Immunohistochemical phenotyping of liver macrophages in normal and diseased human liver

Minoru Tomita, Kazuhide Yamamoto, Haruhiko Kobashi, Masaki Ohmoto, Takao Tsuji – 1 August 1994 – The phenotypical heterogeneity of human liver macrophages was analyzed with monoclonal antibodies that recognize antigens specific for the monocytemacrophage lineage. Most liver macrophages in normal and diseased liver were positive for CD68, whereas fewer matured macrophages were detected by 25–F9. Comparative staining of mirror sections revealed some to be doubly positive and others to be singly CD68 positive.

Profiles of expression of carbohydrate chain structures during human intrahepatic bile duct development and maturation: A lectin‐histochemical and immunohistochemical study

Tadashi Terada, Yasuni Nakanuma – 1 August 1994 – We investigated expression of carbohydrate chain structures during human intrahepatic bile duct development and maturation. Results of staining for ABH antigens were negative in the ductal plate and biliary cells migrating into the mesenchyma but were positive in newly formed bile ducts in the fetal liver and in maturing bile ducts in the postnatal liver. Staining for Lewisa, sialyl Lewisa and Lewisb antigens was negative in the ductal plate but positive in migrating biliary cells, newly formed ducts and maturing ducts.

A prospective randomized trial comparing somatostatin and sclerotherapy in the treatment of acute variceal bleeding

Ramon Planas, Juan Carlos Quer, Jaume Boix, Jaume Canet, Manel Armengol, Eduard Cabre, Teresa Pintanel, Pere Humbert, Benjamin Oller, Marc Antoni Broggi, Miquel Angel Gassull – 1 August 1994 – Somatostatin and endoscopic sclerotherapy are widely used in the treatment of acute variceal bleeding. Although objective evidence does exist about the advantages of either treatment, data comparing both procedures are scarce.

Inactivation of Kupffer cells prevents early alcohol‐induced liver injury

Yukito Adachi, Blair U. Bradford, Wenshi Gao, Heidi K. Bojes, Ronald G. Thurman – 1 August 1994 – It is well recognized that consumption of alcohol leads to liver disease in a dose‐dependent manner; however, the exact mechanisms remain unclear. Hypoxia subsequent to a hypermetabolic state may be involved; therefore, when it was observed recently that inactivation of Kupffer cells prevented stimulation of hepatic oxygen uptake by alcohol, the idea that Kupffer cells participate in early events that ultimately lead to alcohol‐induced liver disease became a real possibility.

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