Protocol, pattern and paper: interactive stabilization of immunohistochemical knowledge.

This paper analyzes the investigation of the distribution of the protein tenascin-C in canine mammary tumors. The method involved immunohistochemistry of tissue slices, performed by the application of an antibody to tenascin-C that specifically can be made visible for microscopic inspection. The first phase of the project is the making of the protocol, the second the deduction of a pattern of tenascin-C distribution in tumors and the third the writing of a paper.

Tenascin-C in chronic canine hepatitis: immunohistochemical localization and correlation with necro-inflammatory activity, fibrotic stage, and expression of alpha-smooth muscle actin, cytokeratin 7, and CD3+ cells.

During fibrosis, the extracellular matrix (ECM) is continuously remodeled and increases in volume due to the production of various proteins. We studied the distribution of tenascin-C (TN-C) and the correlation of TN-C with the necro-inflammatory activity and expression of alpha-smooth muscle actin (alpha-SMA), cytokeratin 7 (CK7), and CD3+ T-lymphocytes in canine chronic hepatitis. This was analyzed using immunohistochemistry and semiquantitative scoring.

Immunohistochemical expression of tenascin in melanocytic tumours of dogs.

The aim of this study was to investigate tenascin-C (TN) immunolabelling and labelling for endothelium by von Willebrand Factor (vWF) in melanocytic tumours of dogs as compared with normal tissues, to evaluate the TN distribution in these types of tumours and to investigate whether a relation could be established between TN and angiogenesis in different types of tumour. Samples of normal dog skin (n=8), benign skin melanocytomas (n=10), malignant oral melanomas (n=9) and malignant toe melanomas (n=5) were studied. The percentages of TN and vWF immunolabelling per total microscopical area were analysed by morphometric methods.

Transforming growth factor beta-1 signalling in canine hepatic diseases: new models for human fibrotic liver pathologies.

Background/aims: The purpose of this study was to validate spontaneous chronic hepatitis and cirrhosis in dogs as a potential large animal model for fibrotic liver disease in humans by evaluating their molecular pathophysiology.

Methods: Transforming growth factor-beta1 (TGF-beta1) signalling was analysed in liver samples of dogs with acute hepatitis (AH), chronic hepatitis (CH), cirrhosis (CIRR), and a specific form of cirrhosis, lobular dissecting hepatitis (LDH), in comparison with human cirrhotic samples from alcohol abuse (ALC) and hepatitis C (HC).

Results: Canine samples were investigated with quantitative real-time PCR (Q-PCR) and Western blotting on TGF-beta1 signalling including Smad2/3 phosphorylation.

Expression of versican in relation to chondrogenesis-related extracellular matrix components in canine mammary tumors.

Versican plays a role in tumor cell proliferation and adhesion and may also regulate cell phenotype. Furthermore, it is one of the pivotal proteoglycans in mesenchymal condensation during prechondrogenesis. We have previously demonstrated accumulation of versican protein in myoepithelial-like spindle cell proliferations and myxoid tissues of complex and mixed mammary tumors of dogs.