75 g OGTT is a useful marker to predict the worst outcome and avoid the adverse effect of LES treatment in liver cirrhosis patients if performed without adequate nutrient conduct by a dietician.

We clarified that TNF-alpha mRNA expression was responsible for the inflammatory activity in UC. However, TNF-alpha mRNA expression was not correlated with the mucosal injury in CD.

Lead nitrate induces liver cell proliferation in rats effect on the liver as well as toxic and teratogenic effect without accompanying liver cell necrosis. However, the on various organs. At least two major types of liver mechanism of this proliferation and its effect on hepato-cell proliferation have been shown in rat experimental cytes remain unknown. Therefore, we examined the models: compensatory regeneration caused by necroliver and blood level of hepatocyte growth factor and genic stimulation and hyperplasia induced by mitotumor necrosis factor a (TNF-a) at various intervals to genic agents. 3 The former includes regeneration after determine whether lead nitrate modifies hepatocyte carbon tetrachloride (CCl 4 ) liver injury, D-galactosproliferation by altering the production of these cytoamine liver injury, and choline deficient diet. treatment with these inhibitors suppresses the increase and cyclosporine. 9 Biological and pathological distincof TNF-a messenger RNA (mRNA) in the liver and pre-tions between liver cell regeneration and hyperplasia vents the hepatocyte proliferation induced by lead ni-have been studied to clarify the mechanism of mitotrate. Hepatocyte proliferation occurred by 24 hours and genic stimulation. For example, compensatory cell proreached a peak 48 hours after a single intravenous injec-liferation enhanced the initiation and promotion of cartion of lead nitrate (100 mmol/kg). TNF-a mRNA exprescinogenesis in rat liver, whereas primary hyperplasia sion in the liver was increased 1, 6, and 12 hours after the induced by lead nitrate and ethylene dibromide was injection, whereas no alteration was observed in liver or not carcinogenic.3,10 Transient increases of expression blood level of hepatocyte growth factor. Pretreatment with dexamethasone (4.0 mg/kg), E3330 (100 mg/kg) of some cell cycle-related genes, c-fos and c-myc, were adenosine (0.3 mmol/kg), and pentoxifylline (100 mg/kg), observed in rat models of compensatory regeneration inhibited both TNF-a mRNA expression and hepatocyte such as partial hepatectomized rat and CCl 4 adminisproliferation 48 hours after the injection. These experi-tration. However, this effect was not detected in the mental results strongly support the hypothesis that experimental models using treatment with lead ni- pathways mediating liver cell proliferation induced by Lead nitrate is a mitogen in vivo and has a powerful these mitogens still remains to be investigated. proliferative effect on rat liver without accompanying Recently, it has been shown that several growth fachistopathological liver cell necrosis.1,2 This mitogen is tors, including hepatocyte growth factor (HGF), transan ubiquitous heavy metal salt and has proliferative forming growth factor a (TGF-a), and transforming growth factor b 1 (TGF-b1), regulate liver cell proliferation in the rat models of compensatory regeneration. 13-20 HowAbbreviations: CCl4, carbon tetrachloride; HGF, hepatocyte growth factor; TGF, transforming growth factor; mRNA, messenger RNA; TNF-a, tumor neever, it has b...

ABSTRACT— This study evaluated whether liver regeneration could take place after massive or submassive necrosis of liver cells in 25 patients with several kinds of hepatic failure by immunohistochemical staining for proliferating cell nuclear antigen (PCNA). PCNA positivity was significantly higher (P<0.01) in the patients who survived than in the patients who died. Furthermore, PCNA‐positive hepatocytes were recognized diffusely in the lobule of the liver in survivors. There was positive correlation between PCNA positivity and plasma concentration of AFP (α‐fetoprotein), (r = 0.77, P<0.01). These results show that liver regeneration could take place after massive necrosis of liver cells in survivors from acute hepatic failure and that immunohistochemical staining for PCNA is useful for prognostic evaluation.

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