Affiliation: The Hebrew University
- Cytokine production in the brain following closed head injury: dexanabinol (HU-211) is a novel TNF-alpha inhibitor and an effective neuroprotectantE Shohami
Department of Pharmacology, Hebrew University, School of Pharmacy, Jerusalem, Israel
J Neuroimmunol 72:169-77. 1997..TNF-alpha modulating agents, if given within the early time window post-injury, may improve the final neurological outcome in victims of brain trauma...
- Dexanabinol; a novel neuroprotective drug in experimental focal cerebral ischemiaR R Leker
Department of Neurology, Hebrew University Hadassah Medical School, Jerusalem, Israel
J Neurol Sci 162:114-9. 1999..No effect could be demonstrated on NOS activity. In conclusion, dexanabinol may be a pluripotent cerebroprotective agent...
- Long term cerebroprotective effects of dexanabinol in a model of focal cerebral ischemiaG Lavie
Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hebrew University Hadassah Medical School, Hadassah University Hospital, Ein Kerem, P O Box 12000, 91120, Jerusalem, Israel
Brain Res 901:195-201. 2001..05 for all). In conclusion, the extended therapeutic window and the multi-mechanistic durable neuroprotective effects of dexanabinol make it a promising candidate for future stroke therapy...
- Closed head injury in the rat induces whole body oxidative stress: overall reducing antioxidant profileE Shohami
Department of Pharmacology, Hebrew University of Jerusalem, Israel
J Neurotrauma 16:365-76. 1999..01) even up to 24 h. We conclude that although the injury was delivered over the left cerebral hemisphere, the whole body appeared to be under oxidative stress, within 24 h after brain injury...
- An endogenous cannabinoid (2-AG) is neuroprotective after brain injuryD Panikashvili
Department of Pharmacology, Medical Faculty, Hebrew University, Jerusalem 91120, Israel
Nature 413:527-31. 2001..The beneficial effect of 2-AG was dose-dependently attenuated by SR-141761A, an antagonist of the CB1 cannabinoid receptor...
- Closed head injury increases extracellular levels of antioxidants in rat hippocampus in vivo: an adaptive mechanism?E Moor
Department of Pharmacology, The Hebrew University of Jerusalem, The School of Pharmacy, Hadassah Ein Kerem, Jerusalem 91120, Israel
Neurosci Lett 316:169-72. 2001..Together with previous results, the current findings suggest that ascorbic acid and uric acid are mobilized from brain cells to the extracellular space...
- Erythropoietin is neuroprotective, improves functional recovery, and reduces neuronal apoptosis and inflammation in a rodent model of experimental closed head injuryI Yatsiv
Department of Pharmacology, School of Pharmacy, Hebrew University Hadassah Medical Center, Jerusalem, Israel
FASEB J 19:1701-3. 2005..vehicle-treated animals. We propose that further studies on Epo in TBI should be conducted in order to consider it as a novel therapy for TBI...
- Dual role of tumor necrosis factor alpha in brain injuryE Shohami
Department of Pharmacology, Hebrew University School of Pharmacy, Jerusalem, Israel
Cytokine Growth Factor Rev 10:119-30. 1999..It is suggested that the appropriate context of mediators, at any given time after brain injury may well determine whether the effect of TNF alpha is protective or toxic...
- Subacute treatment with vascular endothelial growth factor after traumatic brain injury increases angiogenesis and gliogenesisO Thau-Zuchman
Department of Neurology and the Peritz and Chantal Scheinberg Cerebrovascular Research Laboratory, Hadassah Hebrew University Medical Center, Jerusalem, Israel
Neuroscience 202:334-41. 2012..However, treated mice had only insignificant motor improvements in this paradigm, suggesting that the bulk of the beneficial effects observed when VEGF is given early after TBI results from the neuroprotective effects...
- Therapeutic effect of dexamethasone in T-2 toxicosisE Shohami
Department of Pharmacology, Hadassah Medical School, Jerusalem, Israel
Pharm Res 4:527-30. 1987..BW 755c had no consistent effect on the survival of rats in T-2 toxicosis. It is suggested that dexamethasone might be a useful therapeutic agent in T-2 toxicosis in animals and humans, but its mechanism of action remains obscure...
- A peptide derived from activity-dependent neuroprotective protein (ADNP) ameliorates injury response in closed head injury in miceL Beni-Adani
Department of Neurosurgery, The Hebrew University Hadassah Medical Center, Jerusalem, Israel
J Pharmacol Exp Ther 296:57-63. 2001..Thus, NAP provides significant amelioration from the complex array of injuries elicited by head trauma...
- Inactivation of PKMζ in the NAc shell abolished cocaine-conditioned rewardD Shabashov
Institute for Drug Research IDR, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel
J Mol Neurosci 47:546-53. 2012....
