基于能力分析的空间对抗装备体系效能评估方法

首先研究了空间对抗的核心能力要素;然后研究了空间对抗装备体系的构成,即将核心能力要素细化为基本能力要素并映射到空间对抗装备子系统;最后构建由作战能力指标→核心能力指标及权重赋值→基本能力指标及权重赋值→单项效能指标及权重赋值组成的指标体系,并提出基于该指标体系的单项效能评价→系统综合评价→体系综合评价→作战效能评价→结果验证的综合评估途径.     

Two new nematodes,Pseudelzalia longiseta gen. nov., sp. nov. and Paramonohystera sinica sp. nov. (Monhysterida: Xyalidae), from sediment in the East China Sea

Pseudelzalia longiseta gen. nov, sp. nov. and Paramonohystera sinica sp. nov. from subtidal sediment in the East China Sea are described. Pseudelzalia is characterized by 6 labial papillae and 10 cephalic setae, cylindrical buccal cavity, elongate (>2 anal body diameter) spicules, and conico-cylindrical tail devoid of terminal setae. It differs from Elzalia by the absence of terminal setae. Pseudelzalia longiseta sp. nov. is 647–853 μm long, has 7–8 μm long cervical setae, 11–14 μm long caudal setae, 25–41 μm long spicules about 2.1–2.7 anal diameter, and pointed tail-tip. Paramonohystera sinica possesses 12 cephalic setae, a character found in four congeners: Paramonohystera buetschlii (Bresslau and Schuurmans Stekhoven in Schuurmans Stekhoven, 1935, Paramonohystera pilosa Boucher, 1971, Paramonohystera concinna Lorenzen, 1977 and Paramonohystera halerba Fadeeva and Belogurov, 1987. It differs from P. buetschlii by shorter body (933–1023 μm versus 2000–2200 μm); from P. pilosa by the much shorter spicules (79–88 μm versus 167 μm) and narrower head (13–16 µm versus 32 µm); from P.concinna by smooth cephalic setae (versus segmented); and from P. halerba by the absence of two rows of setae on the ventral side of the tail (versus present). Based on the evaluation of nominal species, we recognize 14 valid species and provide an emended diagnosis and a tabular key for Paramonohystera.

http://www.zoobank.org/urn:lsid:zoobank.org:pub:474B8F17-AED7-4078-8176-DFC499B78526     

Exome sequencing of liver fluke-associated cholangiocarcinoma

Opisthorchis viverrini-related cholangiocarcinoma (CCA), a fatal bile duct cancer, is a major public health concern in areas endemic for this parasite. We report here whole-exome sequencing of eight O. viverrini-related tumors and matched normal tissue. We identified and validated 206 somatic mutations in 187 genes using Sanger sequencing and selected 15 genes for mutation prevalence screening in an additional 46 individuals with CCA (cases). In addition to the known cancer-related genes TP53 (mutated in 44.4% of cases), KRAS (16.7%) and SMAD4 (16.7%), we identified somatic mutations in 10 newly implicated genes in 14.8-3.7% of cases. These included inactivating mutations in MLL3 (in 14.8% of cases), ROBO2 (9.3%), RNF43 (9.3%) and PEG3 (5.6%), and activating mutations in the GNAS oncogene (9.3%). These genes have functions that can be broadly grouped into three biological classes: (i) deactivation of histone modifiers, (ii) activation of G protein signaling and (iii) loss of genome stability. This study provides insight into the mutational landscape contributing to O. viverrini-related CCA.     

Common variants at 12q14 and 12q24 are associated with hippocampal volume

Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Our genome-wide association study (GWAS) of dementia-free persons (n = 9,232) identified 46 SNPs at four loci with P values of <4.0 × 10(-7). In two additional samples (n = 2,318), associations were replicated at 12q14 within MSRB3-WIF1 (discovery and replication; rs17178006; P = 5.3 × 10(-11)) and at 12q24 near HRK-FBXW8 (rs7294919; P = 2.9 × 10(-11)). Remaining associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 × 10(-7)) and nine SNPs at 9p33 within ASTN2 (rs7852872; P = 1.0 × 10(-7)); along with the chromosome 12 associations, these loci were also associated with hippocampal volume (P < 0.05) in a third younger, more heterogeneous sample (n = 7,794). The SNP in ASTN2 also showed suggestive association with decline in cognition in a largely independent sample (n = 1,563). These associations implicate genes related to apoptosis (HRK), development (WIF1), oxidative stress (MSR3B), ubiquitination (FBXW8) and neuronal migration (ASTN2), as well as enzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal size and possibly the risk of cognitive decline and dementia.     

Price–Dividend Ratios and Stock Price Predictability

A long‐standing puzzle to financial economists is the difficulty of outperforming the benchmark random walk model in out‐of‐sample contests. Using data from the USA over the period of 1872–2007, this paper re‐examines the out‐of‐sample predictability of real stock prices based on price–dividend (PD) ratios. The current research focuses on the significance of the time‐varying mean and nonlinear dynamics of PD ratios in the empirical analysis. Empirical results support the proposed nonlinear model of the PD ratio and the stationarity of the trend‐adjusted PD ratio. Furthermore, this paper rejects the non‐predictability hypothesis of stock prices statistically based on in‐ and out‐of‐sample tests and economically based on the criteria of expected real return per unit of risk. Copyright © 2011 John Wiley & Sons, Ltd.     

Mutations in SWI/SNF chromatin remodeling complex gene ARID1B cause Coffin-Siris syndrome

We identified de novo truncating mutations in ARID1B in three individuals with Coffin-Siris syndrome (CSS) by exome sequencing. Array-based copy-number variation (CNV) analysis in 2,000 individuals with intellectual disability revealed deletions encompassing ARID1B in 3 subjects with phenotypes partially overlapping that of CSS. Taken together with published data, these results indicate that haploinsufficiency of the ARID1B gene, which encodes an epigenetic modifier of chromatin structure, is an important cause of CSS and is potentially a common cause of intellectual disability and speech impairment.     

A genome-wide association study in Han Chinese identifies new susceptibility loci for ankylosing spondylitis

To identify susceptibility loci for ankylosing spondylitis, we performed a two-stage genome-wide association study in Han Chinese. In the discovery stage, we analyzed 1,356,350 autosomal SNPs in 1,837 individuals with ankylosing spondylitis and 4,231 controls; in the validation stage, we analyzed 30 suggestive SNPs in an additional 2,100 affected individuals and 3,496 controls. We identified two new susceptibility loci between EDIL3 and HAPLN1 at 5q14.3 (rs4552569; P = 8.77 × 10(-10)) and within ANO6 at 12q12 (rs17095830; P = 1.63 × 10(-8)). We also confirmed previously reported associations in Europeans within the major histocompatibility complex (MHC) region (top SNP, rs13202464; P < 5 × 10(-324)) and at 2p15 (rs10865331; P = 1.98 × 10(-8)). We show that rs13202464 within the MHC region mainly represents the risk effect of HLA-B*27 variants (including HLA-B*2704, HLA-B*2705 and HLA-B*2715) in Chinese. The two newly discovered loci implicate genes related to bone formation and cartilage development, suggesting their potential involvement in the etiology of ankylosing spondylitis.