The current Core Curricula of Degree courses in Biomedical areas has enormously compressed the hours dedicated to the student for self-learning in morphological subjects. The result is a reduced student attitude to integrate the information received by attending lectures and practical sessions, with the indispensable consultation of texts dealing with morphological and ‘functional’ subjects, a key experience to autonomously logically identify the rational of the morphology/function relationship in the human body, at the macroscopic and microscopic level. These changes are occurring at a time when new medical imaging technologies become more and more informative in both morphological and functional areas. As a consequence, we are modifying our way of organize lessons compared to the generations of colleagues who have preceded us. More and more frontal lessons are organized with a logical morpho-functional approach. For example, the reference to the anatomy of the living, displayed through invasive or not invasive imaging, is added to the necessary and traditional anatomy of the cadaver. The reference to the pathology helps to define how the alteration of morphological integrity is reflected on function, both at the macro and microscopic level, and so on. However, there are no organized easy-to-use guided tours for the student to allow, in the shortest possible time, to ‘rationally see’ what he has studied, in the various imaging contexts available at the macro- and microscopic level. At the same time, there are no ‘data bank’ of resources for the preparation of the lessons. That is why we have imagined ‘virtual campus’ an integrated digital learning platform for self-learning. The platform has been thought and realized thanks to a group of teachers of ‘morphologic’ and ‘functional’ biomedical subjects and computer engineers belonging to a publishing house. The presentation will explain the rationale behind the platform, its structure and the educational opportunities offered.

Le linkage of some 24 diseases to mutations in proteins of the nuclear envelope has stimulated a major reassessment of the function of the nuclear envelope, and particularly the nuclear lamina, as more than half of these diseases are caused by mutations of the LMNA gene, coding lamin A. As a consequence of these studies, we now envisage the nuclear envelope/lamina functioning not only as a molecular device regulating the transfer of macromolecules between the cytoplasm and the nucleus, but as a key cellular hub in integrating critical functions that include chromatin, organization, modulation of signaling pathways, and transcriptional regulation (1). A fundamental issue in deciphering the molecular basis of the pathogenic mechanisms of laminopathies has been obtained demonstrating that these diseases are not due to a loss of function of lamin A but to a gain of function of immature forms of the protein, referred to as prelamin A, which are differently modified by posttranslational processes (2). Here we review the involvement of defects of prelamin A processing in the pathogenesis of different classes of laminopathies, which include muscular, metabolic, and progeric laminopathies. In particular, we will focus on the pathogenic mechanism of the Hutchinson-Gilford progeric syndrome (HGPS), which involve a particular form of prelamin A, the progerin, whose accumulation in the nucleus affects both chromatin arrangement and transcriptional regulation. The identification of the molecular basis of progeric laminopathies contributed to the development of a targeted therapy on the experimental models of the disease (3). In the last three years encouraging results have been also obtained by pharmacological trials on selected groups of progeric patients. Since low levels of progerin are also accumulated in normal aging, particular attention has been given to differential expression of prelamin A forms in the cells of a particular class of healthy aged subjects, represented by centenarians (4).