Grading alcoholic hepatitis
Ewan Forrest, Saket Singhal, Geoffrey Haydon, Christopher Day, Neil Fisher, Alison Brind, Peter Hayes – 15 July 2005
Ewan Forrest, Saket Singhal, Geoffrey Haydon, Christopher Day, Neil Fisher, Alison Brind, Peter Hayes – 15 July 2005
Michelle Embree‐Ku, Philip A. Gruppuso – 15 July 2005 – During the last 3 days of fetal development in the rodent, a burst of hepatocyte proliferation results in a tripling of liver size. Despite stimulation of mitogenesis via multiple signaling pathways, including some that are considered stress response pathways, little apoptosis accompanies this cell growth.
Saul J. Karpen – 15 July 2005
Carla W. Brady, Andrew J. Muir – 15 July 2005
Steven C. Katz, Venu G. Pillarisetty, Joshua I. Bleier, T. Peter Kingham, Umer I. Chaudhry, Alaap B. Shah, Ronald P. DeMatteo – 15 July 2005 – The contribution of intrahepatic conventional T cells to the unique immunologic properties of the liver has not been clearly defined. We isolated bulk and CD4 T cells from mouse liver and compared their functions with each other and with their splenic counterparts. Unlike bulk spleen T cells, bulk liver T cells reacted minimally to allogeneic or antigen‐loaded syngeneic dendritic cells.
Feng Zhou, Maureen N. Ajuebor, Paul L. Beck, Tai Le, Cory M. Hogaboam, Mark G. Swain – 15 July 2005 – The CD154–CD40 interaction is a critical costimulatory pathway modulating the cellular immune response. Moreover, fulminant hepatitis of various etiologies is characterized by a hepatic influx of CD154‐expressing T cells and an upregulation of CD40 expression on Kupffer cells and hepatocytes, implicating this pathway in the pathogenesis of fulminant hepatitis.
15 July 2005
Claudio E. Lagoa, Yoram Vodovotz, Donna B. Stolz, Franck Lhuillier, Carol McCloskey, David Gallo, Runkuan Yang, Elena Ustinova, Mitchell P. Fink, Timothy R. Billiar, Wendy M. Mars – 15 July 2005 – Hemorrhagic shock (HS) followed by resuscitation (HS‐R) is characterized by profound physiological changes. Even if the patient survives the initial blood loss, these poorly understood changes can lead to morbidity. One of the tissues most often affected is liver. We sought to recognize specific hepatic changes induced by this stressor to identify targets for therapeutic intervention.
Alexander Monto, Lorna M. Dove, Alan Bostrom, Sanjay Kakar, Phyllis C. Tien, Teresa L. Wright – 15 July 2005 – Liver disease in patients coinfected with HIV and hepatitis C virus (HCV) has received increasing attention in recent years. Steatosis is accepted as an important contributor to liver disease in patients with HCV, but despite coinfected patients having several reasons to have steatosis, the prevalence and significance of such changes has received scant attention.
Boris Görg, Matthias Wettstein, Sabine Metzger, Freimut Schliess, Dieter Häussinger – 15 July 2005