Experimental thioacetamide-induced cirrhosis of the liver

Hepatic cirrhosis is a complex disease in which several biological, biochemical and chemical alterations are combined, none of these alone being sufficient for diagnosis. The morphological characteristics of the final stages of cirrhosis are well known, but the initial lesions and intermediate stages still have not been fully clarified. An experimental model of hepatic cirrhosis by chronic administration over 30 weeks of thioacetamide (50 mglkg twice weekly) to female Wistar rats has been produced. In a macroscopic, microscopic and ultrastructural study. The different lesions that appeared were evaluated according to the dose of the toxic agent administered up, until hepatic cirrhosis was finally installed; this was after 60 doses of the toxic agent (30 weeks). Discussion is made of the different types of administration and the doses employed to obtain a suitable survival rate for these cases; in our experiments this was 95%. It has been demonstrated in both human and experimental pathology that once the disease itself has been installed, currently there is no rational or useful treatment for it. A beneficial effect has been demonstrated for certain substances, improving the initial and intermediate lesions. so we conclude by stating that it is necessary to further study the hepatic lesions preceeding cirrhosis. Knowledge of these lesions could form the basis for establishing a useful and rational therapy for such cases

Down regulation of gastric and intestinal phenotypic expression in Epstein-Barr virus-associated stomach cancers

importance of gastric and intestinal phenotypic expression for stomach carcinogenesis. In this study, we focused on Epstein-Barr virus (EBV)-associated stomach cancers, with special attention to Cdx2. Methods and Results: We evaluated the expression of gastric and intestinal phenotypic markers by immunohistochemistry in 35 EBV-positive [EBV (+)] and 75 EBV-negative [EBV (-)] stomach cancers in Colombia. The lesions were divided phenotypically into gastric (G), gastric-and-intestinal mixed (GI), intestinal (I), and null (N) phenotypes. In the EBV (+) cases, the lesions were divided phenotypically into 9 G (25.7%), 1 GI (2.9%), 3 I (8.6%), and 22 N (62.9%) types. Similarly, the EBV (-) lesions were also classified phenotypically as 15 G (20.0%), 19 GI (25.3%), 24 I (32.0%), and 17 N (22.7%) types. The proportion of N type EBV (+) lesions was higher than for their EBV (-) counterparts (P<0.0001). The expression of Cdx2 and MUC2 was also found to be significantly lower in EBV (+) than in EBV (-) stomach cancers (P=0.0001; P<0.0001). Cdx2 expression in the intestinal metaplastic glands present in non-neoplastic mucosa surrounding EBV (+) lesions was also significantly lower than in EBV (-) tumors (P=0.016) despite no evidence of EBV infection by low expression of intestinal phenotype markers, including Cdx2, and only occasional gastric phenotypic expression