Objective discrimination of fur type based on electrophoresis optimized for fur-hair proteins.

The accurate identification of animal species used for fur is important for conserving endangered animals, stopping illegal fur distribution, and addressing consumer concerns. Animal species used for fur are currently differentiated by observing species-specific morphological fur-hair features through a microscope. Although this method is simple, the results may differ among inspectors owing to its subjective nature. To develop an objective approach for differentiating animal species based on fur, we utilized the electrophoretic patterns of fur-hair proteins. First, we optimized protein extraction methods to produce clear electrophoretic patterns from fur-hair proteins. Then, we obtained 324 electrophoretic patterns from 54 fur samples belonging to 24 different animals; 216 of the 324 patterns were used for the construction of a discrimination model using two-way orthogonal partial least squares discriminant analysis. The model correctly discriminated between all the remaining 108 patterns without any false negatives or positives. Moreover, this model could discriminate between fur samples from closely related species that are difficult to distinguish using conventional microscopic identification because of the visual similarity of the fur hairs.

Epithelial Nuclear Factor-x03BA;B Activation in Inflammatory Bowel Diseases and Colitis-Associated Carcinogenesis.

Prolonged inflammatory bowel diseases (IBD) may lead to colitis-associated carcinogenesis (CAC). Previous studies had shown that nuclear factor-x03BA;B (NF-x03BA;B) activation in both macrophages and epithelia in inflamed colonic tissue is associated with CAC development. However, the mechanism by which epithelial NF-x03BA;B activation leading to CAC development had not previously been rigorously studied. We and others had observed the increased expression of the type 2 receptor for tumor necrosis factor (TNFR2/TNFRSF1b/p75) in IBD models. Myosin light chain kinase (MLCK) is suggested to be associated with epithelial permeability via TNF signaling. Therefore, the relationship between epithelial MLCK expression and NF-x03BA;B activation via TNFR2 signaling on CAC development was investigated. Pro-tumorigenic cytokines such as interleukin (IL)-1ß, IL-6 and macrophage inflammatory protein-2 at the lamina propria were increased in the setting of colitis and further increased in tumor tissues with upregulated epithelial TNFR2 and MLCK expressions in an animal model of CAC. The upregulated MLCK expression was also observed in TNF-stimulated colonic epithelial cells in vitro in association with the upregulation of TNFR2 but not TNFR1/TNFRSF1a/p55. Gene silencing of tnfrsf1b, but not tnfrsf1a, resulted in restoration of epithelial tight junction (TJ) associated with decreased MLCK expression. The presence of anti-TNF antibody also resulted in restoration of TJ in association with suppressed MLCK expression, and interestingly, similar results including the suppressed TNFR2 and MLCK expressions were observed by inhibiting MLCK in the epithelial cells. MLCK silencing also led to suppressed TNFR2 expression, suggesting that the restored TJ leads to reduced TNFR2 signaling. Such suppression of MLCK as well as blockade of TNFR2 signaling resulted in reduced CAC development, restored TJ, and decreased pro-tumorigenic cytokines. These imply that TNF-induced NF-x03BA;B activation and MLCK expression may be a potential target for the prevention of IBD-associated carcinogenesis.