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Gerd Otto

Researcher at University of Mainz

Publications -  261
Citations -  10058

Gerd Otto is an academic researcher from University of Mainz. The author has contributed to research in topics: Liver transplantation & Transplantation. The author has an hindex of 51, co-authored 261 publications receiving 9390 citations. Previous affiliations of Gerd Otto include University Hospital Heidelberg & University of Ulm.

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Lymphocyte apoptosis induced by CD95 (APO-1/Fas) ligand-expressing tumor cells--a mechanism of immune evasion?

TL;DR: The data suggest that tumor cells can evade immune attack by down–regulation of the CD95 receptor and killing of lymphocytes through expression of CD95L, which is an important mediator of T–cell cytotoxicity.
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Involvement of the CD95 (APO-1/Fas) receptor and ligand in liver damage.

TL;DR: The findings suggest that liver destruction in hepatitis B may primarily involve killing of hepatocytes by T lymphocytes using the CD95 receptor-ligand system.
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Response to transarterial chemoembolization as a biological selection criterion for liver transplantation in hepatocellular carcinoma

TL;DR: Sustained response to TACE is a better selection criterion for LT than the initial assessment of tumor size or number, according to the multivariate analysis.
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Sirolimus Use in Liver Transplant Recipients With Hepatocellular Carcinoma: A Randomized, Multicenter, Open-Label Phase 3 Trial

Edward K. Geissler, +68 more
- 01 Jan 2016 - 
TL;DR: This trial provides the first high-level evidence base for selecting immunosuppression in LTx recipients with HCC and reveals that low-risk, rather than high- risk, patients benefited most from sirolimus; furthermore, younger recipients (age ⩽60) also benefited, as well siro Limus monotherapy patients.
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Hepatic failure and liver cell damage in acute Wilson's disease involve CD95 (APO-1/Fas) mediated apoptosis.

TL;DR: In patients with fulminant hepatic failure in the course of Wilson's disease and in an in vitro model of copper treated human hepatoma cells, copper overload in vitro resulted in hepatocytic apoptosis which could be reduced with a neutralizing anti-CD95L antibody.