7,162 research outputs found

    Optimal low-complexity detection for space division multiple access wireless systems

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    A symbol detector for wireless systems using space division multiple access (SDMA) and orthogonal frequency division multiplexing (OFDM) is derived. The detector uses a sphere decoder (SD) and has much less computational complexity than the naive maximum likelihood (ML) detector. We also show how to detect non-constant modulus signals with constrained least squares (CLS) receiver, which is designed for constant modulus (unitary) signals. The new detector outperforms existing suboptimal detectors for both uncoded and coded systems

    LFV couplings of the extra gauge boson Z' and leptonic decay and production of pseudoscalar mesons

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    Considering the constraints of the lepton flavor violating (LFV) processes μ3e\mu \rightarrow 3e and τ3μ\tau\rightarrow3\mu on the LFV couplings ZijZ'\ell_{i}\ell_{j}, in the contexts of the E6E_{6} models, the left-right (LR) models, the "alternative" left-right (ALR) models and the 331 models, we investigate the contributions of the extra gauge boson ZZ' to the decay rates of the processes ijνν\ell_{i}\rightarrow\ell_{j}\nu_{\ell}\nu_{\ell}, τμP\tau\rightarrow\mu P and PμeP\rightarrow \mu e with P=π0,ηP=\pi^{0},\eta and η\eta '. Our numerical results show that the maximal values of the branching ratios for these processes are not dependent on the ZZ' mass MZM_{Z'} at leader order. The extra gauge boson ZXZ'_{X} predicted by the E6E_{6} models can make the maximum value of the branching ratio Br(τμνν)Br(\tau\rightarrow\mu\nu_{\ell}\nu_{\ell}) reach 1.1×1071.1\times10^{-7}. All ZZ' models considered in this paper can produce significant contributions to the process τμP\tau\rightarrow\mu P. However, the value of Br(Pμe)Br(P\rightarrow\mu e) is far below its corresponding experimental upper bound.Comment: 14 pages, 2 figures; matches published versio

    Quantum Electroweak Symmetry Breaking Through Loop Quadratic Contributions

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    Based on two postulations that (i) the Higgs boson has a large bare mass mHmh125m_H \gg m_h \simeq 125 GeV at the characteristic energy scale McM_c which defines the standard model (SM) in the ultraviolet region, and (ii) quadratic contributions of Feynman loop diagrams in quantum field theories are physically meaningful, we show that the SM electroweak symmetry breaking is induced by the quadratic contributions from loop effects. As the quadratic running of Higgs mass parameter leads to an additive renormalization, which distinguishes from the logarithmic running with a multiplicative renormalization, the symmetry breaking occurs once the sliding energy scale μ\mu moves from McM_c down to a transition scale μ=ΛEW\mu =\Lambda_{EW} at which the additive renormalized Higgs mass parameter mH2(Mc/μ)m^2_H(M_c/\mu) gets to change the sign. With the input of current experimental data, this symmetry breaking energy scale is found to be ΛEW760\Lambda_{EW}\simeq 760 GeV, which provides another basic energy scale for the SM besides McM_c. Studying such a symmetry breaking mechanism could play an important role in understanding both the hierarchy problem and naturalness problem. It also provides a possible way to explore the experimental implications of the quadratic contributions as ΛEW\Lambda_{EW} lies within the probing reach of the LHC and the future Great Collider.Comment: 10 pages, 2 figures, published versio

    DEVELOPMENTAL REGULATION OF THE DRUG-PROCESSING GENOME IN MOUSE LIVER

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    Despite the recent progress in understanding the expression patterns and regulatory mechanisms of drug-processing genes, namely phase-I and -II drug metabolizing enzymes and transporters in adults, very little is known of the alterations of these genes during liver development. Therefore, newborns and children are potentially at a higher risk of adverse drug reactions. The purpose of my dissertation is to characterize the expression and regulatory mechanisms of the drug-processing genes during postnatal liver maturation. The present study integrated various research technologies, including genetically-engineered mice, messenger RNA and protein assays, ChIP-on-chip, ChIP-Seq, transcription-factor binding assays, LC-MS/MS, and bioinformatics analysis. Cluster analysis demonstrated that the ontogenic expression of 82 drug-processing genes separate into 4 distinct patterns: perinatal enriched, early-adolescent enriched, late-adolescent enriched, and adult enriched. Critical nuclear receptors, including the xenobiotic sensor pregnane X receptor (PXR, N1I2), and the bile-acid sensor farnesoid X receptor (FXR, NR1H4), are crucial in regulating the expression of drug-processing genes during liver development. Initiation of bile-acid signaling, mediated largely via FXR, is a hallmark of the neonatal induction of major liver transporters involved in the enterohepatic circulation of bile acids, whereas PXR is more important for the induction of xenobiotic-processing genes in adolescent and adult period. Because the accessibility of transcription factors to the target genes is determined by chromatin epigenetic mechanisms, I have also determined the correlations between the expression of drug-processing genes and distinct chromatin epigenetic marks, and identified that histone H3 lysine 4 di-methylation (H3K4Me2) appeared to be the choice of nature to induce numerous drug-processing genes during postnatal liver development. In conclusion, in the present dissertation, I have performed a systemic characterization of critical drug-processing genes and transcription factors during postnatal liver maturation. I have demonstrated that the developmental regulation of drug metabolism and transport is a sequential event associated with changes of chromatin epigenetic signatures, which set a permissive environment for ligand-activated nuclear receptors to gain access to the target genes prior to transcription initiation. The current work has generated basic knowledge that will serve as a foundation for further understanding of pediatric pharmacology and toxicology in humans

    Determinants of trade policy responses to the 2008 financial crisis

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    The collapse in trade and contraction of output that occurred during 2008-09 was comparable to, and in many countries more severe than, the Great Depression of 1930, but did not give rise to the rampant protectionism that followed the Great Crash. Theory suggests several hypotheses for why it was not in the interest of many firms to lobby for protection, including much greater macroeconomic"policy space"today, the rise of intra-industry trade (specialization in specific varieties), and the fragmentation of production across global value chains ("vertical"specialization and the associated growth of trade in intermediates). Institutions may also have played a role in limiting the extent of protectionist responses. World Trade Organization disciplines raise the cost of using trade policies for member countries and have proved to be a stable foundation for the open multilateral trading system that has been built over the last fifty years. This paper empirically examines the power of these and other theories to explain the observed pattern of trade policy responses to the 2008 crisis, using trade and protection data for seven large emerging market countries that have a history of active use of trade policy. Vertical specialization (global fragmentation) is found to be the most powerful economic factor determining trade policy responses.Free Trade,Trade Policy,Economic Theory&Research,International Trade and Trade Rules,Debt Markets
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