纳米晶体钒热稳定性的分子动力学模拟

用分子动力学技术, 结合分析型嵌入原子方法模拟计算了平均晶粒尺寸为2.86~7.50 nm的纳米晶体钒的微观结构及其热稳定性. 用原子键对分析技术区分了晶粒与晶界原子, 发现晶界原子所占的比例随晶粒尺寸的减小明显提高, 晶体中原子的平均能量要较普通单晶的高. 从原子平均势能、晶界原子比率以及径向分布函数随温度的变化关系得出纳米晶体钒的热稳定温度, 发现随晶粒尺寸的减小纳米晶体钒的热稳定温度明显降低. 最后还讨论了引起这种热稳定温度降低的原因.     

氢稀释对非晶硅碳(a-SiC:H)合金薄膜生长和光学特性的影响

用PECVD方法, 以固定的甲烷硅烷气体流量比([CH₄]/[SiH₄] = 1.2)和不同的氢稀释比(R_H = [H₂]/[CH₄+SiH₄] = 12, 22, 33, 102和135)制备了一系列的氢化非晶硅碳合金(a-SiC:H)薄膜. 运用紫外-可见光透射谱(UV-VIS)、红外吸收谱(IR)、Raman谱以及光荧光发射谱(PL)测量研究了氢稀释和高温退火对薄膜生长和光学特性的影响. 实验发现氢稀释使薄膜光学带隙展宽(从1.92到2.15 eV). 高氢稀释条件下制备的薄膜经过1250℃退火后在室温下观察到可见光发光峰, 峰位位于2.1 eV. 结合Raman谱分析, 认为发光峰源于纳米硅的量子限制效应, 纳米硅被Si-C和Si-O限制.     

电脉冲作用下Al-22％Si合金的价电子理论研究

基于固体与分子经验电子理论（EET），计算了Al—22％Si合金熔体相价电子结构参数，研究了铝硅合金熔体基元键络对温度（能量）变化的敏感性及其对组织形态的影响．结果表明，低过热铝硅合金熔体中n4值较大的Si-Si团簇为过共晶铝硅合金初生硅形核提供了核心，对其周围的Al—Si团簇产生强烈的“类拖曳”效应；熔体温度的变化较明显地影响了该核心键络的稳定性，从而影响了组织形态；脉冲电场作用于合金熔体后，不可恢复地改变了Si-Si团簇键络稳定性，从而对合金凝固组织形态起到变质作用，施加电脉冲的能量越高，Si—Si团簇越不稳定，电脉冲孕育效果越显著．     

纳米晶体的熔化与过热

本文介绍了纳米晶体尺寸依赖的熔化温度和熔化熵模型,该模型不仅可以预测自由表面纳米晶体随尺寸减小的熔化温度和熔化焓降低,而且可以预测镶嵌纳米晶体随尺寸减小的熔化温度和熔化焓增长,已有的纳米粒子、纳米线和纳米薄膜的实验结果证实了模型的预测。     

铁电体的极化储能效应

三维铁电体的偶极子等概率地分布在晶格取向相关的特定极化方向上.外加电场后,各个方向的偶极子对电场的响应不同,导致了各种场致效应.最基本的效应是电场对极化强度在相变温区的诱导和转向,导致铁电体在相应温区实现了高的储能密度效应.基于铁电体德文希尔理论三维吉布斯自由能与极化强度的关系,得到了二阶相变铁电体偶极子的诱导及取向对极化储能密度和放电能量密度的影响.研究结果显示:低电场下储能峰低于居里温度,并随电场增大接近并超过居里温度;两个铁电参量的比值对铁电体的极化行为、电滞回线和储能密度具有关键影响并使其相互关联.同时还发现介电峰的温度宽度对应电滞回线形状变化的温度宽度和储能密度峰的温度宽度,且储能密度峰越高,峰的温区越窄.     

细晶粒BaTiO3陶瓷的烧结和介电性能研究

采用放电等离子烧结新技术。在９００℃的温度下烧结到得到平均晶粒１７０ｎｍ的致密ＢａＴｉＯ３陶瓷，对样品介电性能的测量发现材料的介电常数随晶粒尺寸的减小而降低，同时介电温度谱出现相变用现象。从晶界面和晶粒相结构两方面分析了导致这一现象的原因。     

进入纳米时代的CMOS设计

本论文着重论述未来ＣＭＯＳ进入纳米尺寸的关键挑战，如电源电压和阈值电压减小、短沟效应、量子效应、杂质数起伏以及互边线延迟等影响。分析了纳米ＣＭＯＳ器件结构的设计，讨论了用于纳米尺寸的新型器件结构，包括ＳＯＩ ＣＭＯＳ、册和环栅ＭＯＳＦＥＴ、凹陷沟道ＭＯＳＦＥＴ、动态阈值ＭＯＳＦＥＴ以及低温ＣＭＯＳ，它们可能把我们带到硅器件设计的最远极限。     

