Giuseppe Morelli, Alan Reed, Roberto J. Firpi, Victor Machicao, Manal F. Abdelmalek, Consuelo Soldevilla‐Pico, David R. Nelson – 30 January 2006
Ahmet Demirkiran, Alice Kok, Jaap Kwekkeboom, Johannes G. Kusters, Herold J. Metselaar, Hugo W. Tilanus, Luc J.W. van der Laan – 30 January 2006 – Immune regulatory CD4+CD25+ T cells play a crucial role in inducing and maintaining allograft tolerance in experimental models of transplantation (Tx). In humans, the effect of Tx and immunosuppression on the function and homeostasis of CD4+CD25+ regulatory T cells (Tregs) is not well characterized.
Pam Kimball, Melissa Baker, Robert A. Fisher – 30 January 2006 – Hepatitis C (HCV) recurrence after liver transplantation is universal although severity varies. We explored whether certain donor cytokine gene polymorphisms may be useful markers of susceptibility to severe recurrence. Allograft tumor necrosis factor (TNF) β and interleukin (IL) 16 gene polymorphisms were correlated with l‐yr clinical outcome among HCV+ recipients. Recipients of donor TNFβ2,2 (n = 8) experienced less recurrence (50% vs. 71%, P < 0.05), less fibrosis (25% vs. 76%, P < 0.01), and less rejection (25% vs.
Kimberly A. Powers, Ruy M. Ribeiro, Keyur Patel, Stephen Pianko, Lisa Nyberg, Paul Pockros, Andrew J. Conrad, John McHutchison, Alan S. Perelson – 30 January 2006 – Improved understanding of hepatitis C virus (HCV) dynamics during and after liver transplantation can be useful in optimizing antiviral therapy in transplant recipients. We analyzed serum HCV ribonucleic acid (RNA) levels during and after cadaveric liver transplantation in 6 HCV patients.
Harmeet Malhi, Gregory J. Gores, John J. Lemasters – 30 January 2006 – Death of hepatocytes and other hepatic cell types is a characteristic feature of liver diseases as diverse as cholestasis, viral hepatitis, ischemia/reperfusion, liver preservation for transplantation and drug/toxicant‐induced injury. Cell death typically follows one of two patterns: oncotic necrosis and apoptosis. Necrosis is typically the consequence of acute metabolic perturbation with ATP depletion as occurs in ischemia/reperfusion and acute drug‐induced hepatotoxicity.
Vito Racanelli, Barbara Rehermann – 30 January 2006 – The liver is a unique anatomical and immunological site in which antigen‐rich blood from the gastrointestinal tract is pressed through a network of sinusoids and scanned by antigen‐presenting cells and lymphocytes. The liver's lymphocyte population is selectively enriched in natural killer and natural killer T cells which play critical roles in first line immune defense against invading pathogens, modulation of liver injury and recruitment of circulating lymphocytes.
Dr. Andres T. Blei – 30 January 2006
Yasuko Iwakiri, Roberto J. Groszmann – 30 January 2006 – The hyperdynamic circulatory syndrome observed in chronic liver diseases is a great example of research that originated from clinical observations and progressed in the last 50 years from the patient to the experimental laboratory. Our knowledge has evolved from the patient to the molecule, using experimental models that serve as a source for understanding the complex pathophysiological mechanisms that govern this complex syndrome.
Nelson Fausto, Jean S. Campbell, Kimberly J. Riehle – 30 January 2006 – During liver regeneration after partial hepatectomy, normally quiescent hepatocytes undergo one or two rounds of replication to restore the liver mass by a process of compensatory hyperplasia. A large number of genes are involved in liver regeneration, but the essential circuitry required for the process may be categorized into three networks: cytokine, growth factor and metabolic. There is much redundancy within each network, and intricate interactions exist between them.
Neil Kaplowitz – 30 January 2006