a novel cytokine by inducing tissue-repairing M2SP macrophages and thus may be developed for pharmacological intervention in diseases involving chronic inflammation and acute injury.
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Inhibitory effect of rapamycin on corneal neovascularization in vitro and in vivo.

TL;DR: Rapamycin strongly inhibited HUVEC migration at doses that did not cause cytotoxicity and apoptosis in this in vitro model and suppressed corneal neovascularization, possibly by inhibiting proinflammatory cytokines, as shown by the in vivo study.