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Thomas S. Weiss

Researcher at University Hospital Regensburg

Publications -  190
Citations -  8542

Thomas S. Weiss is an academic researcher from University Hospital Regensburg. The author has contributed to research in topics: Liver regeneration & Fatty liver. The author has an hindex of 47, co-authored 181 publications receiving 7463 citations. Previous affiliations of Thomas S. Weiss include University of Regensburg & Ludwig Maximilian University of Munich.

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Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.

Patricio Godoy, +94 more
TL;DR: This review encompasses the most important advances in liver functions and hepatotoxicity and analyzes which mechanisms can be studied in vitro and how closely hepatoma, stem cell and iPS cell–derived hepatocyte-like-cells resemble real hepatocytes.
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PD-L1 is induced in hepatocytes by viral infection and by interferon-α and -γ and mediates T cell apoptosis

TL;DR: A novel bidirectional interaction between hepatocytes and lymphocytes modulated by PD-L1 expression in hepatocytes is suggested, which may contribute to the unique immunological properties of the liver.
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GLUT1 Expression Is Increased in Hepatocellular Carcinoma and Promotes Tumorigenesis

TL;DR: It is suggested that increased GLUT1 expression levels in HCC cells functionally affect tumorigenicity, and thus,GLUT1 is proposed as an innovative therapeutic target for this highly aggressive tumor.
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Lipid accumulation in hepatocytes induces fibrogenic activation of hepatic stellate cells.

TL;DR: In vitro data indicate a potential mechanism for the pathophysiological link between hepatic steatosis and fibrogenesis in vivo, and provide an attractive in vitro model to study the molecular mechanisms of steatotic-induced fibrogensesis, and to identify and test novel targets for antifibrotic therapies in fatty liver disease.
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A novel MCP-1 gene polymorphism is associated with hepatic MCP-1 expression and severity of HCV-related liver disease.

TL;DR: In Inheritance of the -2518 MCP-1 G allele, which appears to affect hepatic M CP-1 expression, may predispose HCV patients to more severe hepatic inflammation and fibrosis.