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About the CFS Research Center at Stanford University
The vision of the Chronic Fatigue Syndrome Research Center at Stanford (CFSRC) is to discover a molecular diagnosis, causes, and a cure for CFS. The research will be directed by Dr. Ronald W. Davis, PhD, Professor of Biochemistry and Genetics and Director of the Stanford Genome Technology Center. He does cutting edge, innovative, interdisciplinary research and technology development on cancer, immunology, genetics, infectious disease, novel drug development, and nanofabrication of diagnostic instrumentation. He won the Gruber Prize in Genetics in 2011 ( CFSRC operates within the Stanford Genome Technology Center. The scientists work in collaboration with scientists and doctors from many disciplines, from all over the world. Similarly, for research on CFS, the plan is to recruit world class scientists and doctors with different specialties for collaborations or to fund their independent work. Dr. Davis and his team are already closely collaborating with AndreasKogelnik, M.D., at the Open Medicine Institute and Jose Montoya, M.D. at Stanford.This disease affects many systems of the human body, requiring a diversity of knowledge to unlock its secrets. Increasing the diversity of specialties of the researchers will mean that all aspects of this disease are considered in our effort to understand CFS at the molecular level, not just the “symptom” level. Thus, the Center will increase the participation of the mainstream scientific community in CFS. Involving well known prestigious university and research institute scientists with a track record of government funding will not only impact CFS directly by generating new knowledge, but will also have a ripple effect in generating awareness and legitimacy for this devastating disease. This kind of research will employ a collaborative, multi-disciplinary approach, which will investigate all aspects of CFS in a comprehensive manner. Dr. Ronald W. Davis, who already has demonstrated success in this approach, is uniquely positioned to spearhead this attack on CFS at the molecular level.