二维典型纳米结构的非局域化光学特性研究

由于量子效应的存在,纳米尺度结构所具有的特性很难完全基于经典力学来解释,其光学特性也难以采用经典方法得到.随着时域有限差分(FDTD)方法的发展,其在光学领域中的应用变得越来越广泛.论文基于FDTD方法研究了典型二维纳米结构的非局域光学特性,得到了不同纳米尺度结构的局域和非局域性光学特性存在的条件,分析了结构形状对其消光截面特性的影响.计算与分析结果表明随着纳米结构尺寸的减小及形状的突变,结构的非局域性越明显.我们的理论及结果可为实际小尺度纳米器件的设计提供参考依据.     

生物能量在生命体中传递的新理论及应用

生物能量在生物体当中的传递是生命科学中的一个基本问题，它相关于ATP水解放出的能量沿着蛋白质分子的传递。这种传递与蛋白质的动力学相关。根据ATP分子分布和水解的特性以及蛋白质结构的特点，在Davyclov理论的基础上提出了一个新的生物能量传递的理论。在这个理论当中，Amide振动的集体激发状态用一个两量子准相干态表示，系统的哈密顿量不但包含了Amide振动引起的相邻氨基酸残基的位移，而且包含了相邻Amide之间的共振相互作用所引起的氨基酸残基的相对位置的改变。由这个理论得出的传递生物能量的孤子的寿命可得10^-10秒，在这个时间之内孤子能传递过上千个氨基酸残基，因此它能在生物过程中起着重要的作用。这个理论与E．col．的Ramma谱的实验结果和我们做出的胶原蛋白的红外吸收谱等实验结果相一致，因此它可能是生物体中生物能量传递的一个可利用的和正确的理论。     

高电场下弛豫铁电体的场致效应

弛豫铁电体在热释电、介电、电场调制微波器件和电致伸缩器件方面有着广泛的应用.这些应用均涉及电场的作用.因电场会导致极化强度增大,并连续地延伸到顺电相,从而产生了电场诱导效应.用弯曲近似法对极化强度在电场作用下随温度的连续变化做近似,得到了介电系数峰值在高场下随电场2/3次方的变化规律.与介电峰在电场作用下移动的实验结果基本一致.理论数值模拟发现:存在一个与热力学参量相关的极化温度系数,其值越大,场致介电移峰效应越小,且热释电系数越大;反之,如果场致介电移峰效应越大,电场调制微波器件的介电可调性及可调性的温度稳定性会越好.上述研究结果对掺杂改性研究微波器件的介电可调性和热释电性有一定的参考作用.     

铋层状化合物Na0.5Ho0.5-xYbxBi4Ti4O15陶瓷材料的上转换发光、铁电、介电性能研究

采用传统的固相烧结法,制备了Na0.5Ho0.5-xYbxBi4Ti4O15铋层状结构陶瓷.经X射线衍射（XRD）表征,新合成材料为单相结构,且扫描电子显微镜下的表面和断面图像均为层状,说明合成材料为新型铋层状材料.室温时,在可见光波长范围内,有2个峰,分别为546 nm处的绿光峰和656 nm处的红光峰,分别对应于Ho3＋离子的5F4＋5S2→5I8和5F5→5I8跃迁.为研究其机理,测试了变功率条件下的发光强度,经计算,绿光和红光发射均为双光子过程.研究陶瓷样品在变温（-130~270°C）条件下的发光性能时,发现红光与绿光的强度比值与温度呈线性关系,该材料有望应用于光学温度传感器领域.经介电性能测试发现当Ho：Yb=1：9时,样品的居里温度为686.4°C.研究铁电性能发现当Ho：Yb=3：2时,剩余极化Pr为9.3μC/cm2,矫顽场强为Ec=82 k V/cm,表明具有一定的铁电性能.以上研究结果表明,制得的新材料是一种具有优异光学性能的多功能材料.     

