维普中文期刊产品整合服务
88篇 您的检索式:作者名="Bilzer"
    题名 作者 年代 出处 被引量
1Intravenous administration of glutathione protects parenchymal and non-parenchymal liver cells against reperfusion injury following rat liver transplantation显示文摘AIM:To investigate the effects of intravenous administration of the antioxidant glutathione (GSH) on reperfusion injury following liver transplantation.METHODS:Livers of male Lewis rats were transplanted after 24 h of hypothermic preservation in University of Wisconsin solution in a syngeneic setting. During a 2-h reperfusion period either saline (controls,n=8) or GSH (50 or 100μmol/(h·kg),n=5 each) was continuously administered via the jugular vein.RESULTS:Two hours after starting reperfusion plasma ALT increased to 1 457±281U/L (mean±SE) in controls but to only 908_+187 U/L (P<0.05) in animals treated with 100μmol GSH/(h·kg).No protection was conveyed by 50μmol GSH/(h·kg).Cytoprotection was confirmed by morphological findings on electron microscopy:GSH treatment prevented detachment of sinusoidal endothelial cells (SECs) as well as loss of microvilli and mitochondrial swelling of hepatocytes. Accordingly, postischemic bile flow increased 2-fold. Intravital fluorescence microscopy revealed a nearly complete restoration of sinusoidal blood flow and a significant reduction of leukocyte adherence to sinusoids and postsinusoidal venules. Following infusion of 50μmol and 100 μmol GSH/(h·kg),plasma GSH increased to 65±7mol/L and 97±18μmol/L,but to only 20±3mol/L in untreated recipients.Furthermore, plasma glutathione disulfide (GSSG) increased to 7.5±1.0mol/L in animals treated with 100μmol/(h·kg) GSH but infusion of 50μmol GSH/(h·kg) did not raise levels of untreated controls (1.8±0.5mol/L vs 2.2±0.2mol/L).CONCLUSION:Plasma GSH levels above a critical level may act as a “sink” for ROS produced in the hepatic vasculature during reperfusion of liver grafts.Therefore, GSH can be considered a candidate antioxidant for the prevention of reperfusion injury after liver transplantation, in particular since it has a low toxicity in humans.RolfJ.Schauer SinanKalmuk Alexander L.Gerbes Rosemarie Leiderer Herbert Meissner Friedrich W.Schildberg Konrad Messmer Manfred Bilzer 2004World Journal of Gastroenterology2004,10,6:9
2PI 3-kinase pathway is responsible for antiapoptotic effects of atrial natriuretic peptide in rat liver transplantation显示文摘AIM:To investigate the in vivo effect of atrial natriureticpeptide(ANP)and its signaling pathway during ortho-topic rat liver transplantation.METHODS:Rats were infused with NaCl,ANP(5 μg/kg),wortmannin(WM,16 μg/kg),or a combination ofboth for 20 min.Livers were stored in UW solution(4°C)for 24 h,transplanted and reperfused.Apoptosis wasexamined by caspase-3 activity and TUNEL staining.Phosphorylation of Akt and Bad was visualized by West-ern blotting and phospho-Akt-localization by confocalmicroscopy.RESULTS:ANP-pretreatment decreased caspase-3activity and TUNEL-positive cells after cold ischemia,indicating antiapoptotic effects of ANP in vivo.The an-tiapoptotic signaling of ANP was most likely caused byphosphorylation of Akt and Bad,since pretreatment withPI 3-kinase inhibitor WM abrogated the ANP-inducedreduction of caspase-3 activity.Interestingly,analysis ofliver tissue by confocal microscopy showed translocationof phosphorylated Akt to the plasma membrane of hepa-tocytes evoked by ANP.CONCLUSION:ANP activates the PI-3-kinase pathwayin the liver in vivo leading to phosphorylation of Bad, an event triggering antiapoptotic signaling cascade inischemic liver.Uwe Grutzner Melanie Keller Michael Bach Alexandra K Kiemer Herbert Meissner Manfred Bilzer Stefan Zahler Alexander L Gerbes Angelika M Vollmar 2006World Journal of Gastroenterology2006,12,7:3
