A classical model of educational cooperation in Human Anatomy: the Table Leaders.

This project has been developed for many years in the Human Anatomy courses.Its good outcomes have been confirmed by years of evidence of excellent resultsobtained through the learning of Human Anatomy. This method of teaching andlearning as one allows students who are taking Human Anatomy classes to receivepractical training in small groups and transmit it to their colleagues in the practicaltraining established in the Medical degree. Table Leaders feel rewarded as theylearn to speak in public, regularly transmitting the knowledge obtained, and byhaving to be up to date with their studies. These are all aspects that help, not onlythe Table Leaders process of learning, but also that of their colleagues, who seeclosely and carefully anatomical details that help them understand the subject.This method of supporting practical training is always under the supervision ofthe teacher who develops the practical classes. These Leaders used to pass thetest without additional problems. Thus the note was significantly increased versusthe class colleagues.

Anti-proliferative effect of pro-inflammatory cytokines in cultured beta cells is associated with extracellular signal-regulated kinase 1/2 pathway inhibition: protective role of glucagon-like peptide -1.

Pancreatic beta-cell homeostasis is a balance between programmed cell death (apoptosis) and regeneration. Although autoimmune diabetes mellitus type 1 (DM1) is the most-studied cause of beta-cell mass loss by pro-inflammatory cytokine-induced apoptosis, influences of a pro-inflammatory environment on beta-cell regenerative response have been poorly studied. In this study, we assess the anti-proliferative effect of pro-inflammatory cytokines and glucose concentration on rat pancreatic beta cells and the potential protective role of glucagon-like peptide (GLP-1). Apoptotic and proliferating islet cells were stained using the DeadEnd Fluorimetric TUNEL System and 5-bromo-2'-deoxyuridine label respectively, in the presence-absence of varying concentrations of glucose, pro-inflammatory cytokines, and GLP-1. The potential signaling pathways involved were evaluated by western blot. Considerable anti-proliferative effects of pro-inflammatory cytokines interleukin (IL)-1beta, interferon (IFN)-gamma, and tumour necrosis factor-alpha (TNF-alpha) were observed. The effects were synergistic and independent of glucose concentration, and appeared to be mediated by the inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) activation, the signaling pathway involved in beta-cell replication. GLP-1 completely reversed the cytokine-induced inhibition of ERK phosphorylation and increased beta-cell proliferation threefold in cytokine-treated cultures. While pro-inflammatory cytokines reduced islet cell ERK1/2 activation and beta-cell proliferation in pancreatic islet culture, GLP-1 was capable of reversing this effect. These data suggest a possible pharmacological application of GLP-1 in the treatment of early stage DM1, to prevent the loss of pancreatic beta cells as well as to delay the development of overt diabetes.