Multi-user lattice coding for the multiple-access relay channel

This paper considers the multi-antenna multiple access relay channel (MARC), in which multiple users transmit messages to a common destination with the assistance of a relay. In a variety of MARC settings, the dynamic decode and forward (DDF) protocol is very useful due to its outstanding rate performance. However, the lack of good structured codebooks so far hinders practical applications of DDF for MARC. In this work, two classes of structured MARC codes are proposed: 1) one-to-one relay-mapper aided multiuser lattice coding (O-MLC), and 2) modulo-sum relay-mapper aided multiuser lattice coding (MS-MLC). The former enjoys better rate performance, while the latter provides more flexibility to tradeoff between the complexity of the relay mapper and the rate performance. It is shown that, in order to approach the rate performance achievable by an unstructured codebook with maximum-likelihood decoding, it is crucial to use a new K-stage coset decoder for structured O-MLC, instead of the one-stage decoder proposed in previous works. However, if O-MLC is decoded with the one-stage decoder only, it can still achieve the optimal DDF diversity-multiplexing gain tradeoff in the high signal-to-noise ratio regime. As for MS-MLC, its rate performance can approach that of the O-MLC by increasing the complexity of the modulo-sum relay-mapper. Finally, for practical implementations of both O-MLC and MS-MLC, practical short length lattice codes with linear mappers are designed, which facilitate efficient lattice decoding. Simulation results show that the proposed coding schemes outperform existing schemes in terms of outage probabilities in a variety of channel settings.Comment: 32 pages, 5 figure

3,3′-Bis(3-meth­oxy­benz­yl)-1,1′-(ethane-1,2-diyl)­diimidazolium dibromide dihydrate

In the title compound, C24H28N4O2 2+·2Br−·2H2O, the diimid­azo­lium cation is located on an inversion center. The imidazole and the benzene rings make a dihedral angle of 68.08 (04)°. In the crystal, O—H⋯Br, C—H⋯O and C—H⋯Br hydrogen bonds link the diimidazolium cations, the bromide anions and the water mol­ecules into a two-dimensional network

3,3′-Dibenzyl-1,1′-ethyl­enediimidazolium dibromide

In the title compound, C22H24N4 2+·2Br−, the imidazolium dication is located on a crystallographic inversion center. The imidazole and benzene rings make a dihedral angle of 73.1 (9)°. In the crystal, non-classical inter­molecular C—H⋯Br hydrogen bonds link the ion pairs into a two-dimensional network

3,3′-Bis(4-fluoro­benz­yl)-1,1′-ethyl­enediimidazolium tribromidocuprate(I)

The title compound, (C22H22F2N4)[CuBr3], crystallizes with the cation situated on an inversion center and the anion on a twofold rotation axis along one Cu—Br bond. The two imidazole rings are in an anti configuration. The anion has a trigonal planar coordination geometry

Small molecule-mediated tribbles homolog 3 promotes bone formation induced by bone morphogenetic protein-2.

Although bone morphogenetic protein-2 (BMP2) has demonstrated extraordinary potential in bone formation, its clinical applications require supraphysiological milligram-level doses that increase postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threatening cervical swelling and cyst-like bone formation. Recent promising alternative biomolecular strategies are toward promoting pro-osteogenic activity of BMP2 while simultaneously suppressing its adverse effects. Here, we demonstrated that small molecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibular defect model. Moreover, we successfully elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect by applying high dose BMP2. Phenamil treatment significantly improves the quality of newly formed bone by inhibiting BMP2 induced fatty cyst-like structure and inflammatory soft-tissue swelling. The observed positive phenamil effects were associated with upregulation of tribbles homolog 3 (Trib3) that suppressed adipogenic differentiation and inflammatory responses by negatively regulating PPARγ and NF-κB transcriptional activities. Thus, use of BMP2 along with phenamil stimulation or Trib3 augmentation may be a promising strategy to improve clinical efficacy and safety of current BMP therapeutics