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Tissue engineering can be broadly defined as the combination of biology and engineering to repair or replace lost tissue function. From an industry perspective, the field encompasses implanted biomaterials, cell and tissue transplants and therapies, and even extracorporeal cellular devices. To achieve its goals, tissue engineering must effectively utilize not only multiple aspects of engineering but also several aspects of biology that govern mechanisms of organ development, repair and regeneration. The field has always had a strong focus on application yet the challenge of integrating biological science, engineering and medicine has kept many past efforts from reaching their therapeutic and commercial potential. This chapter covers the evolution of tissue engineering, looking at the change in emphasis from bioengineering to stem cell biology and the potential impact of this shift in focus from an industrial perspective. In addition, we have analyzed four major commercial thrusts from past to present: vascular tissue engineering, cartilage repair, liver-assist devices and skin constructs, paying particular attention to how the biomedical disciplines must be integrated to achieve commercial feasibility and therapeutic success. Each example yields one or more important and practical lessons learnt that could be instructive for most future medical and commercial efforts in tissue engineering.

Of the three human arylamine N-acetyltransferase (NAT) genes, (HUMAN)NAT1 and (HUMAN)NAT2 code for functional enzymes, namely (HUMAN)NAT1 and (HUMAN)NAT2. (HUMAN)NAT1 is expressed early during development and is ubiquitously expressed during adulthood, whereas (HUMAN)NAT2 expression and enzyme activity is primarily restricted to adult liver and intestine. A similar temporal and spatial distribution of the corresponding orthologues has been found in rodent models regularly used to investigate their expression and endogenous function, and to understand their role in the metabolism of aromatic amines (AAs). While NAT1 is considered to have an additional endogenous role, NATs are defined as xenobiotic-phase II conjugating enzymes, which N- or O-acetylate AAs, heterocyclic aromatic amines (HAAs) and their N-oxidised metabolites using acetyl-CoA as a co-substrate. The substrates are mainly environmental chemicals, including carcinogens. While both human NATs deactivate their substrates, especially AAs, through N-acetylation, (HUMAN)NAT2 appears to be extremely important also in the activation of carcinogenic compounds. Their presence and activity in the organs involved in uptake of arylamines (skin, respiratory tract, gastro-intestinal tract), influences AA and HAA loads and their fates, thereby allowing their distribution throughout the body (blood), metabolism (liver), excretion (bladder, intestine), but also provoking tumour formation in specific organs, particularly in the case of carcinogenic AAs and HAAs.