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1.À£¬Áõ´¿½Ü£¬ÌÕºÃϼ£¬µÈ£®ÓÄÃÅÂݸ˾úºã¾ÃѬȾÃɹÅɳÍÁÊóµ¼ÖÂθÑס¢Î¸À£ÑñµÄʵÑéÑо¿.¾üÊÂҽѧ¿ÆѧԺԺ¿¯£¬2003,27 (4):255-258
2.ºú°Øƽ£¬Äß¾². Ô˶¯Ó¦¼¤ÐÔθÀ£Ññ¶¯ÎïÄ£×ӵĽ¨Éè¼°ÆäÐÐΪѧÆÀ¼Û£®ÌåÓý¿Æѧ£¬2007,27 (11):55-60
3.Deoda RS, Kumar D, Bhujbal SS: Gastroprotective Effectof rubia cordifolia !inn. on aspirin plus pylorus-ligated ulcer. Evid Based Complement Altemat Med, 2011, 2011:541624
4.Gana TJ,Huhlewych R,Koo J. Focal gastric mucosa.I blood flow in aspirin- induced ulceration. Ann Surg, 1987, 205 (4):399-403
5.Kaminishi M,Sadalsuki H,Jobjima Y,el al. A new model for production of chronic gastric ulcer by duodenogastric reflux in rals. Gastroenterology, 1987, 92 (6): 1913-1918
6.Marshall B. Helicobacler pylori: pasl, present and future. Keio J Med, 2003, 52(2):80-85
7.Ohkusa T, Okayasu I, M.iwa H, el: al. Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in Mongolian gerbils. Gut, 2003, 52 (6):797-803
8.Rainsford KD. Aspirin and gastric ulceration: light and electron microscopic observations in amodel of aspirin plus stress-induced ulcerogenesis. Br J Exp PatJiol, 1977, 58 (2): 215-219
9.Szabo S. Duodenal ulcer disease. Animal model: cysleamine induced acute and chronic duodenal ulcer in the rat. Am J Pathol, 1978, 93 (1): 273-276