Liver Proliferation Is an Essential Driver of Fibrosis in Mouse Models of Nonalcoholic Fatty Liver Disease

Ashley Cast, Meenasri Kumbaji, Amber D'Souza, Katherine Rodriguez, Anita Gupta, Rebekah Karns, Lubov Timchenko, Nikolai Timchenko – 17 July 2019 – Nonalcoholic fatty liver disease (NAFLD) involves development of hepatic steatosis, fibrosis, and steatohepatitis. Because hepatic steatosis appears first in NAFLD animal models, the current therapy development focuses on inhibition of hepatic steatosis, suggesting that further steps of NAFLD will be also inhibited. In this report, we show that the first event of NAFLD is liver proliferation, which drives fibrosis in NAFLD.

Incidence, Risk Factors, and Outcomes of Transition of Acute Kidney Injury to Chronic Kidney Disease in Cirrhosis: A Prospective Cohort Study

Rakhi Maiwall, Samba Siva Rao Pasupuleti, Chhagan Bihari, Archana Rastogi, Pawan Kumar Singh, Vini Naik, Akanksha Singh, Priyanka Jain, Awinash Kumar, Amar Mukund, R.P. Mathur, Guresh Kumar, Shiv Kumar Sarin – 16 July 2019 – Transition to chronic kidney disease (CKD) after an episode of acute kidney injury (AKI) is known in patients without cirrhosis. We studied the incidence and risk factors for development of CKD in patients with cirrhosis. Competing risk analysis was performed to identify risk factors for CKD development.

Diabetes Is Associated With Increased Risk of Hepatocellular Carcinoma in Patients With Cirrhosis From Nonalcoholic Fatty Liver Disease

Ju Dong Yang, Fowsiyo Ahmed, Kristin C. Mara, Benyam D. Addissie, Alina M. Allen, Gregory J. Gores, Lewis R. Roberts – 15 July 2019 – Diabetes increases the risk of liver disease progression and cirrhosis development in patients with nonalcoholic steatohepatitis (NASH). The association between diabetes and the risk of hepatocellular carcinoma (HCC) in NASH patients with cirrhosis is not well quantified. All patients with the diagnosis of NASH cirrhosis seen at Mayo Clinic Rochester between January 2006 and December 2015 were identified.

Posttranscriptional Inhibition of Protein Tyrosine Phosphatase Nonreceptor Type 23 by Staphylococcal Nuclease and Tudor Domain Containing 1: Implications for Hepatocellular Carcinoma

Nidhi Jariwala, Rachel G. Mendoza, Dawn Garcia, Zhao Lai, Mark A. Subler, Jolene J. Windle, Nitai D. Mukhopadhyay, Paul B. Fisher, Yidong Chen, Devanand Sarkar – 15 July 2019 – Oncoprotein staphylococcal nuclease and tudor domain containing 1 (SND1) regulates gene expression at a posttranscriptional level in multiple cancers, including hepatocellular carcinoma (HCC). Staphylococcal nuclease (SN) domains of SND1 function as a ribonuclease (RNase), and the tudor domain facilitates protein–oligonucleotide interaction.

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