Dynamic analysis of arrest of buckle propagation on a beam on a nonlinear elastic foundation by FEM

Based on the dynamic governing equation of propagating buckle on a beam on a nonlinear elastic foundation, this paper deals with an important problem of buckle arrest by combining the FEM with a time integration technique. A new conclusion completely different from that by the quasi-static analysis about the buckle arrestor design is drawn. This shows that the inertia of the beam cannot be ignored in the analysis under consideration, especially when the buckle propagation is suddenly stopped by the arrestors.

Effects of cell-cycle arrest agents on cleavage and development of loach (Misgurnus anguillicaudatus) embryos

The aim of this study was to determine the lowest concentration of nocodazole and colchicine to arrest blastomere division during the cleavage stage of loach embryos and to assess the reversibility and toxicity of the treatments in the treated embryos. Eight-cell loach embryos were incubated for 4, 8, 12, or 16 h in 1/10x Holtfreter supplemented with either nocodazole, an inhibitor of tubulin polymerization, or colchicine, an inhibitor of tubulin assembly. Complete arrest of cell cycle was observed, at a colchicine concentration of 0.996 mM and at a nocodazole concentration of 0.275 muM, respectively (the lowest effective concentration). No major morphological alteration in chromatin was observed. Reversibility and toxicity of both agents were dose and exposure period dependent. For both agents, prolonging cleavage arrest for more than 4 h (at the effective concentrations) is detrimental to development of embryos. Nocodazole treatment was less cytotoxic, whereas the concentrations of colchicine which induce cleavage arrest were detrimental to development beyond the blastula stage. Toxic effects beyond the blastula stage could be minimized for both agents by reducing the period of treatment and concentration.

Targeted RNA interference of cyclin A(2) mediated by functionalized single-walled carbon nanotubes induces proliferation arrest and apoptosis in chronic myelogenous leukemia K562 cells

Cyclin A(2) plays critical role in DNA replication, transcription, and cell cycle regulation. Its overexpression has been detected and related to many types of cancers including leukemia, suggesting that suppression of cyclin A(2) would be an attractive strategy to prevent tumor progression. Herein, we apply functionalized single wall carbon nanotubes (f-SWNTs) to carry small interfering RNA (siRNA) into K562 cells and determine whether inhibition of cyclin A(2) would be a potential therapeutic target for chronic myelogenous leukemia.

Involvement of p90 ribosomal S6 kinase in termination of cell cycle arrest during development of Artemia-encysted embryos

Artemia has evolved a unique developmental pattern of encysted embryos to cope with various environmental threats. Cell divisions totally cease during the preemergence developmental stage from gastrula to prenauplius. The molecular mechanism of this, however, remains unknown. Our study focuses on the involvement of p90 ribosomal S6 kinase (RSK), a family of serine/threonine kinase-mediating signal transduction downstream of mitogen-activated protein kinase cascades, in the termination of cell cycle arrest during the post-embryonic development of Artemia-encysted gastrula. With immunochemistry, morphology, and cell cycle analysis, the identified Artemia RSK was established to be specifically activated during the post-embryonic and early larval developmental stages when arrested cells of encysted embryos resumed mitoses. In vivo knockdown of RSK activity by RNA interference, kinase inhibition, and antibody neutralization consistently induced defective larvae with distinct gaps between the exoskeleton and internal tissues. In these abnormal individuals, mitoses were detected to be largely inhibited in the affected regions. These results display the requirement of RSK activity during Artemia development and suggest its role in termination of cell cycle (G(2)/M phase) arrest and promotion of mitogenesis. Our findings may, thus, provide insights into the regulation of cell division during Artemia post-embryonic development and reveal further aspects of RSK functions.

Rhein induces apoptosis and cell cycle arrest in human hepatocellular carcinoma BEL-7402 cells

Rhein, an anthraquinone derivative of rhubarb, inhibits the proliferation of various human cancer cells. In this paper, we focused on studying the effects of rhein on human hepatocelluar carcinoma BEL-7402 cells and further understanding the underlying molecular mechanism in an effort to make the potential development of rhein in the treatment of cancers. Using MTT assay and flow cytometry, we demonstrate a critical role of rhein in the suppression of BEL-7402 cell proliferation in a concentration- and time-dependent manner. The increase of apoptosis rate was observed after incubation of BEL-7402 cells with rhein at 50-200 mu M for 48 hours, and the cells exhibit typical apoptotic features including cellular morphological change and chromatin condensation. Moreover, rhein-induced cell cycle S-phase arrest. Additionally, after rhein treatment, expression levels of c-Myc gene were decreased, while those of caspase-3 gene were increased in a dose-dependent manner by using real-time PCR assay. The results demonstrate for the first time that cell cycle S-phase arrest is one of the mechanisms of rhein in inhibition of BEL-7402 cells. Rhein plays its role by inducing cell cycle arrest via downregulation of oncogene c-Myc and apoptosis through the caspase-dependent pathway. It is expected that rhein will be effective and useful as a new agent in hepatocelluar carcinoma treatment in the future.

