Exposure to ionizing radiation during liver transplantation evaluation, waitlist time, and in the postoperative period: A cause for concern

Ser Yee Lee, Michael A. Mooney, Matthew L. Inra, Krishna Juluru, Alyson N. Fox, Sonja K. Olsen, Robert S. Brown, Jean C. Emond, Daniel Cherqui, Michael D. Kluger – 31 July 2013 – Substantial evidence has linked ionizing radiation exposure (RE) to oncogenesis. Patients evaluated for transplantation undergo extensive diagnostic imaging and have increased baseline cancer risk factors. The objective was to examine exposure in a cohort of patients undergoing evaluation and liver transplantation. Radiation exposure from all diagnostic examinations and procedures were retrospectively recorded.

Increased hepatic stiffness as consequence of high hepatic afterload in the fontan circulation: A vascular doppler and elastography study

Shaija S. Kutty, Qinghai Peng, David A. Danford, Scott E. Fletcher, Deborah Perry, Geoffrey A. Talmon, Cynthia Scott, John D. Kugler, Kim F. Duncan, Ruben E. Quiros‐Tejeira, Shelby Kutty, the Liver Adult‐Pediatric‐Congenital‐Heart‐Disease Dysfunction Study (LADS) Group – 31 July 2013 – Hepatic dysfunction is a recognized complication after Fontan palliation of congenital heart disease. We sought to quantitatively measure hepatic stiffness and vascular Doppler indices using ultrasound (US) and shear wave elastography (SWE) in a Fontan cohort.

Hepatitis C virus induced up‐regulation of microRNA‐27: A novel mechanism for hepatic steatosis

Ragunath Singaravelu, Ran Chen, Rodney K. Lyn, Daniel M. Jones, Shifawn O'Hara, Yanouchka Rouleau, Jenny Cheng, Prashanth Srinivasan, Neda Nasheri, Rodney S. Russell, D. Lorne Tyrrell, John Paul Pezacki – 29 July 2013 – MicroRNAs (miRNAs) are small RNAs that posttranscriptionally regulate gene expression. Their aberrant expression is commonly linked with diseased states, including hepatitis C virus (HCV) infection. Herein, we demonstrate that HCV replication induces the expression of miR‐27 in cell culture and in vivo HCV infectious models.

Growth arrest and DNA damage 45G down‐regulation contributes to janus kinase/signal transducer and activator of transcription 3 activation and cellular senescence evasion in hepatocellular carcinoma

Li Zhang, Zhaojuan Yang, Aihui Ma, Yulan Qu, Suhua Xia, Dongxu Xu, Chao Ge, Bijun Qiu, Qiang Xia, Jinjun Li, Yongzhong Liu – 29 July 2013 – Growth arrest and DNA damage 45G (GADD45G), a stress sensor with multiple implications in various biological processes, is down‐regulated in a broad spectrum of cancers. However, little is known about the biological effects of GADD45G on hepatocellular carcinoma (HCC) cells and the related mechanisms. In the present study, we found that GADD45G was commonly down‐regulated in oncogene‐transformed mouse liver cells and in human and mouse HCC.

Risk factors for long‐term persistence of serum hepatitis B surface antigen following acute hepatitis B virus infection in Japanese adults

Kiyoaki Ito, Hiroshi Yotsuyanagi, Hiroshi Yatsuhashi, Yoshiyasu Karino, Yasuhiro Takikawa, Takafumi Saito, Yasuji Arase, Fumio Imazeki, Masayuki Kurosaki, Takeji Umemura, Takafumi Ichida, Hidenori Toyoda, Masashi Yoneda, Eiji Mita, Kazuhide Yamamoto, Kojiro Michitaka, Tatsuji Maeshiro, Junko Tanuma, Yasuhito Tanaka, Masaya Sugiyama, Kazumoto Murata, Naohiko Masaki, Masashi Mizokami, the Japanese AHB Study Group – 29 July 2013 – The proportion of patients who progress to chronicity following acute hepatitis B (AHB) varies widely worldwide.

Hepatitis C virus induced up‐regulation of microRNA‐27: A novel mechanism for hepatic steatosis

Ragunath Singaravelu, Ran Chen, Rodney K. Lyn, Daniel M. Jones, Shifawn O'Hara, Yanouchka Rouleau, Jenny Cheng, Prashanth Srinivasan, Neda Nasheri, Rodney S. Russell, D. Lorne Tyrrell, John Paul Pezacki – 29 July 2013 – MicroRNAs (miRNAs) are small RNAs that posttranscriptionally regulate gene expression. Their aberrant expression is commonly linked with diseased states, including hepatitis C virus (HCV) infection. Herein, we demonstrate that HCV replication induces the expression of miR‐27 in cell culture and in vivo HCV infectious models.

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