Patient Perspectives of High‐Quality Care on the Liver Transplant Waiting List: A Qualitative Study

Nicole T. Shen, Ashley Wu, Karen Farrell, Amanda Ivatorov, Enad Dawod, Michael Raver, Nicholas Russo, Laura Robbins, Monika Safford, Robert S. Brown – 25 September 2019 – The prevalence of advanced liver disease and listing for liver transplantation is increasing. Prior assessments of quality of care neither incorporate nor emphasize the patient perspective on quality of care, which may impact clinical outcomes.

Hyperpolarized Metabolic Imaging Detects Latent Hepatocellular Carcinoma Domains Surviving Locoregional Therapy

Nicholas R. Perkons, Ryan M. Kiefer, Michael C. Noji, Mehrdad Pourfathi, Daniel Ackerman, Sarmad Siddiqui, David Tischfield, Enri Profka, Omar Johnson, Stephen Pickup, Anthony Mancuso, Austin Pantel, Michelle R. Denburg, Gregory J. Nadolski, Stephen J. Hunt, Emma E. Furth, Stephen Kadlecek, Terence P. F. Gade – 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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