[Intranuclear cytoplasmic autophagosomes cause specific nucleolysis and cell death of liver cancer cells and liver cells].

The structure and performance of nuclear cytoplasmic autophagosomes was explored. Seventeen cases of hepatocellular carcinoma and liver cells with other diseases from liver tissues were selected. The nuclear cytoplasm were isolated and degraded by the nuclear membrane. Damaged cytoplasm had damaged its own membrane and the surrounding nuclear tissues other than the nuclear membrane, leading to specific nucleolysis and cell death of liver cancer cells and liver cells.

A study on pathogenicity of hepatitis G virus.

AIM: To study the pathogenicity of hepatitis G virus (HGV) and observe the genesis and pathological process of hepatitis G. METHODS: HGV-RNA in serum was detected by RT-PCR assay. The immunohistochemical assays of liver tissue were performed with HGV monocoloned antibody (McAb) expressed from the region of HGV NS5 nucleic acid sequence. The clinical and pathological data of 52 patients with hepatitis G were discussed. In animal experiment, the Chinese Rhesus monkeys were infected with the serum of a patient with HGV infection. And the dynamic changes in serology and liver histology of animals were observed. RESULTS: One hundred and fifty-four patients with HGV-RNA positive were selected from 1552 patients with various kinds of hepatitis. Of 154 patients with HGV infection, 52 were infected with HGV only, which accounted for 33.8 (52/154) and 102 with positive HGV-RNA were super-infected with other hepatitis viruses, which accounted for 66.2 (102/154). The clinical and pathological observation showed that the acute and chronic hepatitis could be induced by HGV. The slight abnormality of transaminases ALT and AST in serum of monkeys lasted nearly 12 months and histological results showed a series of pathological changes. CONCLUSION: HGV is a hepatotropic virus and has pathogenicty.

Establishment and application of an experimental model of human fetal hepatocytes for investigation of the protective effects of silybin and polyporus umbellalus polysaccharides.

AIM: To establish a new experimental model system of human fetal hepatocytes to study the mechanisms underlying the protective effect of silybin and polyporus umbellalus polysaccharides (PSP) on the cellular ultrastructure. METHODS: Human fetal hepatocytes were obtained from the liver of a human fetus that resulted from a medically necessary induced labor; the mother provided informed consent for sampling, experimental use and publication of findings. The hepatocytes were cultured and then pretreated with silybin or PSP or without either (control), after which the treated cells were exposed to CCl4 for 4 h. Changes in cellular ultrastructure were observed by scanning electron microscopy and transmission electron microscopy, and changes in alanine aminotransferase (ALT), aspartate aminotransferase (AST) and superoxide dismutase (SOD) were assayed. RESULTS: Levels of ALT and AST were significantly decreased, and level of SOD was elevated in the two pretreatment groups following CCl4 exposure, as compared to the control group. The cellular integrity and ultrastructure were well preserved in the two pretreatment groups but were seriously damaged in the control group. CONCLUSION: The CCl4-induced hepatotoxic cell model system of human fetal hepatocytes is an effective tool for studying the hepatoprotective effect of drugs and may be applicable for studies to screen medicines for treatment of hepatitis.

[The nature of "hydropic degeneration" of hepatocytes in severe viral hepatitis].

Specimens were fixed with a mixed fluid of osmium acid potassium ferrocyanide, and embedded with Epon--812. Totally, biopsies from 21 cases of severe chronic viral hepatitis were investigated. When hydropic degeneration of hepatocytes occurred, the clear field in cytoplasm were actually places for accumulating massive glycogen. The granules around the nuclei were convergent mitochondria, endoplasm reticulum and other organelles. Glycogen was best shown in this experiment because of adoption of the mixed fluid as the fixative, which successfully prevented the loss of glycogen during dehydration and the process of uranyl acetate staining. In our opinion this change in hepatocytes might better be termed "glycogen degeneration". It is probably related to infusion of large amount of glucose fluid or due to damage of certain glycogenolytic enzymes in the liver.