Fe、Si对工业纯铝晶粒细化的影响

通过AlTiB晶粒细化剂对高纯铝、工业纯铝的细化及Al-10Ti中间合金、Fe、Si对工业纯铝的细化，研究了Fe、Si在工业纯铝晶粒细化过程中的作用。试验结果表明，0.3％的AlTiB晶粒细化剂对工业纯铝有良好的细化效果，但不能细化高纯铝；Fe、Si作为晶粒细化剂单独加入时，有不同程度的细化作用。分析认为，Fe、Si在工业纯铝晶粒细化过程中有双重作用，即促进型壁晶核的游离和增加α-Al在型壁形核的质点数目。     

基于USB的WSN测试与分析系统

实时监控无线传感器网络（WSN）从单个节点到整个网络的运行状态,是进行无线传感器各类研究及应用开发的关键技术之一,为了克服基于UART的数据传输所存在的速率瓶颈问题,设计了一种基于USB的WSN监测系统,主要包括侦听节点和监测分析系统两部分。侦听节点采用CC2531 USB Dongle,以被动侦听的方式获取无线传感器网络的数据包（符合IEEE802.15.4标准）,封装后通过USB接口上传至上位机监测分析系统。上位机监测系统,通过USB接口读取数据帧、完成帧信息存储、解析。实验结果表明该设计能够实现数据传输并以图形方式动态显示网络运行状态。本监测系统的设计为开展WSN的各类理论及实验研究提供了有力的分析工具。     

高功率窄线宽可调谐 1 064 nm 环形腔激光

文章采用了三镜环形腔内插入标准具获取高功率窄线宽可调谐1064 nm 激光。对环形腔的单向运行、标准具压窄线宽与调谐波长及激光大基模体积运转进行了理论分析与计算,结合实验优化了腔镜曲率与输出耦合率。在808 nm 半导体激光泵浦功率151 W 条件下,获得输出功率33.7 W、光束质量因子 M 2＝1.28、线宽0.1 GHz 的单向1064 nm 激光输出,相应的光转换效率22.3%。采用高精度控温仪对标准具进行精确温控,实现激光波长的精密调谐。改变标准具温度获得1064 nm 波长调谐范围72.6 GHz,调谐精度为220 MHz。波长调谐过程中1064 nm 激光输出功率变化约10%。整个系统稳定可靠,而且相对简单,较易实现,为获得可调谐窄线宽1064 nm 激光提供了实用有效的技术手段。     

基于2D Mesh拓扑结构的NoC模拟器设计

片上网络模拟器的设计涉及到片上网络的拓扑结构、路由器结构、路由算法、性能分析等诸多方面.从NoC模拟器设计的角度,研究并讨论模拟器所采用的拓扑结构,路由器结构及数据包格式,介绍拓扑结构模拟、IP核模拟、路由模拟,并且用面向对象语言C++实现一个NoC模拟器系统.     

个性化学习资源推荐系统研究

通过分析远程网络学习系统中学习者对学习资源的访问历史,以及与学习者有类似访问兴趣的同组学习者的学习偏好,为学习者提供个性化的资源推荐服务,能够有效提高各种学习资源的利用效率,从而提高教学质量.     

考虑循环寿命折损的主动配电网仿射可调鲁棒优化方法

针对主动配电网在源荷储协同下的不确定性优化问题,提出了基于仿射可调鲁棒优化的主动配电网运行策略。首先,考虑分布式光伏的可控模型、循环寿命折损的电池储能模型和ZIP负荷模型,构建了主动配电网优化运行模型。然后,采用椭球集合来描述分布式光伏出力的不确定性,并结合仿射策略形成优化模型中决策变量与分布式光伏出力不确定性变量之间的线性决策机制。最后,通过对偶变换将主动配电网鲁棒优化模型转化为一个确定性的混合整数二阶锥规划模型进行求解。在改进的IEEE33节点算例系统中对比验证了所提出的仿射可调鲁棒优化方法的有效性和优点。     

考虑电池储能老化和需求侧响应的交直流混合配电网动态重构方法

现有的电池储能模型一方面认为电池的充放电功率和效率为固定不变的,另一方面有关电池储能的充放电过程对循环老化的影响缺少考虑,这与电池单元本体的非线性等效电路模型相违背。因此,考虑电池储能的循环老化成本、需求侧响应,提出了交直流混合配电网动态重构方法。通过对实际电池储能的充放电功率的运行区域进行采样,在凸包络的采样点集合中将非理想状态下的电池储能模型重构为线性模型。在此基础上,分别建立了基于累积吞吐电量和放电深度的循环老化成本模型,构建了综合成本最小化的交直流混合配电网动态重构模型。并采用混合整数二阶锥规划方法求解。在改进的33节点算例上仿真验证了所提基于放电深度的循环老化成本模型的经济性,分析了交直流混合配电网重构方法经济性的影响因素。     