高压强脉冲电流对金属裂纹的止裂效果

如何产生高强度脉冲电流是应用电磁热效应遏制金属裂纹扩展的一个关键问题。介绍了高压脉冲放电装置的工作原理，从理论、数值模拟、实验三个方面，通过对不同尺寸的裂纹试件导入强脉冲电流而产生的电磁热效应的止裂效果进行了分析和研究，研究结果表明：强脉冲电流产生的电磁热效应，能够使裂纹尖端处熔化形成微小的焊口，遏制了裂纹的扩展。试件的通流尺寸、电阻率、导入电流密度是影响裂纹尖端温度场和温度梯度场的主要因素。

Crack propagation in structures subjected to periodic excitation

In the present paper, a simple mechanical model is developed to predict the dynamic response of a cracked structure subjected to periodic excitation, which has been used to identify the physical mechanisms in leading the growth or arrest of cracking. The structure under consideration consists of a beam with a crack along the axis, and thus, the crack may open in Mode I and in the axial direction propagate when the beam vibrates. In this paper, the system is modeled as a cantilever beam lying on a partial elastic foundation, where the portion of the beam on the foundation represents the intact portion of the beam. Modal analysis is employed to obtain a closed form solution for the structural response. Crack propagation is studied by allowing the elastic foundation to shorten (mimicking crack growth) if a displacement criterion, based on the material toughness, is met. As the crack propagates, the structural model is updated using the new foundation length and the response continues. From this work, two mechanisms for crack arrest are identified. It is also shown that the crack propagation is strongly influenced by the transient response of the structure.

Mixed-mode fracture mechanisms near the fatigue threshold of aisi-316 stainless-steel

Near threshold, mixed mode (I and II), fatigue crack growth occurs mainly by two mechanisms, coplanar (or shear) mode and branch (or tensile) mode. For a constant ratio of ΔK_I/ΔK_II the shear mode growth shows a self-arrest character and it would only start again when ΔK_I and ΔK_II are increased. Both shear crack growth and the early stages of tensile crack growth, are of a crystallographic nature; the fatigue crack proceeds along slip planes or grain boundaries. The appearance of the fracture surfaces suggest that the mechanism of crack extension is by developing slip band microcracks which join up to form a macrocrack. This process is thought to be assisted by the nature of the plastic deformation within the reversed plastic zone where high back stresses are set up by dislocation pile-ups against grain boundaries. The interaction of the crack tip stress field with that of the dislocation pile-ups leads to the formation of slip band microcracks and subsequent crack extension. The change from shear mode to tensile mode growth probably occurs when the maximum tensile stress and the microcrack density in the maximum tensile plane direction attain critical values.

高压脉冲放电技术在金属裂纹止裂中的应用

如何产生高强度脉冲电流是应用电磁热效应遏制金属裂纹研究的一个关键问题.本文介绍了高压脉冲放电装置的工作原理;从理论上分析了充电电压、回路参数与放电电流幅值、放电周期之间的关系.在此基础上,自主设计、开发了一套高压脉冲放电装置.采用它对金属模具钢中裂纹进行了脉冲放电止裂实验.放电时裂纹尖端熔化形成堆焊和高压应力区,使裂纹尖端钝化,达到了止裂的目的.由于脉冲放电快速加热和冷却,在裂纹尖端处实现了冲击淬火,得到了超细化的隐晶马氏体和细粒碳化物等微观组织,提高了裂纹尖端处的硬度、强韧性和耐磨性,试验结果验证了该装置的有效性,本文的成果为采用电磁热效应对金属模具裂纹止裂提供了实验技术基础.

不同功率下的飞秒激光在水中形成的脉冲压缩和超连续谱

本文研究了飞秒激光脉冲在水中的传输情况.通过改变不同的激光输入功率进行模拟，我们发现从输入功率略高于到远远高于发生自聚焦的临界功率,分别是群速度色散和多光子电离多光子吸收阻止了自聚焦导致的脉冲塌陷，当多光子电离和多光子吸收主导传输时，脉冲能被压缩到几个光学周期.在频域，多光子电离能引起很强的蓝移,而多光子吸收能对这种蓝移起到抑制作用。

C1q-like inhibits p53-mediated apoptosis and controls normal hernatopoiesis during zebrafish embryogenesis

