A 65 year old woman with lupoid hepatitis developed hepatocellular carcinoma which was diagnosed at an early stage. She had no history of blood transfusion and serum hepatitis B virus markers were negative. Prednisolone and 6-mercaptopurine were administered for the treatment of lupoid hepatitis. A hepatocellular carcinoma was detected by the elevation of serum alpha-fetoprotein and imaging studies. A tumour, 1.4 cm in diameter, was located in the lateral segment of the left hepatic lobe. It was resected by hepatic subsegmentectomy. Histological study showed a hepatocellular carcinoma of Edmondson type II against a background of posthepatitic cirrhosis. The patient was in good condition 2.5 years after the operation.

Aged↗

PubMedDate not supplied

Role of heat-shock proteins in the induction of thermotolerance in Chinese hamster V79 cells by heat and chemical agents.

To examine the involvement of heat shock proteins in the induction of thermotolerance in Chinese hamster V79 cells, thermotolerance was induced by heating of the cells at 42 degrees C for 4 h or at 44 degrees C for 20 min, or by treatment of the cells with 50 microM sodium arsenite for 3 h or 20 micrograms/ml puromycin for 4 h. Under unstressed conditions V79 cells synthesized constitutively three major heat-shock proteins, hsp70, hsp85 and hsp105. On exposure to conditions under which thermotolerance was induced, the synthesis of constitutive hsp70, hsp85 and hsp105 increased, but the inducible form of hsp70 was not synthesized, indicating that this inducible form was not necessary for the induction of thermotolerance. Although the amounts of heat-shock proteins synthesized in the cells that acquired thermotolerance were not always more than those synthesized constitutively in unstressed cells, the stressed cells synthesized heat-shock proteins (especially hsp70) preferentially over other proteins. As the level of hsp70 in the thermotolerant cells was almost the same as that in unstressed cells, the specific accumulation of hsp70 seemed not to be required for the acquisition of thermotolerance. From these findings it seemed likely that, for the induction of thermotolerance in V79 cells, hsp70 preferentially synthesized during or after the stress has an important function. Or the synthesis of heat shock proteins may not be important, and constitutively synthesized heat-shock proteins acquire a specific function during or after the stress.

Animals↗

PubMedDate not supplied

Characteristic synthesis and redistribution of 70 kd heat shock protein in thermotolerant Chinese hamster V79 cells.

Upon exposure to heat shock the increased rate of hsp70 synthesis decreased more rapidly in thermotolerant V79 cells than in the non-thermotolerant cells. However, the levels of hsp70 in the thermotolerant cells at 12 h after a heat shock were almost the same as those in the non-thermotolerant cells. On the other hand, the migration of hsp70 from cytoplasm to nucleoli after a heat shock was very rapid in both thermotolerant and non-thermotolerant cells, but hsp70 in the nucleoli disappeared faster in the thermotolerant cells than in the non-thermotolerant cells, and this coincided with the faster decline of hsp70 synthesis in the thermotolerant cells. For the characteristic distribution of hsp70, protein synthesis was not required. Furthermore, the induction and expression of thermotolerance by the cells were little affected by the inhibition of protein synthesis. Thus, the synthesis of hsp70 itself seemed not to be essential for the induction and expression of thermotolerance of the cells, although hsp70 may be essential for thermoresistance of cells. The rapid decrease of hsp70 synthesis and the rapid disappearance of hsp70 from the nucleoli after a heat shock may be essential for the expression of thermotolerance of the cells.

Animals↗

PubMedDate not supplied

Enhanced expression of translation factor mRNAs in hepatocellular carcinoma.

Several studies have demonstrated elevated expression of translation factor mRNAs in malignant tissues. In this study, using primary human hepatocellular carcinoma (HCC) tissues, we examined gene expression of translation factors, including 2 eukaryotic initiation factors (eIFs-4A1, -4E), 4 elongation factors (eEFs-1 alpha, -1 gamma, -1 delta, and -2) and 10 ribosomal proteins (Rps P1, P2, S10, L35, L5, L39, L9, L6, S3a and S17), whose mRNA expression has never been examined in HCC. Our results demonstrated that all the mRNAs examined were up-regulated in HCC tissues. Among 7 HCC tissues of different histological grades, the expression of these mRNAs remained at basal levels in a well to moderately differentiated (W/M-) HCC, was coordinately up-regulated in moderately differentiated (M-) HCCs. In moderately to poorly differentiated (M/P-) HCCs, the expression of eEFs-1 gamma, -1 delta, -2, Rps P0 and L9 mRNAs was further up-regulated along with the histological grading. These results therefore suggest that coordination and specific activation of translation factor genes might be involved in the process of liver carcinogenesis.

Carcinoma, Hepatocellular↗

PubMedDate not supplied

Enhanced expression of S8, L12, L23a, L27 and L30 ribosomal protein mRNAs in human hepatocellular carcinoma.

Differential display (DD) analysis using surgically resected human hepatocellular carcinoma (HCC) and adjacent non-tumorous liver tissues was performed. We identified 5 cDNAs up-regulated in human hepatocellular carcinoma, encoding S8, L12, L23a, L27 and L30 ribosomal protein mRNAs. Northern blot analysis, using total RNAs from thirteen pairs of HCC and abjacent non-tumorous liver tissues demonstrated that these mRNA levels were up-regulated along with the histological grading of tumors. The expression of these mRNAs was also high in three human HCC cell lines (HuH-7, HepG2 and HLF), irrespective of the growth state. These results suggest that activation of these genes is an important manifestation of HCC phenotypes.

Blotting, Northern↗

PubMedDate not supplied

Experimental studies on aconitine-induced atrial fibrillation with microelectrodes.

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Alkaloids↗