A recap on Italian neurolaw: epistemological and ethical issues

Italy is in the forefront of forensic neuroscience practice among European nations. In recent years, the country presented two major criminal cases, the Trieste Case in 2009 and the Como Case in 2011, which were the first cases employing neurogenetic and functional neuroimaging methods in European courts. In this paper we will discuss the consequences that an understanding of the neural and genetic determinants of human (mis)behavior will have on law, especially on the Italian legal context. Some claim that such consequences will actually be revolutionary, while others argue that legal doctrine assumptions won’t be undermined by neuroscientific findings. In the first section of the paper, we introduce the general debate and follow with a section devoted to the two Italian cases. In the third and final section, we discuss epistemological and ethical issues regarding Italian neurolaw. We defend a position which diverges from those prevailing in the debate. While negative outcomes and concerns were usually evidenced, we focus on positive changes coming with the new paradigm of interaction between neuroscience and the law. Our view is that these cases are clearly pioneering ones, anticipating what will happen in the courtrooms of the European Union in the whole, in the near future

HIV-1 proteins gp120 and tat induce the epithelial–mesenchymal transition in oral and genital mucosal epithelial cells

The oral, cervical, and genital mucosa, covered by stratified squamous epithelia with polarized organization and strong tight and adherens junctions, play a critical role in preventing transmission of viral pathogens, including human immunodeficiency virus (HIV). HIV-1 interaction with mucosal epithelial cells may depolarize epithelia and disrupt their tight and adherens junctions; however, the molecular mechanism of HIV-induced epithelial disruption has not been completely understood. We showed that prolonged interaction of cell-free HIV-1 virions, and viral envelope and transactivator proteins gp120 and tat, respectively, with tonsil, cervical, and foreskin epithelial cells induces an epithelial-mesenchymal transition (EMT). EMT is an epigenetic process leading to the disruption of mucosal epithelia and allowing the paracellular spread of viral and other pathogens. Interaction of cell-free virions and gp120 and tat proteins with epithelial cells substantially reduced E-cadherin expression and activated vimentin and N-cadherin expression, which are well-known mesenchymal markers. HIV gp120- and tat-induced EMT was mediated by SMAD2 phosphorylation and activation of transcription factors Slug, Snail, Twist1 and ZEB1. Activation of TGF-β and MAPK signaling by gp120, tat, and cell-free HIV virions revealed the critical roles of these signaling pathways in EMT induction. gp120- and tat-induced EMT cells were highly migratory via collagen-coated membranes, which is one of the main features of mesenchymal cells. Inhibitors of TGF-β1 and MAPK signaling reduced HIV-induced EMT, suggesting that inactivation of these signaling pathways may restore the normal barrier function of mucosal epithelia