基于知识元和有色Petri网的应急实施流程优化方法

合理的应急实施流程对于有效应对突发事件至关重要。在知识元理论与Petri网方法的基础上提出了一种突发事件应急实施流程的优化方法。首先,借鉴共性知识模型,形式化表示活动基元及其内部联系,建立活动基元模型。随后,找到活动基元模型与有色Petri网的映射关系,并使用有色Petri网方法实现活动基元模型以及活动基元间的基本路由关系。在此基础上,结合知识元原理和Petri网方法,提出突发事件应急实施流程的五步优化方法。最后,以化学危险品事故为例说明该优化方法的使用过程。

Study on Tribological Properties of CVT Fluid Containing Inert and Active Functional Elements

The lubricating characteristics of CVTF(continuously variable transmission fluid) mixed with a multi-functional complex additive were studied. The said complex additive contained an organic borate ester and a new type of friction improver comprising phosphorus element and poly-methylmethacrylate(PMMA), and a viscosity index improver. The viscosity-pressure characteristics were evaluated by a high-pressure quartz viscometer, and the anti-wear property was investigated by a four-ball friction tester. The mechanism of lubrication by the CVTF was studied using X-ray photoelectron spectroscopy(XPS). The results showed that CVTF T10, which contained a multi-functional complex additive, exhibited excellent properties, featuring greater solidification pressure and pressure-viscosity coefficient, improved oil film strength, and low wear value. These attributes meet the special CVTF requirements for "high friction and low wear" that make it possible to provide both traction and lubrication. The lubricating mechanism was varied using different functional elements, such as inert and active elements. Sulfur and phosphorus are active extreme pressure elements that can react on the metal friction surface and produce an extreme pressure lubrication film. Boron is an inert functional element and does not react upon the metal surface; boron is only adsorbed onto the metal surface to act as a lubricant for adsorption film and fillers.

Pharmarcogenetic Mechanism of ACE liD Polymorphism Adversely Responding to ACE Inhibitors in Regulating the ACE Promoter Activity in Neurons

The ACE （angiotensin converting enzyme） inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhibitors could activate the c-Jun N-terminal kinase signal to increase the ACE gene expression and that the Alu element of the human ACE gene involved in regulating ACE promoter activity, we aimed to investigate whether there are different pharmacogenetic responses of ACE I/D polymorphism to the ACE inhibitors in neurons. The three reporter vectors, pACEpro（0-SEAP, p-I-ACEpro-SEAP, and p-D-ACEpro-SEAP were used to examine the transcriptional activity of the vectors responding to the lisinopril treatment using a transient-transfection method in SH-SY5Y cells. Our results showed that lisinopril increased the promoter activity of an ACE gene by 16.7%. Additionally, we found the lisinopril enhanced the ACE promoter activity of the I-form vector by 17.2%, but adversely reduced that of the D-form vector by 16.8%, as compared with the respective control without the lisinopril treatment. Firstly, our findings had proved that the UD polymorphism of ACE gene contrarily responds to the ACE inhibitors in regulating the ACE expression in neurons, which provide a novel insight suggesting genetic testing to tailor the treatment regimens in AD （Alzheimer＇s disease） patients.