Large liver cell change in hepatitis B virus–related liver cirrhosis

Haeryoung Kim, Bong‐Kyeong Oh, Massimo Roncalli, Chanil Park, So‐Mi Yoon, Jeong Eun Yoo, Young Nyun Park – 27 August 2009 – Large liver cell change (LLCC) refers to microscopic lesions often found in various chronic liver diseases; however, its nature is still controversial. Thirty‐four formalin‐fixed and 19 fresh frozen hepatitis B virus (HBV)‐related cirrhosis samples were examined for the presence of LLCC, small liver cell change (SLCC), and hepatocellular carcinoma (HCC).

Influence of a single nucleotide polymorphism in the P1 promoter of the furin gene on transcription activity and hepatitis B virus infection

Rui Xiang Lei, Hong Shi, Xiao Mou Peng, Yin Hong Zhu, Jie Cheng, Gui Hua Chen – 27 August 2009 – Hepatitis B e antigen (HBeAg) is a viral strategy of immune response evasion associated with hepatitis B virus (HBV) persistence. Spontaneous HBeAg seroconversion is usually accompanied by liver disease remission. Unfortunately, this goal is difficult to achieve and requires expensive and time‐consuming treatment. Furin, a proprotein convertase, is involved in HBeAg maturation and is therefore a potential therapeutic target or indicator for predicting disease progression and antiviral response.

Fenofibrate differentially regulates plasminogen activator inhibitor‐1 gene expression via adenosine monophosphate–activated protein kinase–dependent induction of orphan nuclear receptor small heterodimer partner

Dipanjan Chanda, Chul Ho Lee, Yong‐Hoon Kim, Jung‐Ran Noh, Don‐Kyu Kim, Ji‐Hoon Park, Jung Hwan Hwang, Mi‐Ran Lee, Kyeong‐Hoon Jeong, In‐Kyu Lee, Gi Ryang Kweon, Minho Shong, Goo‐Taeg Oh, John Y. L. Chiang, Hueng‐Sik Choi – 27 August 2009 – Plasminogen activator inhibitor type I (PAI‐1) is a marker of the fibrinolytic system and serves as a possible predictor for hepatic metabolic syndromes. Fenofibrate, a peroxisome proliferator‐activated receptor α (PPARα) agonist, is a drug used for treatment of hyperlipidemia.

Incidence, risk factors, and outcome of chronic rejection during antiviral therapy for posttransplant recurrent hepatitis C

Inmaculada Fernández, Esperanza Ulloa, Francisco Colina, Manuel Abradelo, Carlos Jiménez, Alberto Gimeno, Juan Carlos Meneu, Carlos Lumbreras, José Antonio Solís‐Herruzo, Enrique Moreno – 29 July 2009 – Antiviral therapy for recurrent hepatitis C in liver transplantation has been associated with the development of chronic rejection. The aim of this study was to assess the incidence, evolution, and risk factors associated with the development of chronic rejection during posttransplant hepatitis C virus antiviral therapy.

No evidence for systemic platelet activation during or after orthotopic liver transplantation

Ilona T. A. Pereboom, Jelle Adelmeijer, Yvonne van Leeuwen, Herman G. D. Hendriks, Robert J. Porte, Ton Lisman – 29 July 2009 – Platelet function is thought to deteriorate during liver transplantation as a result of platelet activation and proteolysis of platelet receptors by plasmin following reperfusion. However, this hypothesis has never been formally tested. Twenty patients undergoing a first or second liver transplant were included in the study. Blood samples were taken at standardized time points during transplantation and up to 10 days after transplantation.

Proliferative alloresponse of T‐cytotoxic cells identifies rejection‐prone children with steroid‐free liver transplantation

Chethan Ashokkumar, Qing Sun, Ankit Gupta, Brandon W. Higgs, Tamara Fazzolare, Lisa Remaley, George Mazariegos, Kyle Soltys, Geoffrey Bond, Rakesh Sindhi – 29 July 2009 – Donor‐induced and third‐party–induced proliferation of T‐helper and T‐cytotoxic (Tc) cells and their naïve and memory subsets was evaluated simultaneously in single blood samples from 77 children who received steroid‐free liver transplantation (LTx) after induction with rabbit anti‐human thymocyte globulin.

CpG oligodeoxynucleotide triggers the liver inflammatory reaction and abrogates spontaneous tolerance

Lian‐Li Ma, Xiudan Gao, Liping Liu, Zhidan Xiang, Timothy S. Blackwell, Philip Williams, Ravi S. Chari, Deng‐Ping Yin – 29 July 2009 – Liver allografts are spontaneously accepted in the liver transplantation mouse model; however, the basis for this tolerance and the conditions that abrogate spontaneous tolerance to liver allografts are incompletely understood. We examined the role of CpG oligodeoxynucleotide (ODN) in triggering the liver inflammatory reaction and allograft rejection.

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