Except for the complement C1q, the immunological functions of other C1q family members have remained unclear. Here we describe zebrafish C1q-like, whose transcription and translation display a uniform distribution in early embryos, and are restricted to mid-hind brain and eye in later embryos. In vitro studies showed that C1q-like could inhibit the apoptosis induced by ActD and CHX in EPC cells, through repressing caspase 3/9 activities. Moreover, its physiological roles were studied by morpholino-mediated knockdown in zebrafish embryogenesis. In comparison with control embryos, the C1q-like knockdown embryos display obvious defects in the head and cramofacial development mediated through p53-induced apoptosis, which was confirmed by the in vitro transcribed C1q-like mRNA or p53 MO co-injection. TUNEL assays revealed extensive cell death, and caspase 3/9 activity measurement also revealed about two folds increase in C1q-like morphant embryos, which was inhibited by p53 MO co-injection. Real-time quantitative PCR showed the up-regulation expression of several apoptosis regulators such as p53, mdm2, p21, Box and caspase 3, and down-regulation expression of hbae1 in the C1q-like morphant embryos. Knockdown of C1q-like in zebrafish embryos decreased hemoglobin production and impaired the organization of mesencephalic vein and other brain blood vessels. Interestingly, exposure of zebrafish embryos to UV resulted in an increase in mRNA expression of C1q-like, whereas over-expression of C1q-like was not enough resist to the damage. Furthermore, C1q-like transcription was up-regulated in response to pathogen Aeromonas hydrophila, and embryo survival significantly decreased in the C1q-like morphants after exposure to the bacteria. The data suggested that C1q-like might play an antiapoptotic and protective role in inhibiting p53-dependent and caspase 3/9-mediated apoptosis during embryogenesis, especially in the brain development, and C1q-like should be a novel regulator of cell survival during zebrafish embryogenesis. (c) 2008 Elsevier Inc. All rights reserved.

面向XML文档的细粒度强制访问控制模型

XML文档存放的信息需要受到访问控制策略的保护.现有的一些面向XML文档的访问控制模型都是基于自主访问控制策略或基于角色的访问控制.高安全等级系统需要强制访问控制来保证系统内信息的安全.首先扩展了XML文档模型使其包含标签信息,并给出了扩展后的文档模型需要满足的规则.然后通过讨论XML文档上的4种操作,描述了面向XML文档的细粒度强制访问控制模型的详细内容.该模型基于XML模式技术,它的控制粒度可以达到文档中的元素或者属性.最后讨论了该模型的体系结构和一些实现机制。

操作系统强制访问控制关键技术研究

强制访问控制能有效地防止用户有意或无意地破坏系统的安全，能够有效地防止病毒和木马以用户的身份破坏系统的安全，是高安全需求操作系统的主要防护手段。业界对操作系统强制访问控制研究起步很早。然而，面对日新月异的应用场景，面对计算机系统及操作系统自身相关技术的迅猛发展，已有的针对操作系统强制访问控制的研究工作不足以兼顾安全性、可用性和灵活性。以上不足集中体现在：1) 当前广泛使用的强制访问控制机制从设计上难以同时满足实用系统对安全性和可用性的要求；2) 强制访问控制的设计缺乏对操作系统所处分布式、网络化环境的考虑；3) 操作系统强制访问控制研发保障技术需要进一步研究。 针对这些问题，本论文从强制访问控制的设计和保障出发，对操作系统强制访问控制关键技术展开研究，并取得了以下几个方面的成果： 第一：强制访问控制格策略模型机制简洁，安全性易验证，在安全操作系统和安全增强操作系统上应用广泛。然而严格地实施格策略会带来可用性的问题。本文针对机密性和完整性强制访问控制格策略模型，分别给出了可监控客体框架和Clark-Wilson可信主体特权状态跃迁监控框架。这些框架具有细的刻画粒度，好的扩展性和简洁性，我们对这些框架给出了数学描述，并对带Clark-Wilson可信主体特权状态跃迁监控框架的完整性格模型给出了理论证明； 第二：针对分布式应用环境，提出了基于可信计算技术和域型实施（Domain and Type Enforcement: DTE）策略的操作系统分布式强制访问控制方案。我们从理论上证明了策略的安全性。相比国内外同类工作，该方案具有细的访问控制粒度，在系统验证的简洁性和部署的灵活性方面是最好的； 第三：实施强制访问控制的中高等级安全操作系统的安全性需要利用形式化方法的严密性进行保证。本文按照TCSEC B2级别的要求，利用Z/EVES形式化工具对SECIMOS安全操作系统进行了形式化保障：给出了安全模型的形式化规范，给出了安全不变量和安全定理，证明了安全定理，描述了形式化安全模型与顶层设计的一致性； 第四：操作系统强制访问控制框架是强制访问控制机制在操作系统上实现的基础。本文提出了针对操作系统强制访问控制框架的自动测试用例生成方案。该方案利用编译器辅助审计代码插入，约束求解器辅助置乱参数生成，测试用例精简等技术为FreeBSD MAC框架生成了一套有效的回归测试用例套件。同时也为基于FreeBSD MAC框架的NFSARK系列安全操作系统提供了坚实的实施基础。 本文的研究成果向圆满解决当前国内操作系统强制访问控制的设计、实施和保障中遇到的问题的目标迈出了坚实的一步。

基于静态分析的强制访问控制框架的正确性验证

现阶段对操作系统的强制访问控制框架的正确性验证的研究主要集中于对授权钩子放置的验证.文中基于TrustedBSD MAC框架对强制访问控制框架的正确性验证问题进行了研究,在授权钩子放置验证的基础上,提出了安全标记的完全初始化验证和完全销毁验证.为了实现上述验证,文中提出了一个路径敏感的、基于用户自定义检查规则的静态分析方法.该方法通过对集成于编译器的静态分析工具mygcc进行扩展来验证强制访问控制框架的钩子放置的准确性和完备性.该方法具有完全的路径覆盖性,且具有低的误报率和时间开销.