Induction of Lysosome‐associated Protein Transmembrane 4 Beta via Sulfatase 2 Enhances Autophagic Flux in Liver Cancer Cells

Yeonjung Ha, Yong Fang, Paola A. Romecin Duran, Ezequiel J. Tolosa, Catherine D. Moser, Martin E. Fernandez‐Zapico, Lewis R. Roberts – 25 September 2019 – Autophagy has been shown to be a key cellular event controlling tumor growth in different neoplasms including hepatocellular carcinoma (HCC). Although this biological role of autophagy has been clearly established, the mechanism underlying its regulation remains elusive.

Clinical Utility of an Increase in Magnetic Resonance Elastography in Predicting Fibrosis Progression in Nonalcoholic Fatty Liver Disease

Veeral H. Ajmera, Amy Liu, Seema Singh, Georg Yachoa, Matthew Ramey, Meera Bhargava, Ava Zamani, Scarlett Lopez, Neeraj Mangla, Ricki Bettencourt, Emily Rizo, Mark Valasek, Cynthia Behling, Lisa Richards, Claude Sirlin, Rohit Loomba – 25 September 2019

LiverLearning®: 2019 Webinar: New Insights Into the Pathogenesis and Management of Cystic Fibrosis-Related Liver Disease

Our understanding of liver disease pathogenesis and manifestations in cystic fibrosis is evolving, as ongoing research and clinical experience expands. This webinar will provide updates on current understanding of CLFD pathogenesis, on strategies for diagnosis and monitoring, and on management of CFLD complications. We will utilize a live webinar format that will be recorded for on-demand viewing on Liver Learning ® .A. Jay Freeman Dr.

Liver Glycogen Phosphorylase Deficiency Leads to Profibrogenic Phenotype in a Murine Model of Glycogen Storage Disease Type VI

Lane H. Wilson, Jun‐Ho Cho, Ana Estrella, Joan A. Smyth, Rong Wu, Tayoot Chengsupanimit, Laurie M. Brown, David A. Weinstein, Young Mok Lee – 24 September 2019 – Mutations in the liver glycogen phosphorylase (Pygl) gene are associated with the diagnosis of glycogen storage disease type VI (GSD‐VI). To understand the pathogenesis of GSD‐VI, we generated a mouse model with Pygl deficiency (Pygl−/−). Pygl−/− mice exhibit hepatomegaly, excessive hepatic glycogen accumulation, and low hepatic free glucose along with lower fasting blood glucose levels and elevated blood ketone bodies.

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