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诺贝尔生理医学奖得主罗宾·沃伦教授讲座
2012-04-20 08:45   审核人:   (点击: )

2005年诺贝尔生理医学奖得主罗宾?沃伦教授讲座通知

讲座题目:幽门螺杆菌的发现

Title: Discovering Helicobacter

讲座时间:2012年4月26日上午11:10

讲座地点:友谊校区东会议室

主 讲 人:2005年诺贝尔生理医学奖得主罗宾?沃伦教授

主讲人简介:

罗宾·沃伦(J. Robin Warren)博士是澳大利亚科学家。曾供职于于南澳大利亚伍德威尔市伊丽莎白皇后医院。1962年成为成为墨尔本皇家医院注册临床病理学医生,之后成为阿德莱德医学与兽医学研究所注册血液病学和临床病理学医师,澳大利亚皇家病理学院研究员,珀斯皇家医院病理学家。

他曾获得过多项奖项,如Warren Alpert基金会奖项,澳大利亚医疗协会奖,拉斯科奖,盖尔德纳基金会国际奖,Paul Ehrlich奖,阿姆斯特丹医学奖,堪培拉佛洛里奖章,英国皇家医学会布坎南奖章,美国富兰克林生命科学奖章,澳大利亚联邦建国百年特殊贡献奖。

1979年华伦首次在胃黏膜中观测到了细小曲形细菌,在接下来的研究中,他发现这种细菌经常出现在胃黏膜中,并和某类胃炎有着极为密切的联系。1981年他结识了巴里—马歇尔并和他进行了卓有成效的合作。他们的研究发现了这种细菌在临床医学上的重大作用。他们对这种细菌进行了培育,并确认为一种新的细菌种类,命名为幽门螺杆菌(Helicobacter pylori,彻底消除这种细菌可以治愈胃炎并使得溃疡不再复发。

罗宾·沃伦与巴里·马歇尔(Barry J. Marshall)发现了幽门螺杆菌(Helicobacter pylori,Hp)以及这种细菌在胃炎和胃溃疡等疾病中的作用,被授予2005年诺贝尔生理或医学奖。幽门螺杆菌及其作用的发现,打破了当时已经流行多年的人们对胃炎和消化性溃疡发病机理的错误认识,被誉为是消化病学研究领域的里程碑式的革命。由于他们的发现,溃疡病从原先难以治愈、反复发作的慢性。涑闪艘恢植捎枚塘瞥痰目股睾鸵炙峒辆涂芍斡募膊。蠓忍岣吡宋咐Q竦然颊呋竦贸沟字斡幕,为改善人类生活质量作出了贡献。这一发现还启发人们去研究微生物与其他慢性炎症疾病的关系。人类许多疾病都是慢性炎症性疾。缇窒扌曰爻ρ、溃疡性结肠炎、类风湿性关节炎、动脉粥样硬化。

讲座内容简介:

Before the 1970’s, well fixed specimens of gastric mucosa were rare. Then the flexible endoscope was introduced. This enabled gastroenterologists to take numerous well-fixed small biopsies from the stomach. Gastric histology and pathology were clearly demonstrated. Whitehead accurately described it in 1972, including a feature he termed ‘active’ gastritis. This involved only the superficial gastric epithelium, with polymorph infiltration and epithelial cell distortion.

In June 1979 I was examining a gastric biopsy showing chronic inflammation and the active change. A thin blue line on the surface showed numerous small curved bacilli. These were clearly visible with a Warthin Starry silver stain. They appeared to grow on the surface of the foveolar epithelial cells.

Over the next two years I collected numerous similar cases. The changes were often much milder or more focal than the original biopsy, but the main features were usually similar, with chronic gastritis and usually some of the active change. These features could show considerable variation, from near normal to severe.

In 1981 I met Barry Marshal and we completed a clinico-pathological study of 100 outpatients referred for gastroscopy. There was little relation between the infection and the patients’ symptoms. Peptic ulcers, particularly duodenal ulcers, were very closely related to the infection. We cultured Helicobacter pylori.

In 1986, with Marshall et al, I studied the effect of eradication of H pylori on the recurrence of duodenal ulcer. I graded the gastritis (0 – 36) using the features seen with active gastritis. The range was 15 – 35 before treatment. After eradication of H pylori, this changed to 5 – 20 within 2 weeks. This provides powerful evidence that H pylori causes the active change.

Duodenal ulcer usually occurs in the duodenal cap. Gastric mucosa normally extends through the pylorus. In this study, the proximal border of all ulcers was either definite gastric mucosa, or scarred and consistent with a gastric origin. This suggests duodenal ulcer is either actually a distal pyloric ulcer or gastro-duodenal. It may well arise in the damaged, inflamed and infected mucosa in the position of maximum stress – the lip of the pyloric sphincter.

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