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Lei Wei

Researcher at Wuhan University

Publications -  320
Citations -  13830

Lei Wei is an academic researcher from Wuhan University. The author has contributed to research in topics: Cartilage & Osteoarthritis. The author has an hindex of 57, co-authored 304 publications receiving 11840 citations. Previous affiliations of Lei Wei include Rhode Island Hospital & Brown University.

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Effect of Cadmium on Cellular Ultrastructure in Mouse Ovary.

TL;DR: The findings elucidated the morphological mechanism that the exposure of cadmium changed the ultrastructure of cells in ovary tissues and clarified the cytotoxicity and pathological effects of Cadmium on the ovary.
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Correlation of insulin-like growth factor 1 and osteoarthritic cartilage degradation: a spontaneous osteoarthritis in guinea-pig.

TL;DR: The decreased level of IGF-1 may play a critical role for maintaining the balance between catabolic and anabolic processes in cartilage metabolism during the development of osteoarthritis, which may be applicable to developing OA therapy.
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MAGI2-AS3 inhibits breast cancer by downregulating DNA methylation of MAGI2

TL;DR: Gene structure and DNA methylation analysis results indicated that MAGI2‐AS3 may act as a cis‐acting regulatory element downregulating theDNA methylation level of the MAGI 2 promoter region, and the DNA demethylase TET1 inhibitor can reverse MAGI1‐ AS3 overexpression caused upregulation of MAGI3 and cellular effects.
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Enhancing Beta-Catenin Activity via GSK3beta Inhibition Protects PC12 Cells against Rotenone Toxicity through Nurr1 Induction

TL;DR: The data suggested that Wnt/β-catenin and Nurr1 are crucial factors in the survival of DA neurons, and the activation of Wnt-β-Catenin pathway exerts protective effects on DA neurons partly by mean of a co-active pattern with Nurr 1.
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Exendin-4 induces myocardial protection through MKK3 and Akt-1 in infarcted hearts

TL;DR: Results reveal that exendin-4 treatment improves cardiac function, attenuates cardiac remodeling, and promotes angiogenesis in the infarcted myocardium through MKK3 and Akt-1 pathway.