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Bijan Eghtesad

Researcher at Cleveland Clinic

Publications -  200
Citations -  7561

Bijan Eghtesad is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Liver transplantation & Transplantation. The author has an hindex of 44, co-authored 183 publications receiving 6721 citations. Previous affiliations of Bijan Eghtesad include University of Pittsburgh & Cleveland Clinic Lerner College of Medicine.

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Tolerogenic immunosuppression for organ transplantation.

TL;DR: The striking ability to wean immunosuppression in these recipients indicates variable induction of tolerance, and systematic application of these principles should allow improvements in quality of life and long-term survival after organ transplantation.
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Near-total human face transplantation for a severely disfigured patient in the USA

TL;DR: The feasibility of reconstruction of severely disfigured patients in a single surgical procedure using composite face allotransplantation is shown and should be taken in consideration as an early option for severelydisfigured patients.
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Three‐dimensional print of a liver for preoperative planning in living donor liver transplantation

TL;DR: A protocol is developed and successfully 3D‐printed synthetic livers (along with their complex networks of vascular and biliary structures) replicating the native livers of 6 patients: 3 living donors and 3 respective recipients who underwent LDLT, to be the first complete 3D-printed livers.
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Posttransplant lymphoproliferative disorders in liver transplantation: a 20-year experience.

TL;DR: While PTLD continues to pose problems in patients receiving liver transplants, improvements in patient survival have been observed over time and it is too early to assess the impact of new advances in prophylaxis, diagnosis, and treatment.
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Hyperammonemia in cirrhosis induces transcriptional regulation of myostatin by an NF-κB–mediated mechanism

TL;DR: It is shown that the expression of myostatin, a negative regulator of skeletal muscle mass, is increased in the cirrhotic muscle and is mediated by increased ammonia concentration, and a mechanism by which sarcopenia develops in cirrhosis patients is suggested.