3Evaluation of serum Cystatin C concentration as a marker of renal function in patients with cirrhosis of the liver显示文摘Gerbes AL Gulberg V Bilzer M 0,,:1
4Glutathione protects the rat liver against reperfusion injury after hypothermic preservation显示文摘Bilzer M Paumgartner G Gerbes A L 1999Gastroenterol1999,117,:1
5The immunopathogenesis of Borna disease virus infection显示文摘Stitz L Bilzer T Planz O 2002Front Biosci2002,7,:1
6Evaluation of serum cystatin C concentration as a marker of renal function in patients with cirrhosis of the liver显示文摘Gerbes A L Gulberg V Bilzer M 2002Gut2002,50,1:1
7The immunopathogenesis of Borna disease virus infection显示文摘Stitz L Bilzer T Planz O 2002Front Biosci2002,7,:1
8Neutralizing antibodies in persistent Borna disease virus infeetion:prophylaetic effect of gp94-specific monoclonal antibodies in preventing encephalitis显示文摘Furrer E Bilzer T Stitz L 2001Journal of Virology2001,75,2:1
9Expression of vimentin and glial fibrillary acidic protein in ethylnitrosourea-induced rat gliomas and glioma cell lines显示文摘Reifenberger G Bilzer T Seitz RJ 1989Acta Neuropathol1989,78,:1
10Role of Kupffer cells in host defense and liver disease 显示文摘Bilzer M Roggel F Gerbes AL 2006Liver Int2006,26,10:1
11MICROCIRCULATORY FAILURE AFTER RAT LIVER TRANSPLANTATION IS RELATED TO KUPFFER CELL-DERIVED OXIDANT STRESS BUT NOT INVOLVED IN EARLY GRAFT DYSFUNCTION1显示文摘Rolf J. Schauer Manfred Bilzer Sinan Kalmuk Alexander L. Gerbes Rosmarie Leiderer Friedrich W. Schildberg Konrad Messmer 2001Transplantation2001,,10:1
12Glutathione treatment protectsthe rat liver against injury after warm ischemia and Kupffercell activation显示文摘Bilzer M Baron A Schauer R 2002Digestion2002,66,1:1
13Long-term therapy and retreatment of hepatorenal syndrome type I with ornipressin and opamine显示文摘Gulberg V Bilzer M C erbes AL 1999Hepatology1999,30,4:1
14Role of Kupffer cells in host defense and liver disease显示文摘Bilzer M Roggel F Gerbes A L 0,,10:1
15Tauroursodeoxycholic acid inserts the apical conjugate export pump, Mrp2, into canalicular membranes and stimulates organic anion secretion by protein kinase C-dependent mechanisms in cholestatic rat liver显示文摘Beuers U Bilzer M Chittattu A 2001Hepatology2001,33,5:1
16Evaluation of serum cystatin C coneentration as a marker of rnal function inpatients with cirrhosis of the oiver显示文摘Gerbes AL Gulberg V Bilzer M 2002Gut2002,50,50:1
17Immunopathogenic role of T-cell subsets inBoma disease virus-induced progressive encephalitis显示文摘Planz 0 Bilzer T Stitz L 1995J Virol1995,69,2:1
18Neutralizing antibodies in persistent Borna disease virus infection: prophylactic effect of gp94-specific monoclonal antibodies in preventing encephalitis显示文摘Furrer E Bilzer T Stitz L 2001J Virol2001,75,2:1
19Role of Kupffer cells in host defense and liver disease 显示文摘Bilzer M Roggel F Gerbes AL 2006Liver Int2006,26,10:1
20CD8 + T cellscontribute to tissue destruction during boma disease 显示文摘Bilzer T Stitz L Immune-niediated brain atrophy 1994J Immunol1994,153,2:1
返回顶部 每页显示:
共5页 首页 上一页 第1页 下一页 末页 /5 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费