Tomando como referência a evolução e as características do sistema brasileiro de educação superior discute-se neste artigo os fundamentos de uma efetiva reforma da educação superior. Procura-se mostrar que a adequação desse sistema para o enfrentamento dos desafios da sociedade do conhecimento, em um país como o Brasil, deve necessariamente resolver três questões: a modernização do sistema, o efetivo aprimoramento da qualidade da educação brasileira em todos os níveis, graus e modalidades e a democratização do ensino promovendo a inclusão social.

This paper aims to present the essential basis for an effective higher education reform. The strategies chosen by the authors to develop and to construct their proposals are based on studies of evolution and special features of the Brazilian Higher Education System. By analyzing this special and highly complex system the authors could conclude that in order to fit the challenges which emerge from the knowledge society the higher education system reform adjusted to a country like Brazil has to be reorganized in order to present solutions to three main questions: the system modernization, the improvement of the quality of the whole brazilian education system and the promotion of social inclusion through the access democratization.

Tomando como referencia la evolución y las características del sistema brasileño de educación superior, en este artículo se discuten los fundamentos de una efectiva reforma de la educación superior. Se intenta mostrar que la adecuación de este sistema para el enfrentamiento de los desafíos de la sociedad del conocimiento, en un país como Brasil, se deben necesariamente resolver tres cuestiones la modernización del sistema, la efectiva mejora de la calidad de la educación brasileña a todos los niveles, grados y modalidades, y, la democratización de la enseñanza promoviendo la inclusión social.

Cem ratos norvégicus, machos, com aproximadamente 3 meses de idade foram distribuídos por sorteio em 2 grupos experimentais: Grupo Controle (GC): com 50 ratos sadios, não diabéticos e Grupo Diabético (GD): com 50 ratos diabéticos, induzidos pela aloxana, sem qualquer tratamento. Cada grupo foi dividido em 5 subgrupos com 10 ratos cada e sacrificados com 1, 3, 6, 9 e 12 meses de seguimento, respectivamente. Parâmetros clínicos (peso, ingestão hídrica e alimentar, e diurese) e laboratoriais (glicemia, glicose urinária e insulina) foram documentados em todos os momentos de avaliação. Um segmento do nervo ciático foi obtido de cada animal, em ambos os grupos, para estudo à MO. e ME. Alterações clínicas e laboratoriais significativas (P<0,01), compatíveis com diabetes grave, foram observadas em todos os animais do GD a partir do 4o dia após a indução. Ratos de ambos os grupos apresentaram alterações no número de fibras mielínicas e nos depósitos intraaxonais de glicogênio que não diferiram, estatisticamente, aos 1, 3 e 6 meses de seguimento. Entretanto, aos 9 e 12 meses, ratos do GD apresentaram diminuição significativa no número de fibras mielínicas, com aumento do número de fibras mielínicas de menor calibre, quando comparados com ratos do GC (P<0,05). Grânulos de glicogênio intraaxonais também foram mais acentuados em ratos do GD no 9o e 12o mês de seguimento. Não foram observadas diferenças na densidade de fibras amielínicas ou alterações ultraestruturais significativas entre os dois grupos, em relação aos espaços intraaxonais e endoneurais, bainhas de mielina e células de Schwann durante todo o estudo.

One-hundred male norvegicus rats, approximately 3-months old, were randomly assigned to two experimental groups: Control Group (CG) included 50 non-diabetic control rats and Diabetic Group (DG) included 50 alloxan untreated-diabetic rats. Each group was further divided into 5 subgroups of 10 rats and sacrificed at 1, 3, 6, 9, and 12 months of follow-up, respectively. Clinical (body weight, water and food intake and urine output) and laboratory parameters (blood glucose, urinary glucose and insulin) were documented in all moments of evaluation. A segment of the sciatic nerve was taken from each animal in both groups for light and eletron microscopy. Significant clinical and laboratory changes (P<0.01), compatibles with severe diabetes, were observed in all animals of DG beginning at 4 th day after diabetes induction. There were no significant changes in the number of myelinic fibers and of glycogen granules in DG rats when compared with CG rats at 1, 3, and 6 months of follow-up. However, DG rats presented a significantly decreased number of myelinic fibers, with increase of the number of smaller myelinic fibers, when compared with CG rats (P < 0.05) at 9 and 12 months of follow-up. Intra-axonal glycogen granules were also more evident in DG rats in these periods. No difference was observed between the two experimental groups in the number of unmyelinated fibers. There was also no structural difference in both groups in the intra-axonal and endoneural spaces, in the myelin sheath or in the Schwann cells all over the study.

We studied the effects of islet of Langerhans transplantation (IT) on the kidney lesions of rats with alloxan-induced diabetes. Forty-five inbred male Lewis rats were randomly assigned to 3 experimental groups: group Gl included 15 non-diabetic control rats (NC), group GIT included 15 alloxan-induced diabetic rats (DC), and group III included 15 alloxan-induced diabetic rats that received pancreatic islet transplantation prepared by nonenzymatic method from normal donor Lewis rats and injected into the portal vein (IT). Each group was further divided into 3 subgroups of 5 rats which were sacrificed at 1, 3, and 6 months of follow-up, respectively. Clinical and laboratorial parameters were recorded in the mentioned periods in the 3 experimental groups. For histology, the kidneys of all rats of each subgroup were studied and 50 glomeruli and 50 tubules of each kidney were analyzed using light microscopy by two different investigators in a double blind study. The results showed progressive glomerular basement membrane thickening (GBMT), mesangial enlargement (ME), and Bowman's capsule thickening (BCT) in the 3 experimental groups throughout the follow-up. These alterations were significantly more severe in DC rats at 6 months when compared to NC rats (p < 0.01). However, the degree of GBMT, ME, and BCT observed in DC rats was not statistically different from IT rats at 1, 3, and 6 months. In addition, Armanni-Ebstein lesions of the tubules (AE) and tubular lumen protein (PRO) observed in DC rats were also observed in IT rats all over the study. These lesions were never present in NC rats. We conclude that IT did not prevent progression of kidney lesions in alloxan-induced diabetic rats within 6 months after transplantation.