用大口径大相对孔径非球面透镜拍摄一步彩虹全息图

本文论述要获得大视场、大面积的一步彩虹全息图必须把狭缝放置在成象透镜上;必须使用发散光波做参考光和再现照明光。为此引入孔径共轭技术。为保证较大的观察角范围和好的成象质量,采用了大口径、大相对孔径的非球面透镜组,利用以上方法作者制作了面积为400mm×400mm一步彩虹全息图,本文叙述了制造过程和关键技术,讨论了狭缝象位置、狭缝象长、景深,色模糊、象模糊、衍射效率与布拉格效应对再现象的影响。     

Random quasi-phase-matching in bulk polycrystalline isotropic nonlinear materials

Three-wave mixing in nonlinear materials--the interaction of two light waves to produce a third--is a convenient way of generating new optical frequencies from common laser sources. However, the resulting optical conversion yield is generally poor, because the relative phases of the three interacting waves change continuously as they propagate through the material. This phenomenon, known as phase mismatch, is a consequence of optical dispersion (wave velocity is frequency dependent), and is responsible for the poor optical conversion potential of isotropic nonlinear materials. Here we show that exploiting the random motion of the relative phases in highly transparent polycrystalline materials can be an effective strategy for achieving efficient phase matching in isotropic materials. Distinctive features of this 'random quasi-phase-matching' approach are a linear dependence of the conversion yield with sample thickness (predicted in ref. 3), the absence of the need for either preferential materials orientation or specific polarization selection rules, and the existence of a wavelength-dependent resonant size for the polycrystalline grains.     

基于LightGBM-SVR-LSTM的停车区车位预测

停车难和交通拥堵现象愈演愈烈,提前告知驾驶员未来一段时间空车位数量,可以减少其寻找有效车位的时间,进而够缓解拥堵情况。基于此,本文提出了一种基于LightGBM-SVR-LSTM的停车区剩余车位预测模型。首先,通过数据预处理,尽可能保留原始数据特征的基础上,修复部分噪声数据;其次,将修复的数据放入轻量级梯度提升机（LightGBM）,提取叶子节点的值作为新的特征,并将其放入支持向量回归模型（SVR）进行预测;然后,利用长短时记忆神经网络（LSTM）进行误差修复。最后,选取某停车区数据,利用均方根误差（RMSE）、平均绝对误差（MAE）、平均百分比误差（MAPE）进行预测效果验证。结果表明,在正常条件和节假日期间,所提出的组合模型精度均有提升,具有一定的鲁棒性。     

老年T2DM患者血清相关指标与糖尿病肾病的相关性

摘 要 为研究老年2型糖尿病患者血清胆红素、糖化血红蛋白（HbA1C）、超氧化物歧化酶（SOD）活性与糖尿病肾病（DKD）的相关性。随机选取2018年10月至2020年10月兰州军区总医院单纯T2DM患者、DKD患者各360例为病例组,同期健康者720例作为对照组,检测各组肾功能指标,采用多元回归模型探讨血清胆红素、HbA1C及SOD活性与DKD的相关性。结果表明与对照组相比,病例组HbA1C明显升高、SOD活性显著下降,且DKD-不良预后组升高或下降最为显著（P<0.05）,而单纯T2DM组总胆红素、间接胆红素水平显著高于DKD组。血清TBIL、IBIL、SOD与肾小球滤过率（eGFR）水平呈正相关关系（P<0.05）,且HbA1C与血尿酸（UA）、肌酐（Cr）呈正相关关系（P<0.05）。多元回归分析结果显示,HbA1C每增加1%,DKD发生风险增加7%（OR=1.07, 95%CI 1.02~1.11）;TBIL、IBIL每增加1 μmol·L-1,SOD每增加1 U·g-1,DKD发生风险分别降低21%、16%、26%。可见老年T2DM患者TBIL、IBIL及SOD水平降低或HbA1C水平升高,均是引发DKD的独立危险因素,DBIL与DKD患病风险无明显相关性,但其对女性患者影响较大。     

拟概率空间上的寿险精算基本公式及模型

将寿险精算理论从经典的概率空间推广到了比其更广泛的一类模糊测度空间--拟概率测度空间上.在此空间上给出了生存函数、拟概率分布函数的概念,导出了在拟概率空间上精算模型的基本公式.使得精算理论模型应用范围更广、更有效.     

合成查尔酮化合物新方法的研究进展

查尔酮化合物是芳香醛酮发生交叉羟醛缩合的产物,它不仅是一种重要的有机合成中间体,还具有多种药理作用和生物活性;综述了最近几年来合成查尔酮化合物的反应体系、合成方法,并介绍了各种反应体系的优点及其合成查尔酮化合物的产率范围,认为查尔酮化合物的合成将以新技术、新方法和无污染的绿色合成为发展方向.     

大跨度桥梁风场模拟及气动力计算

介绍了一种快速高效的用于大跨度桥梁风致振动分析的风场模拟方法,并对模拟风场的统计性质进行了讨论和验证。在此基础上进一步给出了大跨度桥梁抖振力和自激力的时域表达方式,其中针对自激力计算中涉及的参数识别问题,提出了一种简单实用的非线性参数识别方法,本文采用上述理论,获得了作用于香港汀九大桥上的风场和气动力,据此对大桥进行的抖振响应时域分析表明,计算结果与风洞试验结果吻合良好,说明文中述及的这套理论已达     

Crystal structure of a rhomboid family intramembrane protease

Escherichia coli GlpG is an integral membrane protein that belongs to the widespread rhomboid protease family. Rhomboid proteases, like site-2 protease (S2P) and gamma-secretase, are unique in that they cleave the transmembrane domain of other membrane proteins. Here we describe the 2.1 A resolution crystal structure of the GlpG core domain. This structure contains six transmembrane segments. Residues previously shown to be involved in catalysis, including a Ser-His dyad, and several water molecules are found at the protein interior at a depth below the membrane surface. This putative active site is accessible by substrate through a large 'V-shaped' opening that faces laterally towards the lipid, but is blocked by a half-submerged loop structure. These observations indicate that, in intramembrane proteolysis, the scission of peptide bonds takes place within the hydrophobic environment of the membrane bilayer. The crystal structure also suggests a gating mechanism for GlpG that controls substrate access to its hydrophilic active site.     

Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.     

Macrophage migration inhibitory factor (MIF) modulates trophic signaling through interaction with serine protease HTRA1

Macrophage migration inhibitory factor (MIF), a small conserved protein, is abundant in the immune- and central nervous system (CNS). MIF has several receptors and binding partners that can modulate its action on a cellular level. It is upregulated in neurodegenerative diseases and cancer although its function is far from clear. Here, we report the finding of a new binding partner to MIF, the serine protease HTRA1. This enzyme cleaves several growth factors, extracellular matrix molecules and is implicated in some of the same diseases as MIF. We show that the function of the binding between MIF and HTRA1 is to inhibit the proteolytic activity of HTRA1, modulating the availability of molecules that can change cell growth and differentiation. MIF is therefore the first endogenous inhibitor ever found for HTRA1. It was found that both molecules were present in astrocytes and that the functional binding has the ability to modulate astrocytic activities important in development and disease of the CNS.