Banishree Saha, Fatemeh Momen‐Heravi, Istvan Furi, Karen Kodys, Donna Catalano, Anwesha Gangopadhyay, Reka Haraszti, Abhishek Satishchandran, Arvin Iracheta‐Vellve, Adeyinka Adejumo, Scott A. Shaffer, Gyongyi Szabo – 18 December 2017 – A salient feature of alcoholic liver disease (ALD) is Kupffer cell (KC) activation and recruitment of inflammatory monocytes and macrophages (MØs). These key cellular events of ALD pathogenesis may be mediated by extracellular vesicles (EVs).

Tung‐Hung Su, Tai‐Chung Tseng, Jia‐Horng Kao – 18 December 2017

Amanda Brisebois, Kathleen P. Ismond, Michelle Carbonneau, Jan Kowalczewski, Puneeta Tandon – 18 December 2017 – Advance care planning (ACP) and goals of care designation (GCD) are being integrated into modern health care. In cirrhosis, uptake and adoption of these practices have been limited with physicians citing many perceived barriers and limitations. Recognizing the many tangible benefits of ACP and GCD processes in patients with life‐limiting chronic diseases, the onus is on health practitioners to initiate and direct these conversations with their patients and surrogates.

Amanda Brisebois, Kathleen P. Ismond, Michelle Carbonneau, Jan Kowalczewski, Puneeta Tandon – 18 December 2017 – Advance care planning (ACP) and goals of care designation (GCD) are being integrated into modern health care. In cirrhosis, uptake and adoption of these practices have been limited with physicians citing many perceived barriers and limitations. Recognizing the many tangible benefits of ACP and GCD processes in patients with life‐limiting chronic diseases, the onus is on health practitioners to initiate and direct these conversations with their patients and surrogates.

Elizabeth K. Speliotes – 18 December 2017

Chun‐Seok Cho, Hwan‐Woo Park, Allison Ho, Ian A. Semple, Boyoung Kim, Insook Jang, Haeli Park, Shannon Reilly, Alan R. Saltiel, Jun Hee Lee – 18 December 2017 – Obesity commonly leads to hepatic steatosis, which often provokes lipotoxic injuries to hepatocytes that cause nonalcoholic steatohepatitis (NASH). NASH, in turn, is associated with the accumulation of insoluble protein aggregates that are composed of ubiquitinated proteins and ubiquitin adaptor p62/sequestosome 1 (SQSTM1).

Zhao Shan, Xiaodong Liu, Yuan Chen, Meng Wang, Yue Rachel Gao, Liangguo Xu, Wasim A. Dar, Chun Geun Lee, Jack Angel Elias, Pavel Davizon Castillo, Jorge Di Paola, Cynthia Ju – 18 December 2017 – Coagulation is a critical component in the progression of liver disease. Identification of key molecules involved in the intrahepatic activation of coagulation (IAOC) will be instrumental in the development of effective therapies against liver disease.

Xiantong Zou, Prakash Ramachandran, Timothy J. Kendall, Antonella Pellicoro, Elena Dora, Rebecca L. Aucott, Kajal Manwani, Tak Yung Man, Karen E. Chapman, Neil C. Henderson, Stuart J. Forbes, Scott P. Webster, John P. Iredale, Brian R. Walker, Zoi Michailidou – 18 December 2017 – A hallmark of chronic liver injury is fibrosis, with accumulation of extracellular matrix orchestrated by activated hepatic stellate cells (HSCs). Glucocorticoids limit HSC activation in vitro, and tissue glucocorticoid levels are amplified by 11beta‐hydroxysteroid dehydrogenase‐1 (11βHSD1).

Jonathan Quinet, Catherine Jamard, Madeleine Burtin, Matthieu Lemasson, Sylviane Guerret, Camille Sureau, Andrew Vaillant, Lucyna Cova – 18 December 2017 – Nucleic acid polymer (NAP) REP 2139 treatment was shown to block the release of viral surface antigen in duck HBV (DHBV)‐infected ducks and in patients with chronic HBV or HBV/hepatitis D virus infection. In this preclinical study, a combination therapy consisting of REP 2139 with tenofovir disoproxil fumarate (TDF) and entecavir (ETV) was evaluated in vivo in the chronic DHBV infection model.

Eunjeong Kim, Donghyo Kim, Jeon‐Soo Lee, Jeehyun Yoe, Jongmin Park, Chang‐Jin Kim, Dongjun Jeong, Sanguk Kim, Yoontae Lee – 18 December 2017 – Hepatocellular carcinoma (HCC) is developed by multiple steps accompanying progressive alterations of gene expression, which leads to increased cell proliferation and malignancy. Although environmental factors and intracellular signaling pathways that are critical for HCC progression have been identified, gene expression changes and the related genetic factors contributing to HCC pathogenesis are still insufficiently understood.