李永渝
从事医学病理生理学教学与消化系统疾病病因发病学的研究。
个性化签名
- 姓名:李永渝
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学术头衔:
博士生导师
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学科领域:
病理学
- 研究兴趣:从事医学病理生理学教学与消化系统疾病病因发病学的研究。
李永渝,女,1955年12月生,1980年毕业于贵州省遵义医学院(辽宁省大连医学院70年代南迁学校)医疗系,毕业后留校任教;1985年遵义-大连医学院病生专业硕士研究生毕业,获硕士学位。在研究生学习期间加入中国共产党。毕业后继续留校任教。后来通过国家英语水平考试(EPT),先后到德国慕尼黑工业大学医学院、慕尼黑大学医学院、德国莱比锡大学医学院学习和研修3年余,获得莱比锡大学医学院医学博士学位;曾作为邀请教授到加拿大蒙特尼尔大学医学院合作研究半年。
二十多年来,一直从事医学病理生理学教学与消化系统疾病病因发病学的研究,发表科研论文70余篇,主编专著3部,获省部级、厅级成果奖8项。1996年获国务院特殊津贴。2001年作为引进人才到同济大学医学院工作。目前任同济大学医学院病理生理教研室主任、同济大学消化系疾病研究所所长,同时兼任中国病理生理学会消化专业委员会主任委员、中国中西医结合急腹症专业委员会中青年委员、上海生理科学会理事、中国中西医结合外科杂志编委等。
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李永渝, Yong-Yu Li, Xue-Li Li, Cui-Xiang Yang, Hong Zhong, Hong Yao, Ling Zhu
World J Gastroenterol 2003: 9(1): 155-159,-0001,():
-1年11月30日
AIM: Available experimental evidence from both clinical and animal models shows that both Chinese medicines tetrandine (Tet) and Qing Yi Tong (QYT) have positive treatment effects on acute pancreatitis (AP). This investigation was conducted to explore the treatment mechanisms of Tet and QYT on AP at the molecular level and thereby explain their therapeutic affects. It included an investigation of the effects of these drugs on gene expression of both intercellular adhesion molecule 1 (ICAM-1) and superoxide dismutase (Mn-SOD and Cu, Zn-SOD) in a rat model with AP. METHODS: AP in the test rats was induced by subjecting them to laparotomy followed by a retrograde injection of 4% sodium taurocholate into the bilio-pancreatic duct. The test rats with AP were divided into three groups. One was treated with Tet, one with QYT, and one with normal saline solution. The sham-operated control group (SO) rats were only subjected to laparotomy. They were given no further treatment. For the Tet group, Tet was injected intraperitoneally, and for the QYT group, QYT was given with a nose-gastric catheter. These procedures were done at both 10min and 5h after AP induction. The levels of ICAM-1 mRNA expression and of SOD (Mn-SOD and Cu, Zn-SOD) mRNA expression in the pancreas and liver tissues were measured by RT-PCR at 1, 5, and 10 h after AP induction. RESULTS: When compared with the SO group during the observation time, rats with AP showed a higher expression of ICAM and a lower expression of Mn-SOD in both pancreas and liver tissues, and a lower expression of Cu, Zn-SOD in the pancreas. Tet treatment attenuated changes in the expression of both ICAM-1, and SOD (Mn-SOD and Cu, Zn-SOD) to a significant degree. A similar effect on the expression of SOD (Mn-SOD and Cu, Zn-SOD) was also found in the QYT group, but no obvious suppressive effect on ICAM-1 expression was observed. CONCLUSION: The results of this study suggest that one of the main mechanisms of Tet and QYT in treating AP is to enhance anti-oxidation of the body. The results also suggest that the anti-inflammatory effect of Tet is involved in the reduction of ICAM-1 expression. This explains why Tet and QYT are beneficial in treating AP.
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李永渝, ZHANG Hong, LI Yong-Yu, WANG Sheng-Nian, ZHANG Kong-Hua, WU Xian-Zhong
Zhang H et al/Acta Pharmacol Sin 2003 Aug; 24(8): 790-795,-0001,():
-1年11月30日
To investigate the effects of lipopolysaccharides (LPS, endotoxin) on the calcium content in pancreatic acinar cells and the origin of Ca2+ during calcium overload induced by LPS, further to explore the mechanism of LPS in inducing calcium overload and pancreatic acinar cell injury. METHODS: Male rat pancreatic acinar cells were isolated by collagenase digestion and loaded with Fluo-3/AM, then exposed to varying doses of LPS (from 1mg/L to 20mg/L). The dynamic change of [Ca2+] in single pancreatic acinar cell in the absence and presence of Ca2+ in extracellular fluid was determined by laser scanning confocal microscopy. Cell viability was determined by MTT at different time points after treatment with LPS. RESULTS: Under physiological calcium concentration in extracellular fluid, LPS (10mg/L) initiated a rapid, concentration-dependent rise in intracellular [Ca2+]i and consequent cell damage (P<0.05). LPS induced a slight rise of [Ca2+]i in the calcium-free extracellular fluid containing egtazic acid 1mmol/L and addition of extracellular calcium in the presence of LPS resulted in a more immediate and remarkable rise of [Ca2+]i, which reached the peak value within 150 s and maintained the value sustainedly. Egtazic acid attenuated LPS-induced cell damage (P<0.05). The increase in intracellular [Ca2+]i preceded the pathological alteration of pancreatic acinar cells. CONCLUSION: LPS directly induced the injury and the disorder of calcium homeostasis in isolated rat pancreatic acinar cell. Calcium overload is an early event in the pathogenesis of LPSinduced cell damage. Origin of the [Ca2+]i in cytoplasma of pancreatic acinar cells during calcium overload is mainly due to the influx of extracellular Ca2+. Calcium homeostasis disorder may be one of the causes or at least an important mediator of LPS-induced pancreatic acinar cell damage.
lipopolysaccharides, pancreas, acinar cells, calcium, confocal microscopy
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李永渝, Y. Li, * D. Gingras, I. Londono, and M. Bendayan
Cell Stress & Chaperones (2003)8(3), 287-294,-0001,():
-1年11月30日
In pancreatic acinar cells, chaperonin Cpn60 is present in all the cellular compartments involved in protein secretion as well as in mitochondria. To better understand the role Cpn60 plays in pancreatic secretion, we have evaluated its changes under experimental conditions known to alter pancreatic secretion. Quantitative protein A-gold immunocytochemistry was used to reveal Cpn60 in pancreatic acinar cells. Cpn60 immunolabelings in cellular compartments involved in secretion were found to decrease in acute pancreatitis as well as upon stimulation of secretion and in starvation conditions. A major increase in Cpn60 was recorded in diabetic condition. This was normalized by insulin treatment. Although in certain situations changes in secretory enzymes and in Cpn60 correlate well, in others, nonparallel secretion seemed to take place. In contrast, expression of mitochondrial Cpn60 in acinar cells appeared to remain stable in all conditions except starvation, where its levels decreased. Expression of Cpn60 in the secretory pathway and in mitochondria thus appears to behave differently, and Cpn60 in the secretory pathway must be important for quality control and integrity of secretion.
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