Báo cáo sinh học: "Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system. | Journal of Biology BioMed Central Research article Open Access Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system Ruolan Han Yin M Yang Joerg Dietrich1 Anne Luebkeh Margot Mayer-Proschel and Mark Noble Addresses Department of Biomedical Genetics and University of Rochester Stem Cell and Regenerative Medicine Institute University of Rochester Medical Center Elmwood Avenue Rochester NY 14642 USA. tDepartment of Neurology Massachusetts General Hospital Harvard Medical School Fruit Street Wang 835 Boston MA 02114 USA. Department of Neurobiology and Anatomy University of Rochester Medical Center Elmwood Avenue Rochester NY 14642 USA. Correspondence Mark Noble. Email mark_noble@ Published 22 April 2008 Received 19 June 2007 Journal of Biology 2008 7 12 doi jbiol69 VÍseC3 J gy v J Accepted 19 February 2008 The electronic version of this article is the complete one and can be found online at http content 7 4 12 2008 Han et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Cancer treatment with a variety of chemotherapeutic agents often is associated with delayed adverse neurological consequences. Despite their clinical importance almost nothing is known about the basis for such effects. It is not even known whether the occurrence of delayed adverse effects requires exposure to multiple chemotherapeutic agents the presence of both chemotherapeutic agents and the body s own response to cancer prolonged damage to the blood-brain barrier inflammation or other such changes. Nor are there any animal models that could enable the study of this important problem. Results We found that clinically relevant .

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