分布系统中多米诺效应的分析与消除

分布系统中发生故障后,错误信息在进程间的传播,以及由此引起的系统恢复过程中的多米诺效应是分布系统容错恢复技术所面临的最重要与最困难的问题.目前各种研究工作偏重于具体的系统动态恢复技术.本文的研究重点在于首次揭示多米诺效应本身固有的数量特征及其与分布系统技术参数间的联系,给出多米诺效应动态消除技术,引入系统额外开销的下限,并针对动态技术的缺点,探讨多米诺效应的静态消除技术,为解决困难开辟新途径.     

基于完美彩虹表的检查点算法改进研究

本文对完美彩虹表下的检查点算法进行了研究和改进.时间存储折中攻击是由Hellman于1980年提出的一种适用于分组密码和哈希函数的算法.该算法具有可以用空间复杂度来换取时间复杂度的特点,然而由于链之间的碰撞,算法具有较高的误报率.其一个变种,Oechslin于2003年提出的彩虹表算法可以大幅减少碰撞的数量,从而提升效率.2005年,Avoine等人提出了另一种名为"检查点"的改进,该算法从另一个角度,即降低误报的影响来提升效率.然而,检查点的设置问题(数量和位置)仍未得到完全的解答.在本文中,我们对检查点算法在基于完美彩虹表的条件下进行研究,对检查点的设置进行理论分析,推导出最佳位置的计算式,并构造实验来检验最优选择的结果.在空间复杂度相当的条件下,相较于没有设置检查点的彩虹表,攻击时间可以减少10%到30%.     

Increasing processor utilization in hard-real-time systems with checkpoints

Often hard real-time systems require results that are produced on time despite the occurrence of processor failures. This paper considers a distributed system where tasks are periodic and each task occurs in multiple copies which are periodically synchronized in order to handle failures. The problem of preemptively scheduling a set of such tasks is discussed where every occurrence of a task has to be completely executed before the next occurrence of the same task. First, a static scheduling algorithm is proposed which uses periodic checkpoints to tolerate processor failures. Then, the performance of the algorithm is substancially improved employing a mixed strategy which constructs a schedule where high frequency tasks are duplicated, and low frequency tasks are periodically checkpointed. The performance of the solution proposed is evaluated in terms of the minimum achievable processor utilization due to the useful computation of the tasks. Moreover, analytical and simulation studies are used to reveal interesting trade-offs associated with the scheduling algorithm. In particular, if high frequency tasks are less than 70 percent of the total number of tasks then the mixed strategy yields a higher processor utilization than the task duplication scheme.     

Complex Mechanisms of Antimony Genotoxicity in Budding Yeast Involves Replication and Topoisomerase I-Associated DNA Lesions,Telomere Dysfunction and Inhibition of DNA Repair

Antimony is a toxic metalloid with poorly understood mechanisms of toxicity and uncertain carcinogenic properties. By using a combination of genetic, biochemical and DNA damage assays, we investigated the genotoxic potential of trivalent antimony in the model organism Saccharomyces cerevisiae. We found that low doses of Sb(III) generate various forms of DNA damage including replication and topoisomerase I-dependent DNA lesions as well as oxidative stress and replication-independent DNA breaks accompanied by activation of DNA damage checkpoints and formation of recombination repair centers. At higher concentrations of Sb(III), moderately increased oxidative DNA damage is also observed. Consistently, base excision, DNA damage tolerance and homologous recombination repair pathways contribute to Sb(III) tolerance. In addition, we provided evidence suggesting that Sb(III) causes telomere dysfunction. Finally, we showed that Sb(III) negatively effects repair of double-strand DNA breaks and distorts actin and microtubule cytoskeleton. In sum, our results indicate that Sb(III) exhibits a significant genotoxic activity in budding yeast.     

Synergy of Immunostimulatory Genetherapy with Immune Checkpoint Blockade Motivates Immune Response to Eliminate Cancer

