Advance care planning (ACP) for specialists managing cirrhosis: A focus on patient‐centered care

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.

Advance care planning (ACP) for specialists managing cirrhosis: A focus on patient‐centered care

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.

Lipotoxicity induces hepatic protein inclusions through TANK binding kinase 1–mediated p62/sequestosome 1 phosphorylation

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).

Chitinase 3‐like‐1 promotes intrahepatic activation of coagulation through induction of tissue factor in mice

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.

11Beta‐hydroxysteroid dehydrogenase‐1 deficiency or inhibition enhances hepatic myofibroblast activation in murine liver fibrosis

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).

Nucleic acid polymer REP 2139 and nucleos(T)ide analogues act synergistically against chronic hepadnaviral infection in vivo in Pekin ducks

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.

Capicua suppresses hepatocellular carcinoma progression by controlling the ETV4–MMP1 axis

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.

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