Transmit Power Optimization for Relay-Aided Multi-Carrier D2D Communication

In this paper,we consider the power optimization problem in Orthogonal Frequency Division Multiplexing(OFDM)-based relay-enhanced device-to-device(D2D) communication.In a single cell transmission scenario,dualhop communication is assumed in which each D2D user re-uses the spectrum of just one Cellular User(CU).In this work,we formulate a joint optimization scheme under a Decode-and-Forward(DF) relaying protocol to maximize the sum throughput of D2D and cellular networks via power allocation over different sub-carriers.The problem is thus transformed into a standard convex optimization,subject to individual power constraints at different transmitting nodes.We exploit the duality theory to decompose the problem into several sub-problems and use Karush–Kuhn–Tucker(KKT) conditions to solve each sub-problem.We provide simulation results to validate the performance of our proposed scheme.     

一种引入互斥关系的功能单元分配算法

为使条件分支数据通道中功能单元的分配结果得到进一步优化,在数据流图操作相容性分析中引入操作间互斥关系,并构建基于图论的分配模型.使用团划分算法在该模型上进行功能单元分配,同时提出一种针对功能单元分配问题的团划分启发式方法.不仅提高了团划分算法求解功能单元分配问题的计算结果一致性,而且使算法的收敛速度得以提高.根据实验结果,该算法得到的数据通道中所需功能单元平均减少了41%,同时执行速度加快了50%.     

Regulation of the bacterial cell cycle by an integrated genetic circuit

How bacteria regulate cell cycle progression at a molecular level is a fundamental but poorly understood problem. In Caulobacter crescentus, two-component signal transduction proteins are crucial for cell cycle regulation, but the connectivity of regulators involved has remained elusive and key factors are unidentified. Here we identify ChpT, an essential histidine phosphotransferase that controls the activity of CtrA, the master cell cycle regulator. We show that the essential histidine kinase CckA initiates two phosphorelays, each requiring ChpT, which lead to the phosphorylation and stabilization of CtrA. Downregulation of CckA activity therefore results in the dephosphorylation and degradation of CtrA, which in turn allow the initiation of DNA replication. Furthermore, we show that CtrA triggers its own destruction by promoting cell division and inducing synthesis of the essential regulator DivK, which feeds back to downregulate CckA immediately before S phase. Our results define a single integrated circuit whose components and connectivity can account for the cell cycle oscillations of CtrA in Caulobacter.     

Mutations in a new photoreceptor-pineal gene on 17p cause Leber congenital amaurosis

Leber congenital amaurosis (LCA, MIM 204000) accounts for at least 5% of all inherited retinal disease and is the most severe inherited retinopathy with the earliest age of onset. Individuals affected with LCA are diagnosed at birth or in the first few months of life with severely impaired vision or blindness, nystagmus and an abnormal or flat electroretinogram (ERG). Mutations in GUCY2D (ref. 3), RPE65 (ref. 4) and CRX (ref. 5) are known to cause LCA, but one study identified disease-causing GUCY2D mutations in only 8 of 15 families whose LCA locus maps to 17p13.1 (ref. 3), suggesting another LCA locus might be located on 17p13.1. Confirming this prediction, the LCA in one Pakistani family mapped to 17p13.1, between D17S849 and D17S960-a region that excludes GUCY2D. The LCA in this family has been designated LCA4 (ref. 6). We describe here a new photoreceptor/pineal-expressed gene, AIPL1 (encoding aryl-hydrocarbon interacting protein-like 1), that maps within the LCA4 candidate region and whose protein contains three tetratricopeptide (TPR) motifs, consistent with nuclear transport or chaperone activity. A homozygous nonsense mutation at codon 278 is present in all affected members of the original LCA4 family. AIPL1 mutations may cause approximately 20% of recessive LCA, as disease-causing mutations were identified in 3 of 14 LCA families not tested previously for linkage.     

Meta-analysis of genome-wide association studies of asthma in ethnically diverse North American populations

Asthma is a common disease with a complex risk architecture including both genetic and environmental factors. We performed a meta-analysis of North American genome-wide association studies of asthma in 5,416 individuals with asthma (cases) including individuals of European American, African American or African Caribbean, and Latino ancestry, with replication in an additional 12,649 individuals from the same ethnic groups. We identified five susceptibility loci. Four were at previously reported loci on 17q21, near IL1RL1, TSLP and IL33, but we report for the first time, to our knowledge, that these loci are associated with asthma risk in three ethnic groups. In addition, we identified a new asthma susceptibility locus at PYHIN1, with the association being specific to individuals of African descent (P = 3.9 × 10(-9)). These results suggest that some asthma susceptibility loci are robust to differences in ancestry when sufficiently large samples sizes are investigated, and that ancestry-specific associations also contribute to the complex genetic architecture of asthma.     

