We present an experiment-based characterization of passive suppression and active self-interference cancellation mechanisms in full-duplex wireless communication systems. In particular, we consider passive suppression due to antenna separation at the same node, and active cancellation in analog and/or digital domain. First, we show that the average amount of cancellation increases for active cancellation techniques as the received self-interference power increases. Our characterization of the average cancellation as a function of the self-interference power allows us to show that for a constant signal-to-interference ratio at the receiver antenna (before any active cancellation is applied), the rate of a full-duplex link increases as the self-interference power increases. Second, we show that applying digital cancellation after analog cancellation can sometimes increase the self-interference, and thus digital cancellation is more effective when applied selectively based on measured suppression values. Third, we complete our study of the impact of self-interference cancellation mechanisms by characterizing the probability distribution of the self-interference channel before and after cancellation. I. INTRODUCTIONCurrent deployed wireless communication systems employ either a time-division or frequencydivision approach to bidirectional communication. This requires dividing the temporal and/or spectral resources into orthogonal resources and results in half-duplex wireless communication systems. The key deterrent in implementing a full-duplex wireless communication system, which

The COMMD1 protein, implicated in copper homeostasis, is found to regulate endosomal sorting of the copper transporter ATP7A through a novel protein complex containing CCDC22, CCDC93, and C16orf62, which link COMMD1 to the WASH complex.

Abstract-Large-scale (or massive) multiple-input multipleoutput (MIMO) is expected to be one of the key technologies in next-generation multi-user cellular systems based on the upcoming 3GPP LTE Release 12 standard, for example. In this work, we propose-to the best of our knowledge-the first VLSI design enabling high-throughput data detection in single-carrier frequency-division multiple access (SC-FDMA)-based large-scale MIMO systems. We propose a new approximate matrix inversion algorithm relying on a Neumann series expansion, which substantially reduces the complexity of linear data detection. We analyze the associated error, and we compare its performance and complexity to those of an exact linear detector. We present corresponding VLSI architectures, which perform exact and approximate soft-output detection for large-scale MIMO systems with various antenna/user configurations. Reference implementation results for a Xilinx Virtex-7 XC7VX980T FPGA show that our designs are able to achieve more than 600 Mb/s for a 128 antenna, 8 user 3GPP LTE-based large-scale MIMO system. We finally provide a performance/complexity trade-off comparison using the presented FPGA designs, which reveals that the detector circuit of choice is determined by the ratio between BS antennas and users, as well as the desired error-rate performance.Index Terms-Approximate matrix inversion, FPGA design, large-scale (or massive) MIMO, linear soft-output detection, minimum mean square error (MMSE), Neumann series, VLSI.

The immune recognition receptor complex NKG2D-DAP10 on natural killer cells is stimulated by specific ligands carried on virus-infected and malignant cells. Because DAP10 does not have an immunoreceptor tyrosine-based activation motif (ITAM) in its cytoplasmic tail, its ability to trigger killing has been debated. Here we show that a crucial Tyr-Ile-Asn-Met amino acid motif in the cytoplasmic tail of DAP10 couples receptor stimulation to the downstream activation of phosphatidylinositol 3-kinase, Vav1, Rho family GTPases and phospholipase C. Unlike that of ITAM-containing receptors, the activation of NKG2D-DAP10 proceeds independently of Syk family protein tyrosine kinases. Yet the signals initiated by NKG2D-DAP10 are fully capable of inducing killing. Our findings identify a previously unknown mechanism by which receptor complexes that lack ITAM motifs can trigger lymphocyte activation.

NKG2D is an important immunosurveillance receptor that responds to stress-induced ligand expression on tumors and virus-infected cells. Human natural killer cells express NKG2D and require the transmembrane adaptor DAP10 to initiate their full cytotoxic activation. However, DAP10 has no immunoreceptor tyrosine-based activation motif and thus the mechanism of recruiting 'downstream' effector proteins is unclear. We show here that binding of the p85 subunit of phosphatidylinositol-3- kinase to DAP10 could not by itself trigger cell-mediated cytotoxicity and that binding of an intermediate consisting of the DAP10 binding partner Grb2 and the effector molecule Vav1 (Grb2-Vav1) to DAP10 was sufficient to initiate tyrosine-phosphorylation events. For full calcium release and cytotoxicity to occur, both Grb2-Vav1 and p85 had to bind to DAP10. These findings identify a previously unknown mechanism by which NKG2D-DAP10 mediates cytotoxicity and provides a framework for evaluating activation by other receptor complexes that lack immunoreceptor tyrosine-based activation motifs.