Artificial Intelligence as a Means to Moral Enhancement

This paper critically assesses the possibility of moral enhancement with ambient intelligence technologies and artificial intelligence presented in Savulescu and Maslen (2015). The main problem with their proposal is that it is not robust enough to play a normative role in users’ behavior. A more promising approach, and the one presented in the paper, relies on an artifi-cial moral reasoning engine, which is designed to present its users with moral arguments grounded in first-order normative theories, such as Kantianism or utilitarianism, that reason-responsive people can be persuaded by. This proposal can play a normative role and it is also a more promising avenue towards moral enhancement. It is more promising because such a system can be designed to take advantage of the sometimes undue trust that people put in automated technologies. We could therefore expect a well-designed moral reasoner system to be able to persuade people that may not be persuaded by similar arguments from other people. So, all things considered, there is hope in artificial intelli-gence for moral enhancement, but not in artificial intelligence that relies solely on ambient intelligence technologies

Snail1 induces epithelial-to-mesenchymal transition and tumor initiating stem cell characteristics

<p>Abstract</p> <p>Background</p> <p>Tumor initiating stem-like cells (TISCs) are a subset of neoplastic cells that possess distinct survival mechanisms and self-renewal characteristics crucial for tumor maintenance and propagation. The induction of epithelial-mesenchymal-transition (EMT) by TGFβ has been recently linked to the acquisition of TISC characteristics in breast cancer. In HCC, a TISC and EMT phenotype correlates with a worse prognosis. In this work, our aim is to elucidate the underlying mechanism by which cells acquire tumor initiating characteristics after EMT.</p> <p>Methods</p> <p>Gene and protein expression assays and Nanog-promoter luciferase reporter were utilized in epithelial and mesenchymal phenotype liver cancer cell lines. EMT was analyzed with migration/invasion assays. TISC characteristics were analyzed with tumor-sphere self-renewal and chemotherapy resistance assays. <it>In vivo </it>tumor assay was performed to investigate the role of Snail1 in tumor initiation.</p> <p>Conclusion</p> <p>TGFβ induced EMT in epithelial cells through the up-regulation of Snail1 in Smad-dependent signaling. Mesenchymal liver cancer post-EMT demonstrates TISC characteristics such as tumor-sphere formation but are not resistant to cytotoxic therapy. The inhibition of <it>Snail1 </it>in mesenchymal cells results in decreased <it>Nanog </it>promoter luciferase activity and loss of self-renewal characteristics <it>in vitro</it>. These changes confirm the direct role of Snail1 in some TISC traits. <it>In vivo</it>, the down-regulation of <it>Snail1 </it>reduced tumor growth but was not sufficient to eliminate tumor initiation. In summary, TGFβ induces EMT and TISC characteristics through Snail1 and Nanog up-regulation. In mesenchymal cells post-EMT, Snail1 directly regulates <it>Nanog </it>expression, and loss of Snail1 regulates tumor growth without affecting tumor initiation.</p