基于Agent的异常处理在进销存管理系统中的应用

针对基于工作流的进销存管理系统中存在的异常问题,提出了一个基于Agent的工作流异常处理模型,建立了异常监测、分析、处理机制,采用ECA规则建立了异常规则库,利用Agent的自学习性解决系统中出现的不可预测的异常,提高了系统的灵活性和可适应性,增强了系统处理异常的能力.     

铁掺杂纳米氧化锌室温脱硫剂的结构及效能研究

采用均匀沉淀法制备了铁掺杂纳米氧化锌脱硫剂,利用XRD和BET手段对脱硫剂进行了表征,优化了铁的掺杂量,并探讨了焙烧温度、脱硫温度和氧含量等因素对脱除H2S性能的影响。结果表明,铁的掺杂使脱硫剂的比表面积和孔容增大,当Fe∶Zn的摩尔比为5∶100(FZ5.0)时其活性最好。FZ5.0脱硫剂适用于室温脱硫,当样品的焙烧温度为270℃,氧含量为10%,穿透时间达到370 m in时,脱硫性能最佳。     

高动态GPS/INS组合导航算法研究

首先介绍了新型深组合GPS/INS系统原理图及组合导航滤波算法。在该算法中,组合卡尔曼滤波器除完成INS误差及GPS接收机时钟误差的估计外,还参与了GPS码跟踪,即完成传统码跟踪环中环路滤波器的功能。采用自适应码跟踪误差估计器补偿组合卡尔曼滤波器测量值中的相关分量,从而消除了传统组合中不稳定的主要根源。然后进行了计算机仿真计算,仿真结果表明,新型深组合GPS/INS导航算法适用于机动性较高的载体。     

浅谈盾构隧道推进及衬砌拼装

文章针对在松软含水地层中采用手掘式敞胸盾构施工,需辅以气压、人工井点降水及其他地层加固措施,论述了在这种条件下盾构开挖掘进时的几种施工方法.     

<Emphasis Type="Italic">Yersinia pseudotuberculosis</Emphasis> supports Th17 differentiation and limits de novo regulatory T cell induction by directly interfering with T cell receptor signaling

Adaptive immunity critically contributes to control acute infection with enteropathogenic Yersinia pseudotuberculosis; however, the role of CD4⁺ T cell subsets in establishing infection and allowing pathogen persistence remains elusive. Here, we assessed the modulatory capacity of Y. pseudotuberculosis on CD4⁺ T cell differentiation. Using in vivo assays, we report that infection with Y. pseudotuberculosis resulted in enhanced priming of IL-17-producing T cells (Th17 cells), whereas induction of Foxp3⁺ regulatory T cells (Tregs) was severely disrupted in gut-draining mesenteric lymph nodes (mLNs), in line with altered frequencies of tolerogenic and proinflammatory dendritic cell (DC) subsets within mLNs. Additionally, by using a DC-free in vitro system, we could demonstrate that Y. pseudotuberculosis can directly modulate T cell receptor (TCR) downstream signaling within naïve CD4⁺ T cells and Tregs via injection of effector molecules through the type III secretion system, thereby affecting their functional properties. Importantly, modulation of naïve CD4⁺ T cells by Y. pseudotuberculosis resulted in an enhanced Th17 differentiation and decreased induction of Foxp3⁺ Tregs in vitro. These findings shed light to the adjustment of the Th17-Treg axis in response to acute Y. pseudotuberculosis infection and highlight the direct modulation of CD4⁺ T cell subsets by altering their TCR downstream signaling.     

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.     

Mutations in NMNAT1 cause Leber congenital amaurosis and identify a new disease pathway for retinal degeneration

Leber congenital amaurosis (LCA) is a blinding retinal disease that presents within the first year after birth. Using exome sequencing, we identified mutations in the nicotinamide adenine dinucleotide (NAD) synthase gene NMNAT1 encoding nicotinamide mononucleotide adenylyltransferase 1 in eight families with LCA, including the family in which LCA was originally linked to the LCA9 locus. Notably, all individuals with NMNAT1 mutations also have macular colobomas, which are severe degenerative entities of the central retina (fovea) devoid of tissue and photoreceptors. Functional assays of the proteins encoded by the mutant alleles identified in our study showed that the mutations reduce the enzymatic activity of NMNAT1 in NAD biosynthesis and affect protein folding. Of note, recent characterization of the slow Wallerian degeneration (Wld(s)) mouse model, in which prolonged axonal survival after injury is observed, identified NMNAT1 as a neuroprotective protein when ectopically expressed. Our findings identify a new disease mechanism underlying LCA and provide the first link between endogenous NMNAT1 dysfunction and a human nervous system disorder.