L-fuzzy闭包空间的T1与T2分离性

研究了L-fuzzy闭包空间的T1与T2分离性．首先定义了L-fuzzy闭包空间的L与T2分离性的概念,其次用类比、推广的方法讨论了T,与丁2分离性的遗传性,可乘性等性质．证明了一个T1（resp．T2）L-fuzzy闭包空间的子空间仍是T1（resp．,T2）L-fuzzy闭包空间,一族T1（resp．,T2）L-fuzzy闭包空间的乘积空间仍是T1（resp．,T2）L-fuzzy闭包空间的结果．这些结果表明定义的L-fuzzy闭包空间的T1与T2分离性具有遗传性,可乘性．     

Job shop scheduling problem with alternative machines using genetic algorithms

The classical job shop scheduling problem (JSP) is the most popular machine scheduling model in practice and is known as NP-hard. The formulation of the JSP is based on the assumption that for each part type or job there is only one process plan that prescribes the sequence of operations and the machine on which each operation has to be performed. However, JSP with alternative machines for various operations is an extension of the classical JSP, which allows an operation to be processed by any machine from a given set of machines. Since this problem requires an additional decision of machine allocation during scheduling, it is much more complex than JSP. We present a domain independent genetic algorithm (GA) approach for the job shop scheduling problem with alternative machines. The GA is implemented in a spreadsheet environment. The performance of the proposed GA is analyzed by comparing with various problem instances taken from the literatures. The result shows that the proposed GA is competitive with the existing approaches. A simplified approach that would be beneficial to both practitioners and researchers is presented for solving scheduling problems with alternative machines.     

关于弱θ—加细性的遗传性

本证明了弱θ－加强性是Ｆσ遗传的,在完备空间中,弱θ－加细性是遗传的。     

4Cr5Mo2V扁钢中AS14类退火组织成因分析

采用不同温度奥氏体化+贝氏体转变温度范围等温+球化退火工艺,模拟了4Cr5Mo2V扁钢中AS14类退火组织形成过程。利用Leica光学显微镜观察显微组织,采用438VP/KEVEX扫描电镜/能谱仪对试样微区化学成分进行分析,并对不同组织状态扁钢的冲击性能进行了测试。结果表明,终锻温度偏高,锻后在贝氏体转变温度范围停留或缓慢冷却导致钢中形成粗大的竹叶状贝氏体组织;退火时碳化物沿粗大贝氏体组织界面形核长大,而竹叶之间析出碳化物较少,从而形成了AS14类退火组织;AS14类退火组织具有较强的组织遗传性,能够显著降低扁钢的横向冲击性能;较低的终锻温度和冷却过程避免在贝氏体转变温度区间停留或缓慢冷却,可以防止4Cr5Mo2V扁钢形成AS14类退火组织。     

遗传性对称性色素异常症:一例家系报道及DSRAD基因突变的研究

目的报道1例遗传性对称性色素异常症家系,并对家系成员的DSRAD基因突变进行检测。方法PCR扩增该家系患者和健康对照个体DSRAD基因的全部外显子,并进行DNA测序,以100例无亲缘关系的正常人作对照。结果该家系患者DSRAD基因的第14外显子3388碱基发生了一个T→C的杂合突变,导致第1130位半胱氨酸被精氨酸替代,该区域可能存在DSRAD基因的脱氨基酶。家系中健康对照个体及无亲缘关系的正常人均未发现该突变。结论该遗传性对称性色素异常症家系中存在DSRAD基因的特异性突变,该突变引起编码蛋白功能缺陷,导致出现皮肤色素异常的临床表型。