- Experimental closed head injury in rats: prostaglandin production in a noninjured zoneE Shohami
Department of Pharmacology, Hadassah University Hospital, Jerusalem, Israel
Neurosurgery 22:859-63. 1988..Both PGD2 and PGI2 have protective effects in the brain. We suggest that their endogenous increase may be part of a repair mechanism at the periphery of the injured zone...
- Experimental models of head traumaR R Leker
Department of Neurology, Agnes Ginges Center for Human Neurogenetics, Hebrew University Hadassah Medical School, Hadassah University Hospital, Jerusalem, Israel
Acta Neurochir Suppl 83:49-54. 2002..In order to attain these goals adequate animal models for traumatic brain injury are needed. In the following paper the authors will review the various animal models for head trauma and emphasize their potential strengths and weaknesses...
- Endocannabinoids and traumatic brain injuryR Mechoulam
Department of Medicinal Chemistry and Natural Products, Hebrew University Medical Faculty, Ein Kerem Campus, Jerusalem 91120, Israel
Mol Neurobiol 36:68-74. 2007....
- Rapamycin is a neuroprotective treatment for traumatic brain injuryS Erlich
Department of Neurobiochemistry, Tel Aviv University, Ramat Aviv 69978, Israel
Neurobiol Dis 26:86-93. 2007....
- Endocannabinoids and neuroprotectionR Mechoulam
Department of Medicinal Chemistry and Natural Products, Hebrew University Medical Faculty, Jerusalem 91120, Israel
Sci STKE 2002:re5. 2002..2-AG is also a potent modulator of vascular tone, and counteracts the endothelin (ET-1)-induced vasoconstriction that aggravates brain damage; it may thus help to restore blood supply to the injured brain...
- Antioxidant properties of the vasoactive endocannabinoid, 2-arachidonoyl glycerol (2-AG)R M McCarron
Resuscitative Medicine Department, Naval Medical Research Center, Forest Glen, MD, USA
Acta Neurochir Suppl 86:271-5. 2003..These findings provide evidence of 2-AG antioxidant activity and are consistent with the involvement of ROS in the pathomechanism of CHI-induced BBB injury and brain edema...
- Immunohistochemical characterization of Fas (CD95) and Fas Ligand (FasL/CD95L) expression in the injured brain: relationship with neuronal cell death and inflammatory mediatorsM B Grosjean
Center for Dental and Oral Medicine and Cranio maxillofacial Surgery, University of Zurich, Zurich, Switzerland
Histol Histopathol 22:235-50. 2007..Furthermore, Fas and FasL upregulation seems to be independent of neuroinflammation since no differences were found between cytokine-/- and wild-type mice...
- Endothelial-mediated regulation of cerebral microcirculationR M McCarron
Trauma and Resuscitative Medicine Department, Naval Medical Research Center, Bethesda, MD, USA
J Physiol Pharmacol 57:133-44. 2006....
- Apolipoprotein E4 decreases whereas apolipoprotein E3 increases the level of secreted amyloid precursor protein after closed head injuryY Ezra
Department of Neurobiochemistry, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel
Neuroscience 121:315-25. 2003..Similar isoform-specific interactions between apoE and APP may play a role in the acute, short-term effects of head trauma in humans...
- The nitroxide antioxidant tempol is cerebroprotective against focal cerebral ischemia in spontaneously hypertensive ratsR R Leker
Department of Neurology, Agnes Ginges Center for Human Neurogenetics, Hebrew University Hadassah Medical School, Hadassah University Hospital, Jerusalem 91120, Israel
Exp Neurol 176:355-63. 2002..4 +/- 2.38% hemispheric volume, P = 0.02, respectively). In conclusion, treatment with tempol led to significant motor and behavioral improvement and reduced injured tissue volumes both in the short and in the long term after stroke...
- Experimental closed head injury: analysis of neurological outcome, blood-brain barrier dysfunction, intracranial neutrophil infiltration, and neuronal cell death in mice deficient in genes for pro-inflammatory cytokinesP F Stahel
Department of Surgery, University Hospital, Zurich, Switzerland
J Cereb Blood Flow Metab 20:369-80. 2000..Nevertheless, the increased posttraumatic mortality in TNF/LT-alpha-deficient mice suggests a protective effect of these cytokines by mechanisms that have not been elucidated yet...
- Changes in regional energy metabolism after closed head injury in the ratA E Mautes
Neurosurgical Research Laboratory, Saarland University Medical School, Homburg Saar, Germany
J Mol Neurosci 16:33-9. 2001..Cortical glucose and lactate contents could not be discerned over time. Following CHI there is an acute and progressive, yet transient, ischemic cortical profile, which is not reflected in subcortical areas...