Fibroproliferation in liver disease: Role of monocyte factors

Theresa C. Peterson, Richard A. Isbrucker – 1 February 1992 – Fibroproliferation was measured as the uptake of [3H]thymidine into fibroblasts. Human fibroblasts were incubated with 200 μl monocyte‐conditioned medium, the 0.22 μm filtrate from cultured monocytes, in Dulbecco's modified Eagle medium supplemented with controlled process serum replacement 2, a fetal calf serum substitute with low mitogenic activity. Increasing the numbers of fibroblasts resulted in a parallel increase in thymidine uptake to a maximal level.

Portal‐vein obstruction in children leads to growth retardation

Shiv K. Sarin, Anupam Bansal, Shailja Sasan, Aruna Nigam – 1 February 1992 – The portal vein is the main source of blood and hepatotrophic factors to the liver. Partial portal‐vein ligation in rats results in reduced growth compared with that in control rats. To investigate whether extrahepatic portal vein obstruction occurring in early childhood influences growth in humans, anthropometric and nutritional assessments were prospectively carried out in 61 patients with extrahepatic portal vein obstruction.

Lactitol or lactulose in the treatment of chronic hepatic encephalopathy: Results of a meta‐analysis

Pierre Blanc, Jean‐Pierre Daures, Jean‐Michel Rouillon, Pascale Peray, Robert Pierrugues, Dominique Larrey, François Gremy, Henri Michel – 1 February 1992 – Lactitol (β‐galactosido‐sorbitol) has been recently compared with lactulose for the treatment of chronic hepatic encephalopathy in a few studies, each comprising a small number of patients. The results are controversial. We studied the efficiency and tolerance of both compounds by using a meta‐analysis on the basis of published controlled trials.

Evidence that an iron chelator regulates collagen synthesis by decreasing the stability of procollagen mRNA

Hitoshi Ikeda, George Y. Wu, Catherine H. Wu – 1 February 1992 – Iron chelation has been shown previously to decrease collagen synthesis at a posttranslational level by inhibiting prolyl 4‐hydroxylase, one of the key enzymes in collagen metabolism. On the other hand, recent in vivo studies of iron overload in rats suggest that iron could specifically activate collagen gene expression in liver tissues. These findings led us to investigate whether iron chelation might also affect collagen gene expression and posttranslational modification.

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