移动分布式数据库系统中合作事务恢复技术

形式地给出了合作事务定义及事务间由于消息交换而形成的各务间的检验点依赖和恢复依赖，基于这些定义，某一事务记检验点时，所有检验点依赖于该事务也记检验点，当某一事务恢复时，所有恢复依赖于该事务的事务也恢复到其检验点的状态，开发了一种适合于移动环境的事务恢复技术，；在事务正常的消息传送中，通过额外的一点带宽附加传送事务间的依赖关系，在事务记检验点时，尽可能并行地通知所有相关的事务记检验点，实验表明，该事务恢复技术能减少系统检验点的响应时间，提高系统的恢复速度及系统吞吐率，对网络带宽的要求基本没有增加。     

用时间序列分析方法动态确定检查点时间间隔

设置检查点是容错计算机系统进行故障恢复的重要手段。检查点的开销则是影响其性能的一个主要因素。许多文献已指出检查点开销主要是来自于对进程状态的保存。文章采用时间序列分析的方法对进程状态大小变化情况进行分析和预测,动态选择恰当的检查点时间间隔,减少检查点时需保存的进程状态量,从而减小了检查点的开销。     

一种基于虚拟对象的进程检查点实现方法

检查点回卷恢复策略是实现软件容错的一种重要方法。基于虚拟对象策略的进程检查点实现方法把应用层与系统层的直接交互被重定向为应用层与虚拟对象层的交互以及虚拟对象层与系统层的交互。故障恢复时,虚拟对象层重新和系统层捆绑结合,使得进程环境故障前后的差异性对应用层透明。另外,基于虚拟对象的检查点策略不须要进行对象句柄转换,避免了对象句柄转换所带来的开销。该方法具有开销小的特点,并且支持多线程及线程间的同步。     

基于Cluster的并行内存数据库恢复机制的设计与实现

文章提出的恢复子系统模型是根据差分日志记录的特点,将已提交事务的日志经并行日志管理器收集后并行写入到多个磁盘,通过“协调者”全局检验点和站点局部检验点的协调操作,具有更高的并发度和更高的系统吞吐量,并且能快速地支持系统失败恢复．经过验证试验表明该子系统有效地减少了日志信息量,缩短了系统的恢复时间,提高了系统的性能．     

基于检验点的移动云资源调度策略研究

移动云以按需付费的方式交付给用户,其服务可靠性成为了用户最为关心的性能指标之一。容错资源调度策略常用于云平台中提供服务的可靠性,其中检验点技术是云平台中容错资源调度的一种主要手段。对Web云中检验点技术的原理进行了深入分析,重点讨论了基于检验点策略的容错资源调度方法,分别对预设故障概率服从泊松分布的固定间隔周期检验点容错策略及无预设故障概率的动态间隔周期检验点容错策略进行了深入的分析,比较了不同检验点技术的特点和问题。结合移动云的工作特点,提出了移动云环境下检验点技术未来的研究点。     

虚拟机内存轻量级检查点研究

针对传统的虚拟机检查点粒度大和做检查点时停机时间长的问题,采用空闲内存页面排空、写时复制和增量检查点来解决传统虚拟机检查点的问题,通过这三项技术使检查点技术轻量化.空闲内存页面排空通过在检查点中排除空闲页面,可以减少虚拟机检查点文件的大小;写时复制通过在虚拟机内存写入时进行内存页面复制,可以减少做检查点的时间;增量检查点通过内存增量页面的计算,检查点只包含增量信息,可以减少虚拟机检查点文件的大小.在虚拟化平台Xen上的实验结果表明:采用写时复制技术减少了做检查点过程中虚拟机的停机时间,停机时间不超过300ms,并可使检查点这一过程对上层应用透明;采用内存排空技术和增量技术来做检查点,使得检查点文件的大小减少20%.     

