Non-orthogonal multiple access (NOMA) is a potential enabler for the development of 5G and beyond wireless networks. By allowing multiple users to share the same time and frequency, NOMA can scale up the number of served users, increase the spectral efficiency, and improve user-fairness compared to existing orthogonal multiple access (OMA) techniques. While single-cell NOMA has drawn significant attention recently, much less attention has been given to multi-cell NOMA. This article discusses the opportunities and challenges of NOMA in a multi-cell environment. As the density of base stations and devices increases, inter-cell interference becomes a major obstacle in multi-cell networks. As such, identifying techniques that combine interference management approaches with NOMA is of great significance. After discussing the theory behind NOMA, this paper provides an overview of the current literature and discusses key implementation and research challenges, with an emphasis on multi-cell NOMA. I. WHAT DRIVES NOMA?The next generation of wireless networks will require a paradigm shift in order to support massive numbers of devices with diverse data rate and latency requirements. Particularly, the increasing demand for Internet of Things (IoT) devices poses challenging requirements on 5G wireless systems. Two key features of 5G are expected to be a latency of 1ms, compared to 10 ms in the 3rd Generation Partnership Project (3GPP) Long-Term Evolution (LTE), and support for 10 Gbps throughput.To fulfill these requirements, numerous potential technologies have been introduced over the last few years.

Lipoxygenases (LOXs) are a family of nonheme iron dioxygenases that catalyze the regioselective and stereospecific hydroperoxidation of polyunsaturated fatty acids, and are involved in a variety of inflammatory diseases and cancers. The crystal structure of rabbit 15S-LOX1 that was reported by Gillmor et al. in 1997 has played key roles for understanding the properties of mammalian LOXs. In this structure, three segments, including 12 residues in the superficial alpha2 helix, are absent and have usually been described as "disordered." By reinterpreting the original crystallographic data we were able to elucidate two different conformations of the molecule, both having well ordered alpha2 helices. Surprisingly, one molecule contained an inhibitor and the other did not, thereby adopting a closed and an open form, respectively. They differed in the conformation of the segments that were absent in the original structure, which is highlighted by a 12 A movement of alpha2. Consequently, they showed a difference in the size and shape of the substrate-binding cavity. The new model should provide new insight into the catalytic mechanism involving induced conformational change of the binding pocket. It may also be helpful for the structure-based design of LOX inhibitors.

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This tacrolimus population PK model will be a valuable tool in developing rational guidelines and provides a basis for individualized therapy after kidney transplantation in clinical settings of Korea.

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