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702篇 您的检索式:作者名="BAUMERT"
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1Pathogenesis of hepatitis B virus infection显示文摘Infection with hepatitis B virus (HBV) leads to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma. Infection with HBV is one of the most common viral diseases affecting man. Both viral factors as well as the host immune response have been implicated in the pathogenesis and clinical outcome of HBV infection. In this review, we will discuss the impact of virus-host interactions for the pathogenesis of HBV infection and liver disease. These interactions include the relevance of naturally occurring viral variants for clinical disease, the role of virus-induced apoptosis for HBV-induced liver cell injury and the impact of antiviral immune responses for outcome of infection.Thomas F Baumert Robert Thimme Fritz von Weizscker 2007World Journal of Gastroenterology2007,13,1:49
2Interaction of hepatitis C virus envelope glycoprotein E2 with the large extracellular loop of tupaia CD81显示文摘AIM: To further analyze the interaction of tupaia CD81 with hepatitis C virus (HCV) envelope protein E2. METHODS: A tupaia CD81 large extracellular loop (CD81 LEL), which binds to HCV E2 protein, was cloned and expressed as a GST-fusion protein, and interaction of HCV E2 protein with a tupaia CD81 LEL was evaluated by enzyme-linked immunosorbent assay (EIA). RESULTS: Although tupaia and human CD81 LEL differed in 6 amino acid changes, tupaia CD81 LEL was strongly recognized by anti-CD81 antibodies against human CD81 LEL conformation-dependent epitopes. Investigating LEL CD81-E2 interactions by EIA, we demonstrated that binding of tupaia CD81 LEL GST fusion protein to recombinant HCV E2 protein was markedly reduced compared to binding of human CD81 LEL GST fusion protein to recombinant HCV E2 protein. CONCLUSION: These data suggest that the structural differences in-between the tupaia and human CD81 may alter the interaction of the large extracellular loop with HCV envelope glycoprotein E2. These findings may be important for the understanding of the mechanisms of binding and entry of HCV to PTHs.Zhan-Fei Tian Hong Shen Xi-Hua Fu Yi-Chun Chen Hubert E Blum Thomas F Baumert Xi-Ping Zhao 2009World Journal of Gastroenterology2009,15,2:16
3Hepatitis C virus infection and apoptosis显示文摘Apoptosis is central for the control and elimination of viral infections. In chronic hepatitis C virus (HCV) infection, enhanced hepatocyte apoptosis and upregulation of the death inducing ligands CD95/Fas, TRAIL and TNFα occur. Nevertheless, HCV infection persists in the majority of patients. The impact of apoptosis in chronic HCV infection is not well understood. It may be harmful by triggering liver fibrosis, or essential in interferon (IFN) induced HCV elimination. For virtually all HCV proteins, pro- and anti-apoptotic effects have been described, especially for the core and NS5A protein. To date, it is not known which HCV protein affects apoptosis in vivo and whether the infectious virions act pro- or anti- apoptotic. With the availability of an infectious tissue culture system, we now can address pathophysiologically relevant issues. This review focuses on the effect of HCV infection and different HCV proteins on apoptosis and of the corresponding signaling cascades.Richard Fischer Thomas Baumert Hubert E Blum 2007World Journal of Gastroenterology2007,13,36:10
4Hepatitis B virus mutations potentially conferring adefovir/ tenofovir resistance in treatment-naive patients显示文摘Anti-hepatitis B virus(HBV)therapy leads to the emer- gence of mutant viral strains during the treatment of chronic hepatitis B with nucleos(t)ides analogues. The existence of HBV variants with primary antiviral resistance may be important for treatment choice. We studied two patients with chronic HBV infection by sequencing the HBV polymerase gene.They had adefovir-and tenofovir-related mutations in the viral polymerase,although they had never been treated. These mutations were rtV214A/rtN238T in one patient and rtA194T in the other.Thus,mutations in untreated patients deserve cautious surveillance.These data indicate that mutations that can theoretically confer adefovir or tenofovir resistance may emerge in treatmentnaive patients.Rebecca Pastor Franois Habersetzer Samira Fafi-Kremer Michel Doffoёl Thomas F Baumert Jean-Pierre Gut Franoise Stoll-Keller Evelyne Schvoerer 2009World Journal of Gastroenterology2009,15,6:6
