External carcinogens, such as tobacco and alcohol, induce molecular changes in large areas of oral mucosa, which increase the risk of malignant transformation. This condition, known as 'field cancerization', can be detected in biopsy specimens using histochemical techniques, even before histological alterations are identified. The efficacy of these histochemical techniques as biomarkers of early cancerization must be demonstrated in appropriate models. The hamster cheek pouch oral cancer model, universally employed in biological studies and in studies for the prevention and treatment of oral cancer, is also an excellent model of field cancerization. The carcinogen is applied in solution to the surface of the mucosa and induces alterations that recapitulate the stages of cancerization in human oral mucosa. We have demonstrated that the following can be used for the early detection of cancerized tissue: silver staining of nucleolar organizer regions; the Feulgen reaction to stain DNA followed by ploidy analysis; immunohistochemical analysis of fibroblast growth factor-2, immunohistochemical labeling of proliferating cells to demonstrate an increase of epithelial cell proliferation in the absence of inflammation; and changes in markers of angiogenesis (i.e. those indicating vascular endothelial growth factor activity, endothelial cell proliferation and vascular density). The hamster cheek pouch model of oral cancer was also proposed and validated by our group for boron neutron capture therapy studies for the treatment of oral cancer. Clinical trials of this novel treatment modality have been performed and are underway for certain tumor types and localizations. Having demonstrated the efficacy of boron neutron capture therapy to control tumors in the hamster cheek pouch oral cancer model, we adapted the model for the long-term study of field cancerized tissue. We demonstrated the inhibitory effect of boron neutron capture therapy on tumor development in field cancerized tissue with acceptable levels of mucositis, a dose-limiting side-effect.

We developed an experimental didactic proposal to teach both carbohydrate metabolism and lactose intolerance as the disease related to that metabolism. Therefore, we implemented an empirical strategy consisting of inexpensive and nontoxic components for which students do not need to know any of the laboratory techniques. The fact that students were able to discuss their own results obtained from the experiments performed in their classroom gave them an additional motivation to learn the subject.Keywords: Lactose intolerance, carbohydrate metabolism, kit, biological models.Because of its structural characteristics, cellular metabolism is a fundamental issue for the comprehension of the essential processes that occur in organisms. In introductory biology courses, we have noticed that learning biochemistry and cellular basis of an organism and relation between cellular metabolism and the way the multicellular organisms work are difficult tasks for the students. Essentially, they cannot understand, in biochemical terms, the relation between what they see macroscopically and how the cell uses different nutrients [1].We firmly believe that these topics could be more attractive to the students if they were explained with relation to the metabolic pathway of a particular disease. If so, students would be able to analyze the normal metabolic pathway of the disease and hypothesize the functional consequences that can take place when one of the steps of the metabolism is altered.In addition, we consider that if these topics were taught in an empirical way, they would be learnt more easily. However, we are aware that in courses with lots of students, it is really difficult to develop an empirical kind of work due to the lack of laboratories and students' knowledge about the laboratory techniques.Taking these difficulties into consideration, our purpose was to develop an experimental didactic proposal to teach both carbohydrate metabolism (particularly lactose metabolism) and lactose intolerance as the disease related to that metabolism. This proposal is suitable for students in the secondary school and those taking up courses in medicine or nutrition.In normal conditions, mucous cells of the intestine synthesize lactase [2,3], an enzyme that degrades lactose, the sugar present in milk, to its two monomers: glucose and galactose. A number of individuals stop synthesizing lactase when they are 4 years old and can therefore not assimilate lactose [3]. When this happens, lactose reaches the large intestine, where bacteria hydrolyze lactose, producing glucose. As a result of the accumulation and fermentation of the lactose, the person suffers from flatulence and diarrhea [3,4]. In our experience, students tend to confuse lactose intolerance with the other digestive diseases such as Celiac disease.This capacity of intestinal bacteria to hydrolyze and metabolize lactose is shared by Lactobacillus bulgaricus, a bacterium of the Lactobacillus genus, which is used in the milk industry for the production of yoghurt [4]. On the other h...