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| 1 | Toll样受体参与小鼠肝脏缺血再灌注损伤显示文摘目的 探讨Toll样受体是否参与小鼠肝脏缺血再灌注损伤及其机制。方法 用Toll样受体缺损小鼠(C3H/Hej,Hej组)和野生型(C3H/Heouj,Heouj组)小鼠复制部分肝脏缺血再灌注损伤模型,于缺血45min,再灌注1h和3h处死动物,检测血清天门冬氨酸氨基转移酶(AST)和血清肿瘤坏死因子α(TNFα)的含量;并以northern blot及髓过氧化物酶(MPO)试验分别检测缺血肝组织TNFα mRNA的表达和MPO的含量。结果(1)再灌注1、3h,与假手术组相比,小鼠血浆AST明显升高,但Hej组明显低于Heouj组(661.83U/L±106.09U/L和1215.5U/L±174.03U/L,t=-6.65,P<0.01;1145.17U/L±132.43U/L和2958.17U/L±186.81U/L,t=-5.57,P<0.01);(2)再灌注3h时,与假手术组相比,Hej组和Heouj组小鼠血清TNFα浓度明显升高,且前者明显低于后者(152.39pg/ml±43.3pg/ml和249.12pg/ml±51.89pg/ml,t=-3.13,P<0.05);(3)再灌注1h,除假手术组外,Hej组和Heouj组小鼠缺血肝组织内可见TNFα mRNA的表达,但前者的表达水平明显低于后者,杂交带密度分析显示两者之间差异有显著性(80.3±28.8与189.4±24.6,t=-3.25,P<0.05);(4)再灌注3h,与假手术组相比,Hej组和Heouj组小鼠缺血肝组织内MPO含量明显升高,且前者含量明显低于后者(0.059±0.004和0.173±0.025,F=33.49,P<0.01)。结? | 吴河水 王琳 田元 Ori Rotstein | 2003 | 中华肝脏病杂志2003，11，7： | 14 |
| 2 | Toll-like receptor 4 involvement in hepatic ischemia/reperfusion injury in mice显示文摘BACKGROUND: Toll-like receptor 4 (TLR4) is involved in innate immunity by recognizing endotoxin resulting in a burst of inflammatory cascade. We investigated the relation between activation of TLR4 and liver injury in partial hepa- tic ischemia/reperfusion (I/R) injury in mice. METHODS: TLR4-deficient mice ( C3H/Hej) and wild type mice (WT, C3H/Heouj) were used in the model of I/R injury. Partial hepatic ischemia was produced by oc- clusion of inflow to the median and left lobes for 45 mi- nutes. Blood was drawn at 1 and 3 hours after reperfusion. The blood was analyzed for aspartate aminotransferase (AST) and tumor necrosis factor alpha (TNF-α). TNF-α mRNA expression and myeloperoxidase (MPO) level in the ischemic lobes were examined by northern blot and myeloperoxidase assay respectively. RESULTS: AST levels were significantly decreased in TLR4- deficient mice compared with WT mice at both time points (WT: 1215.5 ±174. 03, 2958. 17 ± 186. 81 IU/L at 1 and 3 hours respectively vs TLR4def: 661.83±106.09, 1145.17± 132.43 IU/L at 1 and 3 hours, mean ± SD, 6 mice/group, (=-6.65 and -5.57, P <0.001). Consistent with the role of TNF-α in hepatic I/R, serum TNF-α was decreased in TLR4 deficient mice at 3 hours after reperfusion compared with WT (152.39±43.3 vs 249.12 ± 51.89, n=6, t=-3.13, P<0.05). MPO level in the ischemic lobes in TLR4 defi- cient mice at 3 hours after reperfusion was significantly low- er than that in WT mice (0.059±0.004 vs 0.173±0.025, n=6, F=33.49, P<0.001). This difference appears to be mediated at the gene level since TLR4 deficient mice had decreased TNF-α mRNA expression at 1 hour after reperfu- sion compared with WT mice (80.3±28.8 vs 189.4±24.6, t=-3.25, P<0.05). CONCLUSIONS: Compared with WT mice, TLR4-defi- cient mice appear to have a mild I/R injury. Regulation of TNF-a at mRNA level seems to have a critical effect. These suggest TLR4 be involved in the mechanism of he-patic I/R injury in mice. | Ori Rotstein | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，2： | 9 |
| 3 | Remote Ischemic Preconditioning by Hindlimb Occlusion Prevents Liver Ischemic/Reperfusion Injury: The Role of High Mobility Group-Box 1显示文摘 | Feng Wang Simone E. Birch Ruijan He Patrick Tawadros Katalin Szaszi Andras Kapus Ori D. Rotstein | 2010 | Annals of Surgery2010，，2： | 2 |
