Comparison of peptidoglycan‐polysaccharide and lipopolysaccharide stimulation of Kupffer cells to produce tumor necrosis factor and interleukin‐1

Steven N. Lichtman, Jian Wang, John H. Schwab, John J. Lemasters – 1 April 1994 – Endotoxin (lipopolysaccharide) is a cell wall polymer from gram‐negative bacteria that stimulates Kupffer cell release of cytokines such as tumor necrosis factor‐α and interleukin‐1. Another bacterial cell wall polymer in both gram‐negative and gram‐positive organisms is peptidoglycan‐polysaccharide. Lipopolysaccharide and peptidoglycan‐polysaccharide exist together in the intestinal lumen and can cross the intestinal mucosa, enter the portal vein and activate Kupffer cells.

Inappropriate expression of blood group antigens in hepatic allografts

Stuart Bloom, Ken Fleming, Roger Chapman, James Neuberger, Stefan Hubscher – 1 April 1994 – We examined the expression of blood group antigens of the ABO, Lewis and Kell antigen systems using monoclonal antibodies and immunohistochemical study on 42 liver allograft specimens from 33 patients who underwent liver transplantation between 1986 and 1991 to learn whether altered blood group antigen expression might have a bearing on the immunopathogenesis of transplant rejection.

Multiple viral infection as the most common cause of fulminant and subfulminant viral hepatitis in an area endemic for hepatitis B: Application and limitations of the polymerase chain reaction

Jaw‐Ching Wu, Chih‐Li Chen, Ming‐Chih Hou, Trong‐Zong Chen, Shou‐Dong Lee, Kwang‐Juei Lo – 1 April 1994 – We tested serum samples from 25 fulminant hepatitis and 7 subfulminant hepatitis patients for hepatitis A, B, C, D and E viral markers and nucleic acids by means of polymerase chain reaction to determine the role of each virus on such catastrophic events in an area endemic for hepatitis B.

Hepatitis B virus subtypes and hepatitis C virus genotypes in patients with chronic liver disease in Nepal

Santosh Man Shrestha, Fumio Tsuda, Hiroaki Okamoto, Hajime Tokita, Minoru Horikita, Takeshi Tanaka, Yuzo Miyakawa, Makoto Mayumi – 1 April 1994 – A total of 145 patients with chronic liver disease, including 20 with chronic hepatitis, 63 with cirrhosis and 62 with primary hepatocellular carcinoma from Nepal were tested for markers of hepatitis B virus or hepatitis C virus infection. HBsAg was detected in 57 (39%) and hepatitis C virus RNA in 12 (8%); the cause of liver disease was not known in the remaining 76 (52%).

The role of major histocompatibility complex and non‐major histocompatibility complex encoded antigens in generation of bile duct lesions during hepatic graft‐vs.‐host responses mediated by helper or cytotoxic T cells

Fred H. Williams, Dwain L. Thiele – 1 April 1994 – In these studies, we examined the role of discrete classes of alloantigen differences in generating nonsuppurative cholangitis during graft‐vs.‐host disease. Transfer of C57BL/6J (B6) splenocytes to class I major histocompatibility complex‐disparate bm1 × B6 F1, class II major histocompatibility complex‐disparate B6 × bm12 F1, or multiple non‐major histocompatibility complex antigen‐disparate Balb,B × B6 F1 mice led to the development of periportal inflammatory infiltrates and lymphocyte invasion of bile duct walls.

Role of Na,K‐ATPase in regulating acidification of early rat liver endocytic vesicles

Maan Anbari, Karen V. Root, Rebecca W. Van Dyke – 1 April 1994 – Endocytic vesicles are acidified by an electrogenic proton pump and a parallel chloride conductance; however, acidification might be decreased if electrogenic transporters, such as Na,K‐ATPase, that increase vesicle interior‐positive membrane potential were also present. We examined this issue in early rat liver endosomes using ion substitution and inhibitors to alter Na,K‐ATPase activity.

Murine liver allograft transplantation: Tolerance and donor cell chimerism

Shigwang Qian, Anthony J. Demetris, Noriko Murase, Abdul S. Rao, John J. Fung, Thomas E. Starzl – 1 April 1994 – Nonarterialized orthotopic liver transplantation with no immunosuppression was performed in 13 mouse‐strain combinations. Two strain combinations with major histocompatibility complex class I and class II and minor histocompatibility complex disparity had 20% and 33% survival of more than 100 days, but the other 11 combinations, including four that were fully allogeneic and all with only class I, class II or minor disparities, yielded 45% to 100% survival of more than 100 days.

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