Extracellular vesicles as therapeutic carriers of microRNAs for cholangiocarcinoma
Sergio A. Gradilone – 5 November 2016
Sergio A. Gradilone – 5 November 2016
Yongdong Niu, Meishu Xu, Betty L. Slagle, Haihua Huang, Song Li, Grace L. Guo, Ganggang Shi, Wenxin Qin, Wen Xie – 5 November 2016 – Chronic hepatitis B virus infection is a major risk factor for hepatocellular carcinoma (HCC). Hepatitis B virus X protein (HBx) is a hepatitis B virus protein that has multiple cellular functions, but its role in HCC pathogenesis has been controversial. Farnesoid X receptor (FXR) is a nuclear receptor with activities in anti‐inflammation and inhibition of hepatocarcinogenesis.
Jean‐Louis Delaunay, Alix Bruneau, Brice Hoffmann, Anne‐Marie Durand‐Schneider, Véronique Barbu, Emmanuel Jacquemin, Michèle Maurice, Chantal Housset, Isabelle Callebaut, Tounsia Aït‐Slimane – 5 November 2016 – ABCB4 (MDR3) is an adenosine triphosphate (ATP)‐binding cassette (ABC) transporter expressed at the canalicular membrane of hepatocytes, where it mediates phosphatidylcholine (PC) secretion.
Jagpreet Chhatwal, Sumeyye Samur, Brian Kues, Turgay Ayer, Mark S. Roberts, Fasiha Kanwal, Chin Hur, Drew Michael S. Donnell, Raymond T. Chung – 5 November 2016 – The availability of oral direct‐acting antivirals has altered the hepatitis C virus (HCV) treatment paradigm for both pre–liver transplant (LT) and post‐LT patients. There is a perceived trade‐off between pre‐LT versus post‐LT treatment of HCV—treatment may improve liver function but potentially decrease the likelihood of a necessary LT.
Haider Altaii, Sadeer G. Al‐Kindi, Guilherme H. Oliveira, Zaid Yaqoob, Carlos Romero‐Marrero – 5 November 2016
Veronica L. Massey, Christine E. Dolin, Lauren G. Poole, Shanice V. Hudson, Deanna L. Siow, Guy N. Brock, Michael L. Merchant, Daniel W. Wilkey, Gavin E. Arteel – 5 November 2016 – The extracellular matrix (ECM) consists of diverse components that work bidirectionally with surrounding cells to create a responsive microenvironment. In some contexts (e.g., hepatic fibrosis), changes to the ECM are well recognized and understood. However, it is becoming increasingly accepted that the hepatic ECM proteome (i.e., matrisome) responds dynamically to stress well before fibrosis.
Shuai Yan, Juan Tang, Yuyao Zhang, Yuanyang Wang, Shengkai Zuo, Yujun Shen, Qianqian Zhang, Di Chen, Yu Yu, Kai Wang, Sheng‐Zhong Duan, Ying Yu – 5 November 2016 – Prostaglandin E2 (PGE2) is an important lipid mediator of inflammation. However, whether and how PGE2 regulates hepatic cholesterol metabolism remains unknown. We found that expression of the PGE2 receptor, E prostanoid receptor 3 (EP3) expression is remarkably increased in hepatocytes in response to hyperlipidemic stress.
Eun‐Jeong Joo, Yoosoo Chang, Joon‐Sup Yeom, Seungho Ryu – 5 November 2016 – The presence of an association between chronic hepatitis B virus (HBV) infection and fatty liver is controversial. We examined the association between HBV infection and the development of nonalcoholic fatty liver disease (NAFLD). We conducted a cohort study of 83,339 participants without NAFLD at baseline who underwent serologic testing for hepatitis B surface antigen (HBsAg) between 2002 and 2006 and were followed annually or biennially until December 2014.
Jennifer A. Flemming, W. Ray Kim, Carol L. Brosgart, Norah A. Terrault – 5 November 2016 – Direct‐acting antiviral (DAA) therapy, recently approved for patients with decompensated cirrhosis (DC) secondary to hepatitis C virus (HCV), is associated with improved hepatic function. We analyzed trends in liver transplant (LT) wait‐listing (WL) to explore potential impact of effective medical therapy on WL registration. This is a cohort study using the Scientific Registry of Transplant Recipients database from 2003 to 2015.
Jung Hee Kim, Dong Hyun Sinn, Wonseok Kang, Geum‐Youn Gwak, Yong‐Han Paik, Moon Seok Choi, Joon Hyeok Lee, Kwang Cheol Koh, Seung Woon Paik – 5 November 2016 – The long‐term clinical impact of low‐level viremia (LLV; <2,000 IU/mL) is not well understood. As a result, it is unclear whether the development of LLV during entecavir monotherapy requires a change in therapy.