Publications by authors named "Jiali Wan"

Article Synopsis
  • Mutations in the GABRG2 gene are linked to refractory epilepsy, and the study investigates the potential of SAHA, an HDAC inhibitor, to alleviate seizures associated with this mutation.
  • Research using a zebrafish model with the human mutant GABRG2(F343L) showed that SAHA reduces seizure onset and neuronal activity while enhancing acetylation levels and decreasing HDAC1/10 expression.
  • SAHA treatment helps restore GABA receptor subunit expression by improving gene transcription and protein trafficking, indicating its dual role in histone and non-histone acetylation may provide a new therapeutic approach for managing refractory epilepsy.
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Gold nanorods are a promising nanoscale material in clinical diagnosis and treatment. The physicochemical properties of GNRs, including size, shape and surface features, are crucial factors affecting their cytotoxicity. In this study, we investigated the effects of different aspect ratios and surface modifications on the cytotoxicity and cellular uptake of GNRs in cultured cells and in mice.

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Background And Purpose: Tetrandrine, a bisbenzylisoquinoline alkaloid isolated from the Chinese medicinal herb Stephaniae tetrandrae, has a long history in Chinese clinical applications to treat diverse diseases. Tetrandrine induced apoptosis or, at low concentrations, autophagy of human hepatocellular carcinoma cells. Here we have tested the effects of inhibitors of autophagy such as chloroquine, on the response to low concentrations of tetrandrine in cancer cells.

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Background And Purpose: Sorafenib, a potent inhibitor that targets several kinases associated with tumourigenesis and cell survival, has been approved for clinical treatment as a single agent. However, combining sorafenib with other agents improves its anti-tumour efficacy in various preclinical tumour models. ABT-263, a second-generation BH3 mimic, binds to the anti-apoptotic family members Bcl-2, Bcl-xL and Bcl-w, and has been demonstrated to enhance TNFSF10 (TRAIL)-induced apoptosis in human hepatocarcinoma cells.

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