Activated scramblase and inhibited aminophospholipid translocase cause phosphatidylserine exposure in a distinct platelet fraction

Platelet procoagulant activity is mainly determined by the extent of surface-exposed phosphatidylserine (PS), controlled by the activity of aminophospholipid translocase and phospholipid scramblase. Here, we studied both transport activities in single platelets upon stimulation with various agonists. Besides the formation of procoagulant microparticles, the results show that a distinct fraction of the platelets exposes PS when stimulated. The extent of PS exposure in these platelet fractions was similar to that in platelets challenged with Ca²⁺-ionophore, where all cells exhibit maximal attainable PS exposure. The size of the PS-exposing fraction depends on the agonist and is proportional to the platelet procoagulant activity. Scramblase activity was observed only in the PS-exposing platelet fraction, whereas translocase activity was exclusively detectable in the fraction that did not expose PS. We conclude that, irrespective of the agonist, procoagulant platelets exhibit maximal surface exposure of PS by switching on scramblase and inhibiting translocase activity.Received 8 March 2005; received after revision 19 April 2005; accepted 13 May 2005     

Studies of spin-labeled spectrin]

Spectrin isolated from human erythrocytes has been spin-labeled with five maleimide nitroxides. The mobility of the labels is strongly dependent on their size, and on the temperature. A thermal transition of spectrin is shown to occur above 30 degrees C. Calcium and magnesium provoke a strong immobilization of the labels. This effect is yet more pronounced when spectrin is allowed to reassociate with the cytoplasmic surface of the membrane.     

一种高速铁路无砟轨道混凝土结构疲劳损伤模型

基于连续损伤力学理论和边界面概念,建立了高速铁路无砟轨道混凝土结构在循环荷载作用下的疲劳损伤模型.模型在主坐标系中采用了拉压两个边界面,根据加载面与极限断裂面、边界面之间的位置关系来计算高速铁路无砟轨道混凝土结构在复杂应力状态下的损伤,并由累积损伤与应变能释放率之间的关系确定循环加载中极限断裂面的变化规律.通过将该理论模型嵌入有限元软件ABAQUS的用户材料子程序UMAT,与同类模型进行比较验证了模型的可行性.最后对高速铁路双块式无砟轨道支承层进行了循环动荷载作用下的疲劳累积损伤分析.结果表明该模型不仅能够较好地反映支承层在循环荷载作用下疲劳损伤非线性演变规律,还可以展现其疲劳损伤分布形态的全过程,为研究高速铁路无砟轨道混凝土结构的疲劳损伤与寿命预测,提供了可行的理论分析方法.     

Key role of integrin αIIbβ3 signaling to Syk kinase in tissue factor-induced thrombin generation

The fibrin(ogen) receptor, integrin α(IIb)β(3), has a well-established role in platelet spreading, aggregation and clot retraction. How α(IIb)β(3) contributes to platelet-dependent coagulation is less well resolved. Here, we demonstrate that the potent suppressing effect of clinically used α(IIb)β(3) blockers on tissue factor-induced thrombin generation is linked to diminished platelet Ca(2+) responses and phosphatidylserine (PS) exposure. The same blockers suppress these responses in platelets stimulated with collagen and thrombin receptor agonists, whereas added fibrinogen potentiates these responses. In platelets spreading on fibrinogen, outside-in α(IIb)β(3) signaling similarly enhances thrombin-induced Ca(2+) rises and PS exposure. These responses are reduced in α(IIb)β(3)-deficient platelets from patients with Glanzmann's thrombasthenia. Furthermore, the contribution of α(IIb)β(3) to tissue factor-induced platelet Ca(2+) rises, PS exposure and thrombin generation in plasma are fully dependent on Syk kinase activity. Tyrosine phosphorylation analysis confirms a key role of Syk activation, which is largely but not exclusively dependent on α(IIb)β(3) activation. It is concluded that the majority of tissue factor-induced procoagulant activity of platelets relies on Syk activation and ensuing Ca(2+) signal generation, and furthermore that a considerable part of Syk activation relies on α(IIb)β(3) signaling. These results hence point to a novel role of Syk in integrin-dependent thrombin generation.     

Surface exposure of phosphatidylserine in pathological cells

The asymmetric phospholipid distribution in plasma membranes is normally maintained by energy-dependent lipid transporters that translocate different phospholipids from one monolayer to the other against their respective concentration gradients. When cells are activated, or enter apoptosis, lipid asymmetry can be perturbed by other lipid transporters (scramblases) that shuttle phospholipids non-specifically between the two monolayers. This exposes phosphatidylserine (PS) at the cells outer surface. Since PS promotes blood coagulation, defective scramblase activity upon platelet stimulation causes a bleeding disorder (Scott syndrome). PS exposure also plays a pivotal role in the recognition and removal of apoptotic cells via a PS-recognizing receptor on phagocytic cells. Furthermore, expression of PS at the cell surface can occur in a wide variety of disorders. This review aims at highlighting how PS expression in different cells may complicate a variety of pathological conditions, including those that promote thromboembolic complications or produce aberrations in apoptotic cell removal.Received 26 November 2004; received after revision 3 January 2005; accepted 10 January 2005 Available online 09 March 2005     

