Alpha-fetoprotein reactive to pisum sativum agglutinin (AFP-R-P) in liver tumor tissues, surrounding noncancerous tissues and peripheral blood from 25 cases of primary liver cancer were measured. Their medium and standard deviation were 41 ?26%, 30?27% and 36?25%, respectively. AFP-R-P levels were lower in the tumors with a diameter of less than 3cm, intact capsule, no invasion of surrounding liver tissues and no tumor thrombus. The patients with lower AFP-R-P levels had a longer survival. The results indicate that AFP-R-P is secreted mainly by tumor cells possessing more malignant behaviour, diffused directly in surrounding liver tissues and entered into peripheral blood, resulting in elevated serum AFP-R-P.

AIM: To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) signaling pathway in the Kupffer cells (KCs) production of pro-inflammatory cytokines, tumor necrosis factor-?(TNF-?) and interleukin-1?(IL-1?), in severe acute pancreatitis (SAP) rats. METHODS: Sprague-Dwaley rats were randomized into three groups: ①sham operation rats, ②SAP rats, ③SAP rats given the p38 MAPK inhibitor CNI-1493(10 mg/kg, iv). The SAP model was induced by the bili-pancreatic duct infusion with 5% sterile soduim taurocholate solution. Rats from each group were killed at 12 h after sham operation or SAP and Kupffer cells (KCs) were isolated. The mRNA expressions of TNF-? and IL-1? (by quantitative real-time RT-PCR) and p38 MAPK activity (by Western blot analysis) in KCs were examined. The levels of TNF-? and IL-1? in plasma were determined by ELISA. RESULTS: There was a significant acvitation of p38 MAPK in KCs harvested from SAP rats than those from sham operation rats. SAP also promoted the mRNA expressions of TNF-? and IL-1? in KCs and the plasma levels of TNF-? and IL-1?. These events were significantly inhibited by treatment with CNI-1493.CONCLUSIONS: p38 MAPK activation is one important aspect of the signaling events that may mediate the KCs production of pro-inflammatory cytokines, TNF-? and IL-1?, in SAP rats. The inhibition of the p38 MAPK may be a potential target in the prevention and treatment of SAP.

Overexpression of multidrug resistance gene, (MDR1) is responsible for the resistance of anticancer agents in cancer cells. In this study, we designed three pairs of DNA primers to clone MDR, cDNA from human normal liver by polymerase chain reaction. The sites of these primers in MDR cDNA are (I)-64-46 (5') and 1680-1698 (3'); (II) 1471-1489 (5') and 2905-2923 (3'); (III)2729-2747 (5') and 3845-3863 (3). The three reactions were underwent after the human normal liver mRNA was reverse transcripted into single strand DNA. The lengths of PCR products are 1762bp, 1452 bp and 1134bp, respectively. The former two products were subcloned in pBluscript SK, respectively and the latter product was subcloned in pGEM7Z (named as pMDR1.7, pMDR1.4 and pMDRl.l, respectively). Cloned genes were certificated as MDR1 cDNA by sequence analysis. Full-length MDR, cDNA was obtained after further subcloning. Full-length MDR1 cDNA we obtained will be a very important tool in molecular diagnosis and gene therapy of anticancer drug resistance.

We have cloned full-length MDR1 cDNA from human normal liver tissue in previous study. Using this MDR1 cDNA as probe, we observed the MDR1 gene expression in human hepatocellular carcinoma treated with and without chemotherapy by Northern blot. The results showed that expression of MDR1 gene in hepatocellular carcinoma tissues was higher than that in their adjacent normal liver tissues; and enhanced MDR1 gene expression was also observed in hepatocellular carcinoma treated with chemotherapic agents. We also explored a method for quantitative analysis of MDR1 gene expression in hepatocellular carcinoma by polymerase chain reaction. This study suggests that overexpression of MDR1 gene may be responsible for the intrinsic and acquired drug resistance of human hepatocellular carcinoma, and PCR is a preferable method for quantitative analysis of MDR1 gene expression in hepatocellular carcinoma.