ABSTRACT. A 10-month old male Shi-tzu was presented with a week history of scurfy skin and whitish masses located in the ventral portion of tongue. Grossly, two whitish prominences with diameters of 3 to 4 mm were found on the underside of the tongue. Microscopically, in ulcerative epidermis, deposition of dense, amorphous granular basophilic calcium salts was separated by thin fibrous connective tissue containing mild inflammation. Many fascicles were characterized by replacement of degenerating myofibers with calcification. The precise cause of calcification could not be determined; however, it is interesting that two different lesions shown in calcinosis circumscripta and slight nutritional myopathy were also observed simultaneously only in the tongue. KEY WORDS: calcinosis circumscripta, canine, nutritional myopathy.

Among many detrimental injuries, alcohol is implicated in hepatitis, fatty liver, hepatic fibrosis, and cirrhosis. The purpose of this study was to evaluate the protective effect of bio-active ceramic water on alcohol-induced hepatic injury in pigs. Twelve male Landrace pigs were divided into 3 groups. Groups 1, 2, and 3 were fed with bio-active ceramic water + normal liquid diet, bio-active ceramic water + liquid diet containing 15% ethanol, and tap water + liquid diet containing 15% ethanol for 12 weeks, respectively. For serological, histopathological, and immunohistochemical analysis, all pigs were sacrificed at week 12. In group 3, serum ALT and AST levels increased, and mild fatty change and moderate necrosis were detected in the liver. Collagen fibers, myofibroblasts, and CYP2E1 were also increased or activated in group 3. In group 2, there were mild hepatic injuries compared to group 3. However, injuries and activations were not observed in the liver in group 1. We suggest that the bio-active ceramic water used in the present study had protective capability against ethanol-induced hepatic injury and that having no toxic effect on the pig liver. The bio-active ceramic water might be useful as a therapeutic drinking water in patients suffering from alcoholic liver diseases.

A stillborn bovine male fetus with abdominal distention, arthrogryposis and atresia ani was presented for diagnostic evaluation. At necropsy, this fetus had a large amount of ascites, urachal obstruction and marked bladder distention. The ventral surface of the bladder had ruptured and attached to the abdominal wall by fibrinous adhesions. There was bilateral hydronephrosis with moderate pelvic dilatation and cortical attenuation. The rectum was filled with meconium but the anus was imperforate. The right forelimb was contracted. The cause(s) of these abnormalities could not be determined; however, we believe that developmental abnormalities during embryogenesis may be the result of chromosomal abnormalities.

Hepatitis C virus (HCV) has become a major public health issue. It is prevalent in most countries. HCV infection frequently begins without clinical symptoms, before progressing to persistent viremia, chronic hepatitis, cirrhosis and hepatocellular carcinoma (HCC) in the majority of patients (70% to 80%). Alcohol is an independent cofactor that accelerates the development of HCC in chronic hepatitis C patients. The purpose of the current study was to evaluate ethanol-induced hepatic changes in HCV core-Tg mice and mutant core Tg mice. Wild type (NTG), core wild-Tg mice (TG-K), mutant core 116-Tg mice (TG-116) and mutant core 99-Tg mice (TG-99) were used in this investigation. All groups were given drinking water with 10% ethanol and 5% sucrose for 13 weeks. To observe liver morphological changes, we performed histopathological and immunohistochemical examinations. Histopathologically, NTG, TG-K and TG-116 mice showed moderate centrilobular necrosis, while severe centrilobular necrosis and hepatocyte dissociation were observed in TG-99 mice with increasing lymphocyte infiltration and piecemeal necrosis. In all groups, a small amount of collagen fiber was found, principally in portal areas. None of the mice were found to have myofibroblasts based on immunohistochemical staining specific for α-SMA. CYP2E1-positive cells were clearly detected in the centrilobular area in all groups. In the TG-99 mice, we also observed cells positive for CK8/18, TGF-β1 and phosphorylated (p)-Smad2/3 and p21 around the necrotic hepatocytes in the centrilobular area (p < 0.01). Based on our data, alcohol intake induced piecemeal necrosis and hepatocyte dissociation in the TG-99 mice. These phenomena involved activation of the TGF-β1/p-Smad2/3/p21 signaling pathway in hepatocytes. Data from this study will be useful for elucidating the association between alcohol intake and HCV infection.