鲁米诺体系的多通道电致化学发光

本文综述了鲁米诺体系在金属、非金属以及半导体电极上的电位分辨电致化学发光行为和机理,揭示了鲁米诺电致化学发光的多通道性及其对电极材料、电极电位和电极表面状态的依赖性。     

氧化酪蛋白对小鼠组织抗氧化能力及血液肽组成的影响

目的研究酪蛋白经过加热氧化和脂质过氧化物MDA氧化后，对小鼠体内氧化还原状态及小鼠血液中肽组成的影响。方法酪蛋白经100℃加热（0、30、60、90min）和丙二醛（MDA）氧化（MDA终浓度0、0．2、20、200mmol／L）处理，测定其羰基、巯基含量及表面疏水性的变化。小鼠分为四组，分别灌胃生理盐水、正常酪蛋白、加热90rain、MDA氧化酪蛋白，测定0、30、60、90、120、160min血液中自由基水平，并采用HPLC-MS分析灌胃后120min小鼠血浆肽组分的变化，测定小鼠的肝脏、空肠、十二指肠组织抗氧化能力指标（总抗氧化能力T—AOC、丙二醛MDA、还原型谷胱甘肽GSH）。结果酪蛋白经过两种氧化处理，羰基含量均随氧化程度呈显著上升，巯基含量呈下降趋势。加热氧化后酪蛋白表面疏水性比正常酪蛋白低，而MDA氧化导致疏水性上升。小鼠血液中自由基最高峰出现在灌胃后160min。灌胃两种方式处理的酪蛋白，血液中自由基的含量均显著高于灌胃正常酪蛋白组（P〈0．05），肝脏、空肠、十二指肠还原型谷胱甘肽（GSH）含量和总抗氧化能力（T-AOC）均低于正常酪蛋白组，丙二醛（MDA）含量显著提高（P〈0．05）。HPLC—MS分析显示，灌胃MDA氧化酪蛋白组血液中肽组成与对照组不同，出现c7H15N4O含羰基类的物质：结论氧化会导致酪蛋白理化性质的改变，摄入氧化酪蛋白引起机体的氧化应激，降低组织抗氧化能力。     

Protein oxidation and 20S proteasome-dependent proteolysis in mammalian cells

The generation of reactive oxygen species is an inevitable aspect of aerobic life. In addition to being exposed to free radicals in the environment, aerobic organisms must also deal with oxygen radicals generated as byproducts of a number of physiological mechanisms - for example, by the mitochondrial and endoplasmic reticulum electron transport chains, and by cells of the immune system. Although most organisms are equipped with several lines of defense against oxidative stress, these defensive mechanisms are not 100% effective, and oxidatively modified forms of proteins accumulate during aging, and in many pathological conditions.?Oxidatively modified proteins can form large aggregates due to covalent cross-linking or increased surface hydrophobicity. Unless repaired or removed from cells, these oxidized proteins are often toxic and can threaten cell viability. Mammalian cells exhibit only limited direct repair mechanisms, and oxidatively damaged proteins appear to undergo selective proteolysis, primarily by the major cytosolic proteinase, the proteasome. Interestingly, it appears that the 20S 'core' proteasome conducts the recognition and elimination of oxidized proteins in an ATP-independent and ubiquitin-independent pathway. Received 31 May 2001; accepted 26 June 2001     

Glycoprotein IIb/IIIa blockade inhibits platelet aminophospholipid exposure by potentiating translocase and attenuating scramblase activity

The present study investigated the mechanisms underlying the inhibition of platelet phosphatidylserine (PS) exposure by GPIIb/IIIa blockade. Platelet PS exposure induced by thrombin stimulation was cell-cell contact dependent. GPIIb/IIIa blockade by c7E3 or SR121566 inhibited thrombin-induced platelet PS exposure. Thrombin stimulation induced mild, while A23187 induced extensive platelet-derived microparticle (PDMP) generation. Thrombin-induced PDMP generation was not inhibited by GPIIb/IIIa blockade. Aminophospholipid translocase activity was reduced upon platelet activation by thrombin. The reduction of non-PS-exposing platelets was attenuated by GPIIb/IIIa blockade, while little translocase activity was seen in PS-exposing platelets. Thrombin increased scramblase activity slightly in non-PS-exposing platelets, which was inhibited by GPIIb/IIIa blockade, and markedly enhanced scramblase activity in PS-exposing platelets. Activation of platelet calpain and caspase-3 or cytosolic calcium mobilization were not altered by GPIIb/IIIa inhibition. Thus, GPIIb/IIIa blockade inhibits platelet PS exposure by enhancing translocase activity and attenuating scramblase activity, but does not inhibit PDMP generation. Received 13 December 2006; received after revision 5 February 2007; accepted 9 March 2007