Pak H. Chan
Academic Appointments
- Professor, Neurosurgery
- Professor (By courtesy), Neurology & Neurological Sciences
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 498-4457
Professional Overview
Administrative Appointments
- Director of Research, Department of Neurosurgery, Stanford University School of Medicine (1997 - 2012)
Honors and Awards
- James R. Doty Professor of Neurosurgery and Neurosciences, Stanford University (2007)
- Mencius Type A & Type B Scholarships, Chinese University of Hong Kong (1960-1961)
- University Scientific Achievement Scholarship, Chinese University of Hong Kong (1962-1963)
- Jacob Javits Neuroscience Investigator Award, National Institutes of Health (1997-2004)
- Bugher Foundation Award, American Heart Association (2001-2004)
- Chairman, 22nd Princeton Conference on Cerebrovascular Disease (2000)
Professional Education
| BS: | Chinese University of Hong Kong, Biology (1964) |
| MA: | UCLA, Biochemistry (1970) |
| PhD: | UCLA, Biology (1972) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
My primary research interest is to understand the molecular and cellular mechanisms of cell death in the CNS following acute injuries such as ischemia and trauma and chronic neurodegenerative diseases. We focus on the role of oxidative stress, mitochondrial dysfunction, DNA damage and repair, various gene expressions (gene family of HSP72, Bcl-2, c-fos and COX-2) and various transcription factors (NF-kappaB, AP1, p53) in the pathogenesis of necrosis and/or apoptosis. Various transgenic and knockout mutant mice of CuZn-superoxide dismutase (SOD1) and mitochondrial manganese SOD (SOD2) have been generated to address the role of superoxide radicals in these cell death processes. In addition, human SOD1 transgenic rats have been established as a model for the study of oxidative mechanisms and acute and chronic CNS injuries. The long-term goal of our research is to derive therapeutic strategies at the cellular and molecular level to ameliorate cell death in CNS injuries.
Publications
- Prevention of JNK phosphorylation as a mechanism for rosiglitazone in neuroprotection after transient cerebral ischemia: activation of dual specificity phosphatase. J Cereb Blood Flow Metab. 2013; (1): 106-14
- Interleukin 6-preconditioned neural stem cells reduce ischaemic injury in stroke mice. Brain. 2012; (Pt 11): 3298-310
- Minocycline-preconditioned neural stem cells enhance neuroprotection after ischemic stroke in rats. J Neurosci. 2012; (10): 3462-73
- Neural stem cells genetically modified to overexpress cu/zn-superoxide dismutase enhance amelioration of ischemic stroke in mice. Stroke. 2012; (9): 2423-9
- Release of mitochondrial apoptogenic factors and cell death are mediated by CK2 and NADPH oxidase. J Cereb Blood Flow Metab. 2012; (4): 720-30
- Consistent injury to medium spiny neurons and white matter in the mouse striatum after prolonged transient global cerebral ischemia. J Neurotrauma. 2011; (4): 649-60
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