Ravi Chhatrala, M. Bilal Siddiqui, R. Todd Stravitz, Carolyn Driscoll, Arun Sanyal, Carol Sargeant, Velimir Luketic, Amit Sharma, Richard Sterling, Scott Matherly, Puneet Puri, M. Shadab Siddiqui – 11 March 2015 – Although cardiovascular disease (CVD) is the leading cause of long‐term mortality in liver transplant recipients (LTRs), the role of recently identified biomarkers of CVD risk in liver transplantation is unknown. We aimed to evaluate an extensive CVD risk profile in LTRs.

Takanori Funaki, Kensuke Shoji, Ippei Miyata, Seisuke Sakamoto, Mureo Kasahara, Hironori Yoshii, Isao Miyairi, Akihiko Saitoh – 11 March 2015 – After liver transplantation (LT), live attenuated vaccines (LAVs) are generally contraindicated. LAVs are recommended before LT for patients ≥ 6 months of age. However, the evidence supporting this practice is limited. Patients were enrolled before and after LT. Clinical data for patients were obtained from medical records. Serum antibody titers were evaluated at the time of enrollment and prospectively.

Sung‐Gyu Lee, Sung‐Hwan Moon, Hee‐Je Kim, Ji Yoon Lee, Soon‐Jung Park, Hyung‐Min Chung, Tae‐Yong Ha, Gi‐Won Song, Dong‐Hwan Jung, Hojong Park, Tae‐Won Kwon, Yong‐Pil Cho – 11 March 2015 – The study was designed (1) to examine the hypothesis that circulating progenitor cells play a role in the process of de novo regeneration in human liver transplants and that these cells arise from a cell population originating in, or associated with, the bone marrow and (2) to investigate whether the transplanted liver volume has an effect on the circulating recipient‐derived progenitor cells that generate

Javier Michelena, José Altamirano, Juan G. Abraldes, Silvia Affò, Oriol Morales‐Ibanez, Pau Sancho‐Bru, Marlene Dominguez, Juan Carlos García‐Pagán, Javier Fernández, Vicente Arroyo, Pere Ginès, Alexandre Louvet, Philippe Mathurin, Wajahat Z. Mehal, Juan Caballería, Ramón Bataller – 11 March 2015 – Alcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in the absence of an infection.

Solenne Marmier, Renaud Dentin, Martine Daujat‐Chavanieu, Hervé Guillou, Justine Bertrand‐Michel, Sabine Gerbal‐Chaloin, Jean Girard, Sophie Lotersztajn, Catherine Postic – 11 March 2015 – Carbohydrate responsive element binding protein (ChREBP) is central for de novo fatty acid synthesis under physiological conditions and in the context of nonalcoholic fatty liver disease. We explored its contribution to alcohol‐induced steatosis in a mouse model of binge drinking as acute ethanol (EtOH) intoxication has become an alarming health problem.

Julien Rogier, Stéphanie Roullet, François Cornélis, Matthieu Biais, Alice Quinart, Philippe Revel, Paulette Bioulac‐Sage, Brigitte Le Bail – 11 March 2015 – Fatty liver disease, including liver steatosis, is a major health problem worldwide. In liver transplantation, macrovesicular steatosis in donor livers is a major cause of graft failure and remains difficult to assess. On one hand, several imaging modalities can be used for the assessment of liver fat, but liver biopsy, which is still considered the gold standard, may be difficult to perform in this context.

Kostas Pantopoulos – 11 March 2015

Frank A. Anania – 10 March 2015

Viktor V. Chirikov, Fadia T. Shaya, Charles D. Howell – 7 March 2015 – Patient‐ and county‐level characteristics associated with advanced liver disease (ALD) at hepatitis C virus (HCV) diagnosis were examined in three Medicare cohorts: (1) elderly born before 1945; (2) disabled born 1945‐1965; and (3) disabled born after 1965. We used Medicare claims (2006‐2009) linked to the Area Health Resource Files. ALD was measured over the period of 6 months before to 3 months after diagnosis.

Toshifumi Hoki, Koji Miyanishi, Shingo Tanaka, Kohichi Takada, Yutaka Kawano, Akira Sakurada, Masanori Sato, Tomohiro Kubo, Tsutomu Sato, Yasushi Sato, Rishu Takimoto, Masayoshi Kobune, Junji Kato – 7 March 2015 – Increased hepatic iron accumulation is thought to be involved in the pathogenesis of nonalcoholic steatohepatitis (NASH). Hepatic iron accumulation, as well as oxidative DNA damage, is significantly increased in NASH livers. However, the precise mechanism of iron accumulation in the NASH liver remains unclear.