Clinical Investigations Section - Division of Intramural Research

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John M. Hallenbeck Image

 John M.  Hallenbeck  M.D., Senior Investigator

Dr. Hallenbeck received his M.D. degree from the University of Pennsylvania. After a medical internship and neurology residency at the University of Michigan, he entered the United States Navy. At the Naval Medical Research Institute his research focused on CNS decompression sickness and air embolism and later the study of inflammatory and immune mechanisms in acute brain ischemia. In 1983, he was appointed Chief of the Navy's neurology training program at the National Naval Medical Center and Professor, Vice-Chairman and Chairman for Research in the Department of Neurology, Uniformed Services University of the Health Sciences. In 1991 he came to the NINDS as Chief of the newly created Stroke Branch. He received the Mihara Cerebrovascular Disorder Research Prize. Dr. Hallenbeck's laboratory is studying the cellular regulation of ischemic tolerance and inflammatory and immune mechanisms in the initiation and progression of stroke.

Laboratory Staff

Yong Chen, M.D., Ph.D. Senior Research Fellow  301-402- 6936
Joelle Hillion, Ph.D. Research Fellow  301-594- 2597
Kachikwu Illoh, M.D. Clinical Fellow  301-594- 2514
Dace Klimanis, M.Sc   301-402- 2338
Yixin Li, Ph.D. Special Expert  301-594- 2579
Shinici Miyake, Ph.D. Postdoctoral Fellow  301-451- 5003
Zurab  Nadareishvili, M.D., Ph.D. Research Fellow  301-594- 2498
Christl Reutzler, B.A. Research Assistant  301-496- 8111
Asako Takanohashi, Ph.D. Postdoctoral Fellow  301-435- 6559
Hideaki Wakita, M.D. Research Fellow  301-435- 7654



Research Interests

The Clinical Investigations Section of the Stroke Branch conducts translational research on stroke prevention and stroke treatment. In spontaneously hypertensive, stroke-prone rats, we are studying ways of preventing development of spontaneous brain infarcts. This work is focused on immunologic approaches that suppress the endothelial activation produced by inflammatory cytokines such as TNF and IL-1. Mucosal tolerization to E-selectin targets immunomodulation to vascular segments that are becoming activated and suppresses spontaneous strokes and hemorrhages. This work is being translated into clinical trials.

Selected Recent Publications

Chen Y Ruetzler C Pandipati S Spatz M McCarron RM Becker K Hallenbeck JM
Mucosal tolerance to E-selectin provides cell-mediated protection against ischemic brain injury.  - Proc Natl Acad Sci U S A   100  15107-12  2003

Dirnagl U Simon RP Hallenbeck JM
Ischemic tolerance and endogenous neuroprotection.  - Trends Neurosci   26  248-54  2003

Hallenbeck JM
The many faces of tumor necrosis factor in stroke - Nature Medicine  8 1363-1368 2002

Ginis I, Jaiswal R, Klimanis D, Liu J, Greenspon J, Hallenbeck JM
TNF-alpha-induced tolerance to ischemic injury involves differential control of NFkappaB transactivation: the role of NFkappaB association with p300 adaptor - J Cereb Blood Flow Metab  22 142-152 2002

Takeda H, Spatz M, Ruetzler C, McCarron R, Becker K, Hallenbeck J
Induction of mucosal tolerance to E-selectin prevents ischemic and hemorrhagic stroke in spontaneously hypertensive genetically stroke-prone rats - Stroke  33 2156-63 2002



Contact Information

Clinical Investigations Section Stroke Branch, NINDS  Building 49, Room 2A10, MSC 4476  49 Convent Drive Bethesda MD  20892-4476

Telephone: 301-496- 6231 (office), 301- 496-6231 (laboratory), 301-402- 2769 (fax), Email: HallenbJ@ninds.nih.gov