Key Documents
Pak H. Chan
Academic Appointments
- Professor, Neurosurgery
Contact Information
- Academic
Offices
Personal Information Email
Professional Snapshot
Administrative Appointments
- Director of Research, Department of Neurosurgery, Stanford University School of Medicine (1997 - present)
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)
Professional Education
| BS: | Chinese University of Hong Kong, Biology (1964) |
| MA: | UCLA, Biochemistry (1970) |
| PhD: | UCLA, Biology (1972) |
Postdoctoral Advisees
Hai Chen , Gab Seok Kim , Nobuya Okami , Hiroyuki Sakata , Hideyuki Yoshioka
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
- Oxidative stress increases phosphorylation of IkappaB kinase-alpha by enhancing NF-kappaB-inducing kinase after transient focal cerebral ischemia. J Cereb Blood Flow Metab. 2010
- Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia. Biochim Biophys Acta. 2010; (1): 92-9
- Potential role of PUMA in delayed death of hippocampal CA1 neurons after transient global cerebral ischemia. Stroke. 2009; (2): 618-25
- Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival. J Neurochem. 2009: 133-8
- Inhibition of NADPH oxidase is neuroprotective after ischemia-reperfusion. J Cereb Blood Flow Metab. 2009; (7): 1262-72

