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Jan M. Langrehr

Researcher at Charité

Publications -  250
Citations -  10227

Jan M. Langrehr is an academic researcher from Charité. The author has contributed to research in topics: Transplantation & Liver transplantation. The author has an hindex of 47, co-authored 250 publications receiving 9761 citations. Previous affiliations of Jan M. Langrehr include University of Pittsburgh & Free University of Berlin.

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Adjuvant chemotherapy with gemcitabine vs observation in patients undergoing curative-intent resection of pancreatic cancer: a randomized controlled trial.

TL;DR: The results support the use of gemcitabine as adjuvant chemotherapy in resectable carcinoma of the pancreas by significantly delayed the development of recurrent disease after complete resection of pancreatic cancer compared with observation alone.
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Supply of pre- and probiotics reduces bacterial infection rates after liver transplantation--a randomized, double-blind trial.

TL;DR: The aim is to study if a combination of different LAB and fibers would further improve outcome, which recently reported significant progress with a synbiotic composition, consisting of one lactic acid bacteria and one fiber.
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Fibrosis progression after liver transplantation in patients with recurrent hepatitis C.

TL;DR: These data provide information on the course of recurrent hepatitis C and may be helpful to individualize the treatment of transplanted patients and to identify risk factors, which may play a role in the development of severe fibrosis stages.
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Long-term outcome of liver transplants for chronic hepatitis C: a 10-year follow-up.

TL;DR: The analysis of causes leading to graft failure in patients with HCV showed that HCV recurrence is responsible for one of three deaths in HCV-positive patients, and new antiviral treatments, as well as adapted immunosuppressive protocols, will be necessary to further improve the outcome of HCV -positive patients after liver transplantation.
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Alloantigen-induced activation of rat splenocytes is regulated by the oxidative metabolism of L-arginine.

TL;DR: Inhibition of rat SPL proliferation to alloantigen seems not to be caused by the lack of production of cytokines able to induce T cell proliferation, or by an indirect deleterious effect on the mitochondrial respiration and viability of macrophages that oxidatively metabolize L-arginine.