5Neutralizing antibodies in hepatitis C virus infection显示文摘Hepatitis C virus (HCV) is a major cause of hepatitis world-wide. The majority of infected individuals develop chronic hepatitis which can then progress to liver cirrhosis and hepatocellular carcinoma. Spontaneous viral clearance occurs in about 20%-30% of acutely infected individuals and results in resolution of infection without sequaelae. Both viral and host factors appear to play an important role for resolution of acute infection. A large body of evidence suggests that a strong, multispecific and long-lasting cellular immune response appears to be important for control of viral infection in acute hepatitis C. Due too the lack of convenient neutralization assays, the impact of neutralizing responses for control of viral infection had been less defined. In recent years, the development of robust tissue culture model systems for HCV entry and infection has finally allowed study of antibody-mediated neutralization and to gain further insights into viral targets of host neutralizing responses. In addition, detailed analysis of antibody-mediated neutralization in individual patients as well as cohorts with well defined viral isolates has enabled the study of neutralizing responses in the course of HCV infection and characterization of the impact of neutralizing antibodiesfor control of viral infection. This review will summarize recent progress in the understanding of the molecular mechanisms of antibody-mediated neutralization and its impact for HCV pathogenesis.Mirjam B Zeisel Samira Fafi-Kremer Isabel Fofana Heidi Barth Franoise Stoll-Keller Michel Doffo■l Thomas F Baumert 2007World Journal of Gastroenterology2007,13,36:3
6Entry of hepatitis B and C viruses — recent progress and future impact显示文摘Thomas F Baumert Luke Meredith Yi Ni Daniel J Felmlee Jane A McKeating Stephan Urban 2013Current Opinion in Virology2013,,:3
7Hepatitis C Virus Infects the Endothelial Cells of the Blood-Brain Barrier显示文摘Nicola F. Fletcher Garrick K. Wilson Jacinta Murray Ke Hu Andrew Lewis Gary M. Reynolds Zania Stamataki Luke W. Meredith Ian A. Rowe Guangxiang Luo Miguel A. Lopez–Ramirez Thomas F. Baumert Babette Weksler Pierre–Olivier Couraud Kwang Sik Kim Ignacio A. R 2012Gastroenterology2012,,3:2
8A prophylactic hepatitis C virus vaccine: A distant peak still worth climbing显示文摘Thomas F. Baumert Catherine Fauvelle Diana Y. Chen Georg M. Lauer 2014Journal of Hepatology2014,,1:2
9Characterization of Hepatitis C Virus Particle Subpopulations Reveals Multiple Usage of the Scavenger Receptor BI for Entry Steps显示文摘Viet Loan Dao Thi Christelle Granier Mirjam B. Zeisel Maryse Guérin Jimmy Mancip Ophélia Granio Fran?ois Penin Dimitri Lavillette Ralf Bartenschlager Thomas F. Baumert Fran?ois-Lo?c Cosset Marlène Dreux 2012Journal of Biological Chemistry2012,,37:2
10Pseudomonas exotoxin antisense RNA selectively kills hepatitis B virus infected cells显示文摘AIM: To present an approach for selectively killing retrovirus-infected cells that combines the toxicity of Pseudomonas exotoxin (PE) and the presence of reverse transcriptase (RT) in infected cells. METHODS: PE antisense toxin RNA has palindromic stem loops at its 5' and 3' ends enabling self-primed generation of cDNA in the presence of RT. The RT activity expressed in retrovirus-infected cells converts 'antisense-toxin-RNA' into a lethal toxin gene exclusively in these cells. RESULTS: Using cotransfection studies with PE-expressing RNAs and β-gal expressing reporter plasmids, we show that, in HepG2 and HepG2.2.15 hepatoma cells as well as in duck hepatitis B virus (DHBV) infected cells, HBV or DHBV-polymerase reverse transcribe a lethal cDNA copy of an antisense toxin RNA, which is composed of sequences complementary to a PE gene and eukaryotic transcription and translation signals. CONCLUSION: This finding may have important implications as a novel therapeutic strategy aimed at the elimination of HBV infection.Peter Hafkemeyer Ulrich Brinkmann Elizabeth Brinkmann Ira Pastan Hubert E Blum Thomas F Baumert 2008World Journal of Gastroenterology2008,14,18:2
11Hepatitis C virus structural proteins assemble into virus-like particles in insect cells 显示文摘 Ito S Wong DT 1998JVirol1998,72,5:1
12Elevated levels of interleukin-18 predict the development of type 2 diabetes: results from the MONICA/KORA Augsburg Study, 1984-2002 显示文摘THORAND B KOLB H BAUMERT J 2005Diabetes2005,54,10:1
13Radiation treatment planning with an integrated positron emission and computer tomography(PET/CT): a feasibility study显示文摘Ciernik IF Dizendorf E Baumert BG 2003Int J Radiat Oncol Biol Phys2003,57,3:1
14Laparoscopicradical prostatectomy : oncological evaluation after 1 000cases a montsouris institute 显示文摘Guillonneau B Fettouh H Baumert H 2003J Urol2003,169,4:1
15GI-5005, a yeastvector vaccine expressing an NS3-core fusion protein for chronicHCV infection 显示文摘Habersetzer F Baumert TF Stoll-Keller F 2009Curr Opin Mol Ther2009,11,4:1
16Relation between QT interval variability and cardiac sympathetic activity'in hyper- tension显示文摘Baumert M Schlaich MP Nalivaiko E 2011Am J Physiol Heart Circ Physiol2011,300,4:1
17Aortoiliac and lower extremity arteries assessed with 16-detector row CT angiography:prospective comparison with digital subtraction angiography显示文摘Willmann JK Baumert B Schertler T 0,,:1
18The Determinants of Regional Innovation in Europe: A Combined Factorial and Regression Knowledge Production Function Approach 显示文摘Buesa M Heijs J Baumert T 2010Research Policy2010,39,6:1
19A variant in the ABO gene explains the variation in soluble E-selectin levels-results from dense genotyping in two independent populations显示文摘Karakas M Baumert J Kleber ME 2012PLo S One2012,7,51:1
20Effect of macrophage migration inhibitory factor (MlF) gene variants and MIF serum concentrations on the risk of type 2 diabetes: results from the MONICA/KORA Augsburg Case-Cohort Study, 1984-2002显示文摘HERDER C KLOPP N BAUMERT J 2008Diabetologia2008,51,2:1
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