A ten-year-old dog was presented with pancreatitis and increased hepatic enzymes. On necropsy a large firm mass was observed in the liver extending to the gall bladder. Smaller masses with similar texture were found in multiple organs including lung, stomach, pancreas, lymph nodes, omentum, and mesentery. Neoplastic cells were spindle shaped with prominent osteoid production and occasional trabeculae of woven bone. Tumor cell emboli were observed in the blood vessels and lymphatics of the omentum and stomach. Hepatic osteosarcoma with systemic metastasis is very rare and may serve to broaden the diagnostic spectrum of hepatic and pancreatic diseases in dogs.

The study was designated to investigate the electron microscopic findings following diethylnitrosamine (DEN) treatment in rats. Forty four male (Srague Dawley) rats were continuously given water containing 0.01% DEN for 13 weeks and livers of five rats with more tumor lesions at 16 and 17 weeks after initial treatment were used as EM materials. In transmission electron microscopic findings, most small-sized hepatocytes were active cells containing large mount of organelles, but light (pale staining) hepatocyte among small-sized hepatocytes were injured cells containg disorganized organelles. Tumor cells among small-sized hepatocytes were irregularly arranged and have ;leomorphic nuclei containing electron dense chromatin but the organelles in cytoplasm were swelled. Large-sized hepatocytes were active cells with condensed chromatin but the cytoplasm of these cells were pale due to be injured and dilated organelles. Dark hepatocytes were apoptotic cells with homogenous pyknotic nuclei and cytoplasm, and the cytoplasm of these cells contained dilated smooth endoplasmic reticulum (sER) but these sER were non-vesiculated. Cholangiocarninoma cells were crowed and were pale by far less number of organelles in cytoplasm and nuclei. In scanning electron microscopic findings, the lumens of portal veins, bile canaliculi, bile ductules, bile ducts and sinusoids were dilated and have irregular folded inner surface by protruded parenchyma.

Perfluorooctanoic acid (PFOA), a member of the perfluoroalkyl acids that have wide commercial applications, is persistent organic pollutants widely spread throughout the environment and human population. But little is known about the adverse biological effects of the PFOA. In the present study, the toxicological effects of PFOA were investigated in rats. Sprague-Dawley rats (N = 10 in each group) were orally administered with PFOA in drinking water for 4 weeks (0, 100, 200, or 400 ppm in male, and 0, 200, 400, or 800 ppm in female). These female rats given 800 ppm died during the study. PFOA treatment decreased the body weight gain and increased the liver weights in both genders. Serum biochemical investigations revealed significant increases in the aspartate aminotransferase, alanine transaminase, alkaline phosphatase, blood urea nitrogen, total cholesterol, and total bilirubin in male but in female. Serum estradiol (E2) levels were increased in all treated in all treated rats. Histopathologically, hepatocellular hypertrophy around central vein was noted in the liver of treated rats. No significant histopathological change were noted in other organs. In conclusion, PFOA induced toxicological changes in the liver and increased serum E2 level which was not related to histopathological changes of endocrine and reproductive system.

The insulin-like growth factor-I(IGF-I) is an important metabolic factor involved in cell growth and metabolism. Although secretion of IGF-I in rat liver is regulated by growth hormone, the effects of forskolin, adenylate cyclase activator, on secretion of IGF-I have not been reported. Therefore, a modified perfused rat liver model was used to investigate the regulatory effects of forskolin on IGF-I secretion in this experiment. The results were summerized as follows: 1. Modified perfused rat liver model was not changed to aspartate aminotransferase(AST), alanine aminotransferase(ALT) and lactic dehydrogenase(LDH) secretion in time. 2. The IGF-I secretion in hepatic cell was increased by forskolin(10-5, 10-6 and 10-7M) in a dose-dependent manner as compared with those of the controls, and significantly increased by 10-5 and 10-6M forskolin(p0.05). 3. Secretion of glucose in hepatic cell significantly was decreased by 10-5M forskolin as compared with those of controls(p0.05). These results suggest that forskolin may be involved in the regulation of IGF-I secretion in the perfused rat liver.

A new sudden death in rabbits appeared in China and Korea in 1984 and 1985, respectively, and was recognized to be an acute infectious disease caused by a virus. The disease was reported as a "new viral disease", and thereafter, a tentative name of "viral hemorrhagic disease", "hemorrhagic pneumonia" or "viral hemorrhagic pneumonia" has been described in the case reports. But authors had called the viral disease "rabbit viral hepatitis" due to picornavirus infection, because the principal lesion of the disease was an acute hepatitis. The purpose of this report is to describe the electron microscopic findings on the livers in experimentally infected rabbits. All the livers of the affected rabbits were shown to have degenerative changes of a type that is characteristic of acute hepatitis. In the liver cells, there were dilation of rER and mitochondria, vacuole formation of various sizes, and appearances of many virus-like particles in the vicinity of rER, granular bodies and crystalline arrays of viral particles in the cytoplasm with necrotic changes of the nucleus. Clusters of virus-like particles and viral crystals appeared in the cytoplasm of sinusoid endothelial cells and Kupffer's cells with morphological changes of organelles. Also viral crystals were demonstrated in the cytoplasm of macrophages among the liver cells. On the whole, the liver cells had many virus-like particles and a few crystalline arrays of viral particles. Therefore, this implies that the liver cells are the main site of the viral replication in inducing the viremia. It was concluded that the liver was the primary target organ of this viral disease, and the pathological and the ultrastructural evidence suggest that the virus may belong to genus enterovirus