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1.
Summary. Both 1,4-benzoquinones and 1,4-naphthoquinones were attached to the non-proteinogenic amino acid taurine to form N-quinonyl
taurine derivatives. The products were formed via the direct Michael-like addition or by substitution of a good leaving group.
An attempt to bridge the two moieties via an ureido spacer resulted in the formation of a bis-quinonylamino isocyanurate derivative.
Preliminary MO calculations provided internal ground-state geometries and orbital coefficients of the HOMO levels in two representing
taurine conjugates.
Received May 6, 2002 Accepted August 13, 2002 Published online December 18, 2002
Acknowledgments This research was supported by the Israel Science Foundation founded by the Academy of Science and Humanities. We wish to
thank Ms. Ethel Solomon for skilled technical help.
Authors' address: Prof. Shmuel Bittner, Department of Chemistry, Ben-Gurion University of the Negev, P.O. Box 653, Beer-Sheva 84105, Israel,
Fax: (972)-8-6472943, E-mail: bittner@bgumail.bgu.ac.il 相似文献
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Nico Melzer Sven G. Meuth Delany Torres-Salazar Stefan Bittner Alla L. Zozulya Christian Weidenfeller Alexandra Kotsiari Martin Stangel Christoph Fahlke Heinz Wiendl 《PloS one》2008,3(9)
In multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE), impairment of glial “Excitatory Amino Acid Transporters” (EAATs) together with an excess glutamate-release by invading immune cells causes excitotoxic damage of the central nervous system (CNS). In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a β-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in “Myelin Oligodendrocyte Glycoprotein” (MOG)-induced EAE. Ceftriaxone profoundly ameliorated the clinical course of murine MOG-induced EAE both under preventive and therapeutic regimens. However, ceftriaxone had impact neither on EAAT2 protein expression levels in several brain areas, nor on the radioactive glutamate uptake capacity in a mixed primary glial cell-culture and the glutamate-induced uptake currents in a mammalian cell line mediated by EAAT2. Moreover, the clinical effect of ceftriaxone was preserved in the presence of the EAAT2-specific transport inhibitor, dihydrokainate, while dihydrokainate alone caused an aggravated EAE course. This demonstrates the need for sufficient glial glutamate uptake upon an excitotoxic autoimmune inflammatory challenge of the CNS and a molecular target of ceftriaxone other than the glutamate transporter. Ceftriaxone treatment indirectly hampered T cell proliferation and proinflammatory INFγ and IL17 secretion through modulation of myelin-antigen presentation by antigen-presenting cells (APCs) e.g. dendritic cells (DCs) and reduced T cell migration into the CNS in vivo. Taken together, we demonstrate, that a β-lactam antibiotic attenuates disease course and severity in a model of autoimmune CNS inflammation. The mechanisms are reduction of T cell activation by modulation of cellular antigen-presentation and impairment of antigen-specific T cell migration into the CNS rather than or modulation of central glutamate homeostasis. 相似文献
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Stephen A. Matlin M.Amelia Prazeres Magalis Bittner Mario Silva 《Phytochemistry》1984,23(12):2863-2866
Rimuene and nubigenol have been identified in Podocarpus saligna for the first time, and the structures of three new norditerpene dilactones, salignones K, L and M, isolated from this species have been elucidated. 相似文献
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