A5026882540- Neuroinflammation and Neurodegeneration Mechanisms
- Immune Response and Inflammation
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Vagus Nerve Stimulation Research
- Medicinal Plants and Bioactive Compounds
- Blood Coagulation and Thrombosis Mechanisms
- Cellular transport and secretion
- Alzheimer's disease research and treatments
- Tryptophan and brain disorders
- Signaling Pathways in Disease
- Medicinal Plants and Neuroprotection
- Protease and Inhibitor Mechanisms
- Acute Ischemic Stroke Management
- Protein Degradation and Inhibitors
- Biotin and Related Studies
- Pharmacological Effects of Natural Compounds
- Inflammasome and immune disorders
- S100 Proteins and Annexins
National University of Singapore
2015-2021
The University of Queensland
2012-2016
Ischemic stroke causes a high rate of deaths and permanent neurological damage in survivors. triggers the release damage-associated molecular patterns (DAMPs) such as high-mobility group box 1 (HMGB1), which activate toll-like receptors (TLRs) receptor for advanced glycation endproducts (RAGE) affected area, leading to an exaggerated inflammatory response cell death. Both TLRs RAGE are transmembrane pattern recognition (PRRs) that have been shown contribute ischemic stroke-induced brain...
Intravenous immunoglobulin (IVIg) preparations obtained by fractionating blood plasma, are increasingly being used as an effective therapeutic agent in treatment of several inflammatory diseases. Its use a potential for stroke and Alzheimer's disease has been proposed, but little is known about the neuroprotective mechanisms IVIg. In this study, we investigated effect IVIg on downstream signaling pathways that involved neuronal cell death experimental models disease. Treatment cultured...
Glioblastoma (GBM) is a uniformly lethal disease driven by glioma stem cells (GSCs). Here, we use chemical biology approach to unveil previously unknown GBM dependencies. By studying sulconazole (SN) with anti-GSC properties, find that SN disrupts biotin distribution the carboxylases and histones. Transcriptomic metabolomic analyses of SN-treated GSCs reveal metabolic alterations are characteristic biotin-deficient cells, including intracellular cholesterol depletion, impairment oxidative...