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Dawei Wang

Researcher at Harbin Medical University

Publications -  18
Citations -  5208

Dawei Wang is an academic researcher from Harbin Medical University. The author has contributed to research in topics: Reperfusion injury & Cell cycle. The author has an hindex of 12, co-authored 17 publications receiving 4203 citations. Previous affiliations of Dawei Wang include Chinese Academy of Sciences & The Chinese University of Hong Kong.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Gold and iron oxide hybrid nanocomposite materials

TL;DR: Underpinning the fundamental requirements for effectively forming Au-Fe(x)O(y) hybrid nanocomposite materials would shed light on future development of nanotheranostics, nanomedicines, and chemical technologies.
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Enhanced cellular uptake of aminosilane-coated superparamagnetic iron oxide nanoparticles in mammalian cell lines

TL;DR: Wang et al. as discussed by the authors presented Yi-Xiang J Wang and Ken Cham-Fai Leung Institute of Creativity and Department of Chemistry at The Chinese University of Hong Kong, Shatin, NT, Hong Kong.
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Hydroxytyrosol, a natural molecule from olive oil, suppresses the growth of human hepatocellular carcinoma cells via inactivating AKT and nuclear factor-kappa B pathways.

TL;DR: The results show that HT could inhibit proliferation, induce G2/M cell cycle arrest and apoptosis in human HCC cells, and Mechanically, HT could suppress the activation of AKT and nuclear factor-kappa B (NF-κB) pathways.
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The role of AKT1 and autophagy in the protective effect of hydrogen sulphide against hepatic ischemia/reperfusion injury in mice.

TL;DR: H2S protects against hepatocytic A/R and hepatic I/R injuries, at least in part, through AKT1 activation but not autophagy, consequently.