Disruption of P2RY5, an orphan G protein-coupled receptor, underlies autosomal recessive woolly hair

The genetic determinants of hair texture in humans are largely unknown. Several human syndromes exist in which woolly hair comprises a part of the phenotype; however, simple autosomal recessive inheritance of isolated woolly hair has only rarely been reported. To identify a gene involved in controlling hair texture, we performed genetic linkage analysis in six families of Pakistani origin with autosomal recessive woolly hair (ARWH; OMIM 278150). All six families showed linkage to chromosome 13q14.2-14.3 (Z = 17.97). In all cases, we discovered pathogenic mutations in P2RY5, which encodes a G protein-coupled receptor and is a nested gene residing within intron 17 of the retinoblastoma 1 (RB1) gene. P2RY5 is expressed in both Henle's and Huxley's layers of the inner root sheath of the hair follicle. Our findings indicate that disruption of P2RY5 underlies ARWH and, more broadly, uncover a new gene involved in determining hair texture in humans.     

WDR62 is associated with the spindle pole and is mutated in human microcephaly

Autosomal recessive primary microcephaly (MCPH) is a disorder of neurodevelopment resulting in a small brain. We identified WDR62 as the second most common cause of MCPH after finding homozygous missense and frame-shifting mutations in seven MCPH families. In human cell lines, we found that WDR62 is a spindle pole protein, as are ASPM and STIL, the MCPH7 and MCHP7 proteins. Mutant WDR62 proteins failed to localize to the mitotic spindle pole. In human and mouse embryonic brain, we found that WDR62 expression was restricted to neural precursors undergoing mitosis. These data lend support to the hypothesis that the exquisite control of the cleavage furrow orientation in mammalian neural precursor cell mitosis, controlled in great part by the centrosomes and spindle poles, is critical both in causing MCPH when perturbed and, when modulated, generating the evolutionarily enlarged human brain.     

Forced Oscillations of a Class of Nonlinear Dispersive Wave Equations and their Stability

It has been observed in laboratory experiments that when nonlinear dispersive waves are forced periodically from one end of undisturbed stretch of the medium of propagation, the signal eventually becomes temporally periodic at each spatial point. The observation has been confirmed mathematically in the context of the damped Korteweg-de Vries （KdV） equation and the damped Benjamin-Bona-Mahony （BBM） equation. In this paper we intend to show the same results hold for the pure KdV equation （without the damping terms） posed on a finite domain. Consideration is given to the initial-boundary-value problem {ut＋ux＋uux＋uxxx=0, u（x,0）=φ（x）, 0〈x〈1, t〉0,u（0,t）=h（t）, u（1,t） = 0, ux（1,t） = 0, t〉0.It is shown that if the boundary forcing h is periodic with small ampitude, then the small amplitude solution u of （＊） becomes eventually time-periodic. Viewing （＊） （without the initial condition） as an infinite-dimensional dynamical system in the Hilbert space L^2（0, 1）, we also demonstrate that for a given periodic boundary forcing with small amplitude, the system （＊） admits a （locally） unique limit cycle, or forced oscillation, which is locally exponentially stable. A list of open problems are included for the interested readers to conduct further investigations.     

Predicting multistage financial distress: Reflections on sampling,feature and model selection criteria

This research proposes a prediction model of multistage financial distress (MSFD) after considering contextual and methodological issues regarding sampling, feature and model selection criteria. Financial distress is defined as a three‐stage process showing different nature and intensity of financial problems. It is argued that applied definition of distress is independent of legal framework and its predictability would provide more practical solutions. The final sample is selected after industry adjustments and oversampling the data. A wrapper subset data mining approach is applied to extract the most relevant features from financial statement and stock market indicators. An ensemble approach using a combination of DTNB (decision table and naïve base hybrid model), LMT (logistic model tree) and A2DE (alternative N dependence estimator) Bayesian models is used to develop the final prediction model. The performance of all the models is evaluated using a 10‐fold cross‐validation method. Results showed that the proposed model predicted MSFD with 84.06% accuracy. This accuracy increased to 89.57% when a 33.33% cut‐off value was considered. Hence the proposed model is accurate and reliable to identify the true nature and intensity of financial problems regardless of the contextual legal framework.