CD57+/CD28- T cells in untreated hemato-oncological patients are expanded and display a Th1-type cytokine secretion profile, ex vivo cytolytic activity and enhanced tendency to apoptosis

Protopolystoma (Monogenea, Polystomatidae) is strictly specific to the anuran amphibian genus Xenopus. The host group is characterised by a polyploid series in which chromosome numbers reflect diploid, tetraploid, octoploid and dodecaploid constitutions; the series is considered to have evolved through interspecies hybridisation and genome duplication. This study correlates information on host evolutionary relationships with patterns of parasite speciation and host specificity. Protopolystoma is restricted to one subgenus (Xenopus) with multiples of 36 chromosomes, and is absent from the subgenus Silurana (with multiples of 20 chromosomes). Molecular, biochemical and karyotype evidence distinguishes three subgroups within Xenopus. Representative species from each subgroup, Xenopus muelleri, Xenopus fraseri and Xenopus laevis, have been examined for polystomatid infection. Two species of Protopolystoma occur in each of these host species. In X. muelleri, the two Protopolystoma species reflect parasite co-speciation corresponding with the divergence of two sibling host species. Xenopus fraseri and X. laevis (both with 2n = 36 chromosomes) are implicated in the hybrid origin of two octoploid species, Xenopus wittei and Xenopus vestitus (both 2n = 72). The relationships of the Protopolystoma species in these Xenopus taxa reflect this presumed ancestry. Xenopus wittei carries two species of Protopolystoma, one shared with X. fraseri and the other shared with X. laevis. Xenopus vestitus carries a single species of Protopolystoma which is shared with X. laevis but there is no "heirloom" which reflects its hybrid origin involving X. fraseri. In addition to these shared parasite species which may reflect shared host genes, X. fraseri and X. laevis each carry separate species-specific Protopolystoma which do not occur in other Xenopus species even where there is evidence of common genetic information (as in the allopolyploid wittei and vestitus). This case study may be interpreted as indicating a powerful influence of host genetic factors on susceptibility to infection, host-specificity, and parasite speciation.     

Comparison of CT and MR imaging in staging of neck metastases

OBJECTIVE: To determine whether adaptive cytoprotection exists in human intestinal cells under in vitro conditions and what role, if any, endogenous prostaglandins or calcium may play in mediating this protective response. SUMMARY BACKGROUND DATA: Adaptive cytoprotection can be defined as that process whereby the administration of a low concentration of a damaging agent, termed a "mild irritant," which by itself is not injurious, can attenuate gastrointestinal mucosal injury subsequently induced by the application of higher concentrations of the same or other necrotizing agents. Despite substantial investigation, the mediator or mediators of adaptive cytoprotection remain poorly understood. METHODS: Postconfluent Caco-2 cells were used in all experiments. Cellular death was quantitated using a dual-component fluorescent assay. Changes in intracellular calcium concentration were quantitated by measuring fluorescent signal changes of the single wavelength calcium indicator (Fluo-3). Finally, prostaglandin E2 release into the media was quantitated by radioimmunoassay. RESULTS: Pretreatment of Caco-2 cells with low concentrations of ethanol (mild irritant) significantly attenuated injury induced by higher damaging concentrations of ethanol. The protection conferred by the mild irritant was directly dependent on both the concentration of the irritant used and the duration of exposure and was abrogated when cells were pretreated with an endogenous prostaglandin inhibitor (indomethacin) or if the mild irritant was administered in calcium-free media. Cells exposed to ethanol had a significant and concentration-dependent increase in intracellular calcium concentration, an effect that was highly related to cellular injury. Pretreatment with a mild irritant significantly decreased intracellular calcium increases induced by not only ethanol but also by a calcium ionophore (A23187). Cells treated with low concentrations of ethanol demonstrated no significant elevation in prostaglandin E2 release. CONCLUSIONS: Adaptive cytoprotection induced by ethanol exists in human colonocytes under in vitro conditions independent of mucosal blood flow, neural innervation, or circulating humoral factors. The authors' data suggest that this response does not require endogenous prostaglandin synthesis but may involve processes whereby intracellular calcium accumulation is prevented.