In-band full-duplex (IBFD) operation has emerged as an attractive solution for increasing the throughput of wireless communication systems and networks. With IBFD, a wireless terminal is allowed to transmit and receive simultaneously in the same frequency band. This tutorial paper reviews the main concepts of IBFD wireless. Because one the biggest practical impediments to IBFD operation is the presence of self-interference, i.e., the interference caused by an IBFD node's own transmissions to its desired receptions, this tutorial surveys a wide range of IBFD self-interference mitigation techniques. Also discussed are numerous other research challenges and opportunities in the design and analysis of IBFD wireless systems.

This paper describes the design and implementation of a network virtualization substrate ( ) for effective virtualization of wireless resources in cellular networks. Virtualization fosters the realization of several interesting deployment scenarios such as customized virtual networks, virtual services, and widearea corporate networks, with diverse performance objectives. In virtualizing a base station's uplink and downlink resources into slices, meets three key requirements-isolation, customization, and efficient resource utilization-using two novel features: 1) introduces a provably optimal slice scheduler that allows existence of slices with bandwidth-based and resource-based reservations simultaneously; and 2) includes a generic framework for efficiently enabling customized flow scheduling within the base station on a per-slice basis. Through a prototype implementation and detailed evaluation on a WiMAX testbed, we demonstrate the efficacy of . For instance, we show for both downlink and uplink directions that can run different flow schedulers in different slices, run different slices simultaneously with different types of reservations, and perform slice-specific application optimizations for providing customized services.

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T cells generate adaptive immune responses mediated by the T cell receptor (TCR)-CD3 complex comprising an αβ TCR heterodimer noncovalently associated with three CD3 dimers. In early T cell activation, αβ TCR engagement by peptide-major histocompatibility complex (pMHC) is first communicated to the CD3 signaling apparatus of the TCR-CD3 complex, but the underlying mechanism is incompletely understood. It is possible that pMHC binding induces allosteric changes in TCR conformation or dynamics that are then relayed to CD3. Here, we carried out NMR analysis and molecular dynamics (MD) simulations of both the α and β chains of a human antiviral TCR (A6) that recognizes the Tax antigen from human T cell lymphotropic virus-1 bound to the MHC class I molecule HLA-A2. We observed pMHC-induced NMR signal perturbations in the TCR variable (V) domains that propagated to three distinct sites in the constant (C) domains: 1) the Cβ FG loop projecting from the Vβ/Cβ interface; 2) a cluster of Cβ residues near the Cβ αA helix, a region involved in interactions with CD3; and 3) the Cα AB loop at the membrane-proximal base of the TCR. A biological role for each of these allosteric sites is supported by previous mutational and functional studies of TCR signaling. Moreover, the pattern of long-range, ligand-induced changes in TCR A6 revealed by NMR was broadly similar to that predicted by the MD simulations. We propose that the unique structure of the TCR β chain enables allosteric communication between the TCR-binding sites for pMHC and CD3.

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