| 4 | Integrity of Cell-Cell Contacts Is a Critical Regulator of TGF-β1-Induced Epithelial-to-Myofibroblast Transition显示文摘 | András Masszi Lingzhi Fan László Rosivall Christopher A. McCulloch Ori D. Rotstein István Mucsi András Kapus | 2004 | The American Journal of Pathology2004，，6： | 1 |
| 5 | Integrity of Cell-Cell Contacts Is a Critical Regulator of TGF-β1-Induced Epithelial-to-Myofibroblast Transition显示文摘 | András Masszi Lingzhi Fan László Rosivall Christopher A. McCulloch Ori D. Rotstein István Mucsi András Kapus | 2004 | The American Journal of Pathology2004，，6： | 1 |
| 6 | FGL2/Fibroleukin mediates hepatic reperfusion injury by induction of sinusoidal endothelial cell and hepatocyte apoptosis in mice显示文摘 | Nazia Selzner Hao Liu Markus U. Boehnert Oyedele A. Adeyi Itay Shalev Agata M. Bartczak Max Xue-Zhong Justin Manuel Ori D. Rotstein Ian D. McGilvray David R. Grant Melville J. Phillips Gary A. Levy Markus Selzner | 2011 | Journal of Hepatology2011，，1： | 1 |
| 7 | Twenty-five percent albumin prevents lung injury following shock/resuscitation显示文摘 | Kinga A. Powers Andras Kapus Rachel G. Khadaroo Ruijuan He John C. Marshall Thomas F. Lindsay Ori D. Rotstein | 2003 | Critical Care Medicine2003，，9： | 1 |
| 8 | Training in translational research for graduate students at the University of Toronto显示文摘The Institute of Medical Science (IMS) was established as an institute within the School of Graduate Studies at the University of Toronto in 1968 to serve as a graduate unit for the Clinical Departments in the Faculty of Medicine. In this role,the IMS offers a doctoral stream program in medical science leading to the Master of Science and Doctor of Philosophy degrees. Translational research,as a means of moving new discovery to improvement in patient outcome,has become a central theme of graduate education in our Institute. To this end,we have developed a curriculum offering which is intended to provide all new students with a defined skill set relevant to Translational Research and at the same time,to provide students with flexible offerings which would enhance their specific research programs. The course,spread over two years,will have three separate components:(1) there will be lectures focusing on research fundamentals and the basics of translational research; (2) there will be student presentations to hone presentation skills and get valuable feedback from fellow students and faculty mentors; (3) there will be elective modules,where students can select from a number of course offerings in order to round out training. These modules include subjects such as the fundamentals of clinical trials,the basics of qualitative research,an approach to the role of proteomics and genomics in research and the business of science. As part of this modular program,we have created a program 'clinical exposure for non-clinicians' with the hope that graduate students will be able to gain some understanding of the clinical relevance of their research activities. Over time,these modular offerings will be expanded based on a needs assessment from our students. The presentation will describe the IMS and its mission and will overview the structure and content of this course offering. | Ori D. Rotstein | 2009 | 中国病理生理杂志2009，25，11： | 0 |
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