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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Tumor necrosis factor-mediated inhibition of interleukin-18 in the brain: a clinical and experimental study in head-injured patients and in a murine model of closed head injury. | Journal of Neuroinflammation BioMed Central Short report Open Access Tumor necrosis factor-mediated inhibition of interleukin-18 in the brain a clinical and experimental study in head-injured patients and in a murine model of closed head injury. Oliver I Schmidt1 Maria Cristina Morganti-Kossmann2 Christoph E Heyde1 Daniel Perez3 Ido Yatsiv4 Esther Shohami4 Wolfgang Ertel1 and Philip F Stahel 1 Address Department of Trauma and Reconstructive Surgery Charité University Medical School Campus Benjamin Franklin Berlin Germany 2Department of Trauma Surgery The Alfred Hospital Monash University Melbourne Australia 3Department of Surgery University Hospital Zurich Switzerland and 4Department of Pharmacology The Hebrew University Hadassah Medical School Jerusalem Israel Email Oliver I Schmidt - olischmidt@web.de Maria Cristina Morganti-Kossmann - cristina.morganti-kossmann@med.monash.edu.au Christoph E Heyde - ceheyde@aol.com Daniel Perez - danielperezch@yahoo.com Ido Yatsiv - idoyat@yahoo.com Esther Shohami - esty@huji.ac.il Wolfgang Ertel - wolfgang.ertel@charite.de Philip F Stahel - pfstahel@aol.com Corresponding author Published 28 July 2004 Received 18 June 2004 Journal of Neuroinflammation 2004 1 13 doi 10.1186 1742-2094-1-13 Accepted 28 July 2004 This article is available from http www.jneuroinflammation.cOm content 1 1 1 3 2004 Schmidt et al licensee BioMed Central Ltd. This is an open-access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Tumor necrosis factor TNF and interleukin- IL -18 are important mediators of neuroinflammation after closed head injury CHI . Both mediators have been previously found to be significantly elevated in the intracranial compartment after brain injury both in patients as well as in experimental model systems. However the interrelation
