AI as an “autonomous author” urges the law to rethink authorship. Policy makers should consider a reformative conception of AI in copyright law looking at innovative theories in robot law, where new frames for a legal personhood of artificial agents are proposed.

The ultimate resource for designers, engineers, and analyst working with calculations of loads and stress.

An invaluable guide to how modern chess openings are played. This major new work surveys all chess openings, providing a guide to every critical main line and featuring extensive descriptions of the typical strategies for both sides. These commentaries will be welcomed by all club and tournament players, as they will better help them handle middlegame positions arising from each opening.

In chess, sacrificing material is the most dramatic way to try to seize the advantage. Most sacrifices have a forcing aim in mind, but most profound of all are positional sacrifices where the end is impossible to foresee and thus fine judgment, understanding and intuition are required. Such sacrifices are usually a mystery to average players, but acclaimed author and grandmaster Mihai Suba explains the secrets of this technique in entertaining fashion.

This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.