1. 毕业设计（论文）的内容和要求
论文内容：
设计并合成新的来氟米特类似物，并对合成条件进行优化，力争缩短合成步骤，提高产率。
论文要求：
2. 参考文献
[1] 张木兰,类风湿关节炎的临床表征[J].国防医学杂志，1991，12，109-112。[2] Conaghan, P.G.；Green, M.J.；Emery, P. Established rheumatoid arthritis. Baillieres Clin. Rheumatol. 1999, 13(4), 561-575.[3] Arnett, F.C.；Edworthy, S.M.；Bloch, D.A. et al. The American rheumatism association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis and Rheumatism. 1988, 31, 315-324.[4] Lee, S.S. The treatment of rheumatoid arthritis. Best Pract. Res. Clin. Reheumatol. 2004, 18(4), 507-538.[5] Feldmann, M.；M；Maini, R.N. Discovery of TNF-α as a therapeutic target in rheumatoid arthritis：preclinical and clinical studies. Joint Bone Spine. 2002, 69, 12-18.[6] Bingham, S.J. Rheumatoid arthritis. Best Pract. Res. Clin. Haematol. 2004, 17(2), 263-276.[7] Desoky, E.I. Pharmacotherapy of rheumatoid arthritis：An overview. Cur. Therapeut. Res. 2001, 62(2), 92-112.[8] Manfred Schattenirchner. The use of leflunomide in the treatment of rheumatoid arthritis：an experimental and clinical review. Immunopharmacology. 2000, 47, 291-298.[9] Strand, V. Recent advances in the treatment of rheumatoid arthritis. Office Rheumatology. 2(2), 38-50.[10] Cash, J.M. and Klippel, J.H. Second-line drug therapy for rheumatoid arthritis. N. Eng. J. Med. 1994, 330, 1365-1375.[11] Schuna, A.A.；Upate on treatmentof rheumatoid. J Am Pharm Assoc. 1998, 38, 728-737.[12] Urban, M.K. COX-2 specific inhibition offer improved advantages over traditional NSAIDs. Orthopedics. 2000, 23 (suppl 7), S761-S764.[13] Luong, B.T.；Chong, B.S.；Lowder, D.M. Treatment options for rheumatoid arthritis：Celecoxib, leflunomide, etanercept, and infliximab. Ann Pharmacother. 2000, 34, 743-760.[14] Schuna, A.A.；Megeff, C. New drugs for the treatment of rheumatoid arthritis. Am J Health-Syst Pharm. 2000, 57, 225-234.[15] Tugwell, P.; Pincus, T.; Yocum, D. et al. Combination therapy with cyclosporine and methotrexate in severe rheumatoid arthritis. N. Engl. J. Med. 1995, 333, 137-141.[16] Boers, M.; Verhoeven, A.C.; Markusse, H.M. et al. Randomised comparison of combined step-down prednisolone, methotrexate and sulphasalazine with sulphasalazine alone in early rheumatoid arthritis. Lancet. 1997, 350, 309-318.
[17] Huang, W.H.; Lee, A.R.; Hsieh, Y.H.; Chien, P.Y.; Yang, C.L. Pharmacological action, structural modification and drug design of leflunomide as novel immunosuppressants. J. Med. Sci. 2001, 21, s27-s38.
[18] Fox, R.I.；Herrmann, M.L.；Frangou, C.G. et al. Short analytical review menchanism of action for leflunomide in rheumatoid arthritis. Clin. Immunol. 1999, 93 (3), 198-208.[19] Li, E.K.；Tam, L.S.；Tomlinson, B. Leflunomide in the treatment of rheumatoid arthritis. Clin. Therapeut. 2004, 26(4), 447-459.[20] Fujimura, H.A. The immunosuppressant leflunomide blocks the yeast Saccharomyces cerevisiae cell cycle at the G1 phase. FEMS Microbiology Letters. 1996, 143, 273-277.[21] Hamilton, L.C.; Vojnovic, I.; Warner, T.D.; A771726, the active metabolite of leflunomide, directly inhibits the activity of cyclo-oxygenase-2 in vitro and in vivo in a substrate-sensitive manner. Br. J. Pharmacol. 1999,127(7),1589-1596.[22] Miljkovic, D.; Samardzic, T. et al. Leflunomide inhibits activation of inducible nitric oxide synthase in rat astrocytes. Brain. Res. 2001, 889(1-2), 331-338.[23] Manna, S.K.; Mukhopadhyay, A.; Aggarwal, B.B. Leflunomide suppresses TNF-induced cellular responses: effects on NF-B, activator protein-1, c-Jun N-terminal protein kinase, and apoptosis. J. Immunol. 2000, 165, 5962-5969.[24] Jankovic, V.; Samardzic, T.; Stosic-Grujicic, S.; Popadic, D.; Trajkovic, V. Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide. Cellular Immunol. 2000, 199, 73-80.[25] Kremer, J.M. Rational use of new and existing disease-modifying agents in rheumatoid arthritis. Ann. Intern. Med. 2001, 17, 695-706.
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