VxWorks中任务恢复机制的设计与实现

软件容错技术是保证系统高可靠性及高可信性的有力工具。设计并实现了一种在VxWorks系统下基于检查点的任务恢复机制。通过对VxWorks系统下检查点文件内容的分析,采用3种方法来解决检查点的任务恢复问题:基于内存预先分配的主动内存管理,解决任务恢复时数据内存地址变化的问题;建立系统内核对象池,实现支持多任务之间同步和通信的内核对象的恢复;设计用户层任务恢复中间件,实现用户级检查点设置和任务恢复。最后设计基于VxWorks和PowerPC的计算平台原理样机,通过对单任务、多个单任务、多任务通讯、以及多任务协调工作4个测试用例的分析表明,所设计的基于检查点的任务恢复实现方案能正确保存任务关键信息及保证任务恢复的正确性和一致性。     

Sea urchin embryo as a model for analysis of the signaling pathways linking DNA damage checkpoint,DNA repair and apoptosis

DNA integrity checkpoint control was studied in the sea urchin early embryo. Treatment of the embryos with genotoxic agents such as methyl methanesulfonate (MMS) or bleomycin induced the activation of a cell cycle checkpoint as evidenced by the occurrence of a delay or an arrest in the division of the embryos and an inhibition of CDK1/cyclin B activating dephosphorylation. The genotoxic treatment was shown to induce DNA damage that depended on the genotoxic concentration and was correlated with the observed cell cycle delay. At low genotoxic concentrations, embryos were able to repair the DNA damage and recover from checkpoint arrest, whereas at high doses they underwent morphological and biochemical changes characteristic of apoptosis. Finally, extracts prepared from embryos were found to be capable of supporting DNA repair in vitro upon incubation with oligonucleotides mimicking damage. Taken together, our results demonstrate that sea urchin early embryos contain fully functional and activatable DNA damage checkpoints. Sea urchin embryos are discussed as a promising model to study the signaling pathways of cell cycle checkpoint, DNA repair and apoptosis, which upon deregulation play a significant role in the origin of cancer. Received 10 April 2007; accepted 23 April 2007     

Mitotic regulation of the anaphase-promoting complex

Orderly progression through mitosis is regulated by the anaphase-promoting complex/cyclosome (APC/C), a large multiprotein E3 ubiquitin ligase that targets key mitotic regulators for destruction by the proteasome. APC/C has two activating subunits, Cdc20 and Cdh1. The well-established view is that Cdc20 activates APC/C from the onset of mitosis through the metaphase-anaphase transition, and that Cdh1 does so from anaphase through G1. Recent work, however, indicates that Cdh1 also activates APC/C in early mitosis and that this APC/C pool targets the anaphase inhibitor securin. To prevent premature degradation of securin, the nuclear transport factors Nup98 and Rae1 associate with APC/C^Cdh1-securin complexes. In late metaphase, when all kinetochores are attached to spindle microtubules and the spindle assembly checkpoint is satisfied, Nup98 and Rae1 are released from these complexes, thereby allowing for prompt ubiquitination of securin by APC/C^Cdh1. This, and other mechanisms by which the catalytic activity of APC/C is tightly regulated to ensure proper timing of degradation of each of its mitotic substrates, are highlighted. Received 8 October 2006; received after revision 24 November 2006; accepted 8 January 2007     

Protein kinase TTK interacts and co-localizes with CENP-E to the kinetochore of human cells

Spindle checkpoint is an important biochemical signaling cascade during mitosis which monitors the fidelity of chromosome segregation, and is mediated by protein kinases Mps1 and Bub1/BubR1. Our recent studies show that kinesin-related motor protein CENP-E interacts with BubR1 and participates in spindle checkpoint signaling. To elucidate the molecular mechanisms underlying spindle checkpoint signaling, we carried out proteomic dissection of human cell kinetochore and revealed protein kinase TTK, human homologue of yeast Mps1. Our studies show that TTK is localized to the kinetochore of human cells, and interacts with CENP-E, suggesting that TTK may play an important role in chromosome segregation during mitosis.