Normalizing the tumor-induced immune deficiency in the immunosuppressive tumor microenvironment (TME) through increasing the efficient infiltration and activation of antitumoral immunity in TME is the core of promising immunotherapy. Herein, a Cyclo(Arg-Gly-Asp-d -Phe-Lys) (RGD) peptides-modified combinatorial immunotherapy system based on the self-assembly of the nanoparticles named RGD-DMA composed of RGD-PEG-PLA, methoxy poly(ethylene glycol)-poly(lactide) (MPEG-PLA) and 1,2-Dioleoyl-3-trimethylammonium-propane (DOTAP) is used to codeliver the immunostimulatory chemokine CCL19-encoding plasmid DNA (CCL19 pDNA) and immune checkpoint ligand PD-L1 inhibitor (BMS-1). The RGD-DMA/pCCL19-BMS-1 system not only exhibited significant inhibition of tumor progression but also induced locally high concentrations of immunostimulatory cytokines at tumor sites without causing an obviously systemic inflammatory response. The immunosuppressive TME is efficaciously reshaped by the coadministration of RGD-DMA/pCCL19 and BMS-1, as indicated by the activated T lymphocytes, increased intratumoral-infiltration of mature dendritic cells (DCs), and the repolarization of macrophages from pro-tumoral M2-phenotype toward tumoricidal M1-phenotype. The upregulated PD-L1 expression at tumor sites caused by the increased IFN-γ levels after immunostimulatory gene therapy further demonstrated the synergistic effects of BMS-1 in counteracting the inhibitory role of PD-L1 expression in antitumor immunity. Therefore, the combination of immunostimulating therapy and immune checkpoint inhibitor that synergistically target multiple immune regulatory pathways demonstrates significant potential as a novel immunotherapy approach.     

基于闯关翻转课堂的高职《PLC及其应用》课程整体设计

以超星泛雅网络课程平台为依托,根据电气自动化专业的岗位要求,结合《PLC及其应用》课程的培养目标,按照闯关翻转课堂的模式完成课程的整体设计。     

Cytotoxic T Cell Expression of Leukocyte-Associated Immunoglobulin-Like Receptor-1 (LAIR-1) in Viral Hepatitis C-Mediated Hepatocellular Carcinoma

Virus-related hepatocellular carcinoma (HCC) pathogenesis involves liver inflammation, therefore, despite successful treatment, hepatitis C virus (HCV) may progress to HCC from initiated liver cirrhosis. Cytotoxic T cells (Tcs) are known to be involved in HCV-related cirrhotic complications and HCC pathogenesis. The inhibitory checkpoint leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is expressed on Tcs. Therefore, we aimed to determine whether the Tc expression level of LAIR-1 is associated with HCC progression and to evaluate LAIR-1 expression as a noninvasive biomarker for HCC progression in the context of liver cirrhosis related to HCV genotype 4 (G4) in Egyptian patients’ peripheral venous blood liquid biopsy. A total of 64 patients with HCC and 37 patients with liver cirrhosis were enrolled in this case-controlled study, and their LAIR-1 expression on Tc related to the progression of liver cirrhosis was examined and compared to that of the apparently healthy control group (n = 20). LAIR-1 expression was analyzed using flow cytometry. Results: The HCC group had significantly higher LAIR-1 expression on Tc and percentage of Tc positive for LAIR-1 (LAIR-1+Tc%) than the HCV G4-related liver cirrhosis group. LAIR-1+Tc% was correlated with the HCC surrogate tumor marker AFP (r = 0.367, p = 0.001) and insulin resistance and inflammation prognostic ratios/indices. A receiver operating characteristic (ROC) curve revealed that adding LAIR-1+Tc% to AFP can distinguish HCC transformation in the Egyptian patients’ cohort. Upregulated LAIR-1 expression on Tc could be a potential screening noninvasive molecular marker for chronic inflammatory HCV G4 related liver cirrhosis. Moreover, LAIR-1 expression on Tc may be one of the players involved in the progression of liver cirrhosis to HCC.     

支持构件迁移的分布式系统容错算法

随着分布式应用技术的发展,构件的静态性限制了分布式系统在运行期间适应其可用资源变化的要求.为了动态适应系统可用资源,提高系统性能,支持构件可迁移的分布式应用研究受到广泛关注.针对提高构件可迁移分布式应用的可靠性,提出一种分布式系统容错算法.在准同步检查点算法的基础上,通过引入shadow-chain和通讯录机制,实现了构件间通信的可靠性和构件重定位的透明性,从而使得系统能够在较低代价下设置检查点,并能将出错后的系统回卷到一致性状态.     

A fully informed model-based checkpointing protocol for preventing useless checkpoints

Checkpointing and rollback recovery are widely used techniques for handling failures in distributed systems. When processes involved in a distributed computation are allowed to take checkpoints independently without any coordination with each other, some or all of the checkpoints taken may not be part of any consistent global checkpoint, and hence, are useless for recovery. Communication-induced checkpointing algorithms allow processes to take checkpoints independently and also ensure that each checkpoint taken is part of a consistent global checkpoint by forcing processes to take some additional checkpoints. It is well known that it is impossible to design an optimal communication-induced checkpointing algorithm (i.e. a checkpointing algorithm that takes minimum number of forced checkpoints). So, researchers have designed communication-induced checkpointing algorithms that reduce forced checkpoints using different heuristics. In this paper, we present a communication-induced checkpointing algorithm which takes less number of forced checkpoints when compared to some of the existing checkpointing algorithms in its class.