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As a promising downlink multiple access scheme for future radio access (FRA), this paper discusses the concept and practical considerations of non-orthogonal multiple access (NOMA) with a successive interference canceller (SIC) at the receiver side. The goal is to clarify the benefits of NOMA over orthogonal multiple access (OMA) such as OFDMA adopted by Long-Term Evolution (LTE). Practical considerations of NOMA, such as multi-user power allocation, signalling overhead, SIC error propagation, performance in high mobility scenarios, and combination with multiple input multiple output (MIMO) are discussed. Using computer simulations, we provide system-level performance of NOMA taking into account practical aspects of the cellular system and some of the key parameters and functionalities of the LTE radio interface such as adaptive modulation and coding (AMC) and frequency-domain scheduling. We show under multiple configurations that the system-level performance achieved by NOMA is higher by more than 30% compared to OMA.Keywords − non-orthogonal multiple access, future radio access, power-domain, successive interference canceller

Traumatic injury in the central nervous system induces inflammation; however, the role of this inflammation is controversial. Precise analysis of the inflammatory cells is important to gain a better understanding of the inflammatory machinery in response to neural injury. Here, we demonstrated that leukotriene B4 plays a significant role in mediating leukocyte infiltration after spinal cord injury. Using flow cytometry, we revealed that neutrophil and monocyte/macrophage infiltration peaked 12 hours after injury and was significantly suppressed in leukotriene B4 receptor 1 knockout mice. Similar findings were observed in mice treated with a leukotriene B4 receptor antagonist. Further, by isolating each inflammatory cell subset with a cell sorter, and performing quantitative reverse transcription-PCR, we demonstrated the individual contributions of more highly expressed subsets, ie, interleukins 6 and 1␤, tumor necrosis factor-␣, and FasL, to the inflammatory reaction and neural apoptosis. Inhibition of leukotriene B4 suppressed leukocyte infiltration after injury, thereby attenuating the inflammatory reaction, sparing the white matter, and reducing neural apoptosis, as well as inducing better functional recovery. These findings are the first to demonstrate that leukotriene B4 is involved in the pathogenesis of spinal cord injury through the amplification of leukocyte infiltration, and provide a potential therapeutic Spinal cord injury (SCI) causes severe motor/sensory dysfunction with limited functional recovery. Mechanical trauma rapidly leads to blood-brain barrier disruption, neuronal cell death, edema, axonal damage, and demyelination, followed by a cascade of secondary injuries that expand the inflammatory reaction, which is characterized by immune cell infiltration and activation of systemic immunity at the lesion area.

Cell differentiation is mediated by lineage-determining transcription factors. We show that chromodomain helicase DNA-binding domain 2 (Chd2), a SNF2 chromatin remodelling enzyme family member, interacts with MyoD and myogenic gene regulatory sequences to specifically mark these loci via deposition of the histone variant H3.3 prior to cell differentiation. Directed and genome-wide analysis of endogenous H3.3 incorporation demonstrates that knockdown of Chd2 prevents H3.3 deposition at differentiation-dependent, but not housekeeping, genes and inhibits myogenic gene activation. The data indicate that MyoD determines cell fate and facilitates differentiation-dependent gene expression through Chd2-dependent deposition of H3.3 at myogenic loci prior to differentiation.

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