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Joel H. Greenberg, Ph.D.


Research Professor of Neurology,
Department of Neurology
School of Medicine
415 Stemmler Hall/6063
(215) 662-6351 FAX: (215) 349-5629
email:   joel@med.upenn.edu

Click here for selected publications since Dr. Greenberg's arrival at Penn



RESEARCH INTERESTS

Cerebrovascular physiology in both normal states and pathophysiological states; positron emission tomography; metabolic tissue changes during cerebral ischemia; activation-flow coupling; functional reorganization following ischemia

RESEARCH TECHNIQUES

Quantitative multiple label autoradiography; local cerebral glucose metabolism; regional blood flow utilizing radio labeled microspheres; positron emission tomography (PET); single photon emission tomography; measurement of nitric oxide in vivo; small animal stroke models;optical imaging of blood flow and oxygen

RESEARCH SUMMARY

Stroke: A crucial factor determining the prognosis of patients in cerebral ischemia is the ability of tissue to recover from biochemical and hemodynamic derangements. We are investigating the factors that contribute to irreversibility of tissue damage in focal cerebral ischemia. Studies are being conducted in cats and rats in which the middle cerebral artery is temporarily occluded. Parameters that are measured include local cerebral glucose metabolism, local cerebral blood flow, tissue metabolites (high energy phosphates) and, tissue nitric oxide concentrations. These parameters are correlated with regional histological damage.

Activity dependent plasticity studies are being undertaken in the rat to examine the effect of somatosensory deafferentation on the relationship between local cerebral blood flow and local cerebral glucose metabolism. Double label autoradiography is being used.

Studies are currently in progress to examine reorganization of the blood flow, metabolic, and functional response following focal cerebral ischemia of the somatosensory cortex of the rat. A novel compression ischemia model has been developed to facilitate these studies.

KEY WORDS:
Cerebral blood flow; cerebral ischemia; glucose metabolism; emission tomography; nitric oxide; reorganization

 
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