Potential epidemiologic, economic, and budgetary impacts of current rates of hepatitis C treatment in medicare and non‐medicare populations

John Wittenborn, Joanne Brady, Michelle Dougherty, David Rein – 30 March 2017 – We forecast the health and budgetary impact of hepatitis C (HCV) treatment on the Medicare program based on currently observed rates of treatment among Medicare and non‐Medicare patients and identify the impact of higher rates of treatment among non‐Medicare populations.

Interferon‐alpha‐induced hepatitis C virus clearance restores p53 tumor suppressor more than direct‐acting antivirals

Yucel Aydin, Animesh Chatterjee, Partha K Chandra, Srinivas Chava, Weina Chen, Anamika Tandon, Asha Dash, Milad Chedid, Martin W Moehlen, Frederic Regenstein, Luis A Balart, Ari Cohen, Hua Lu, Tong Wu, Srikanta Dash – 28 March 2017 – The mechanism why hepatitis C virus (HCV) clearance by direct‐acting antivirals (DAAs) does not eliminate the risk of hepatocellular carcinoma (HCC) among patients with advanced cirrhosis is unclear. Many viral and bacterial infections degrade p53 in favor of cell survival to adapt an endoplasmic reticulum (ER)‐stress response.

Identification of a novel alpha‐fetoprotein‐expressing cell population induced by the Jagged1/Notch2 signal in murine fibrotic liver

Yasuhiro Nakano, Sachie Nakao, Hideaki Sumiyoshi, Kenichiro Mikami, Yuri Tanno, Minako Sueoka, Daigo Kasahara, Hiroshi Kimura, Tadashi Moro, Akihide Kamiya, Katsuto Hozumi, Yutaka Inagaki – 27 March 2017 – The liver is well known to possess high regenerative capacity in response to partial resection or tissue injury. However, liver regeneration is often impaired in the case of advanced liver fibrosis/cirrhosis when mature hepatocytes can hardly self‐proliferate. Hepatic progenitor cells have been implicated as a source of hepatocytes in regeneration of the fibrotic liver.

Disrupted ER‐to‐Golgi trafficking underlies anti‐HIV drugs and alcohol‐induced cellular stress and hepatic injury

Hui Han, Yuxin He, Jay Hu, Rhema Lau, Harrison Lee, Cheng Ji – 27 March 2017 – Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) are involved in anti‐human immunodeficiency virus (HIV) drugs and alcohol‐induced liver disease in a significant number of patients infected with HIV. However, the precise mechanism by which the drugs and alcohol cause ER stress remains elusive.

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