P Mathurin, D Vidaud, M Vidaud, P Bedossa, V Paradis, V Ratziu, J Chaput, T Poynard – 1 January 1996 – It has previously been shown that, in heavy drinkers, serum apolipoprotein A‐I (ApoA‐I) levels are closely related to the degree of liver injury: they are at a maximum in patients with steatosis, begin to decrease in patients with fibrosis, and reach a minimum in patients with severe cirrhosis. In contrast with serum ApoA‐I variations, serum apolipoprotein B (ApoB) levels are stable.

H O Conn – 1 January 1996

1 January 1996

Thomas A. Gonwa – 1 January 1996

Gilbert R. Park – 1 January 1996

Maria P. Leon, Margaret F. Bassendine, Paul Gibbs, Alistair D. Burt, Michael Thick, John A. Kirby – 1 January 1996 – Intrahepatic biliary epithelial cells were immunomagnetically purified from specimens of disaggregated human liver and were propagated in vitro. After three passes in culture, the cells were shown to be over 85% pure with contaminating leukocytes and endothelial cells constituting less than 2% of the population.

David J. Plevak, David J. Plevak – 1 January 1996

Y Kubo, M Yasunaga, M Masuhara, S Terai, T Nakamura, K Okita – 1 January 1996 – Lead nitrate induces liver cell proliferation in rats without accompanying liver cell necrosis. However, the mechanism of this proliferation and its effect on hepatocytes remain unknown. Therefore, we examined the liver and blood level of hepatocyte growth factor and tumor necrosis factor α (TNF‐α) at various intervals to determine whether lead nitrate modifies hepatocyte proliferation by altering the production of these cytokines.

1 January 1996

Y Zhu, M J Fillenwarth, D Crabb, L Lumeng, R C Lin – 1 January 1996 – Acetaldehyde, the first product of alcohol metabolism, is highly reactive. Several proteins have been shown to be covalently modified by acetaldehyde in vivo. We have previously reported the detection of a cytosolic 37‐kd protein‐acetaldehyde adduct (‐AA) in the liver of alcohol‐fed rats.