加气加油站车行道下管道的埋设方式及计算探讨

依据HG／T20645－1998《化工装置管道机械设计规定》推荐的埋地管道应力计算式结合加气加油站内埋地管道的实际情况进行计算和分析,提出埋地管道可直接埋地敷设的方式提出一些粗浅的看法供设计参考。     

基于改进自适应遗传算法的固定结合面动态特性参数优化识别

针对固定结合面传统建模方法精度较低和结合面的动态特性参数难以确定的问题,改进了基于弹簧阻尼单元的建模方法,提出了基于实验模态分析和改进自适应遗传算法的固定结合面动态特性参数的优化识别方法。该方法以有限元计算的理论固有频率和阻尼比与其对应实验模态分析结果的相对误差最小为目标函数,使用改进的自适应遗传算法优化识别固定结合面的刚度和阻尼参数。以自行设计制作的固定结合面模型为研究对象进行了建模、实验、参数识别等分析,分析结果表明：所提出的方法是正确的、有效的,参数识别误差在5%以内,达到了较高的识别精度。     

KVLQT1 C-terminal missense mutation causes a forme fruste long-QT syndrome

BACKGROUND: KVLQT1, the gene encoding the alpha-subunit of a cardiac potassium channel, is the most common cause of the dominant form of long-QT syndrome (LQT1-type), the Romano-Ward syndrome (RWS). The overall phenotype of RWS is characterized by a prolonged QT interval on the ECG and cardiac ventricular arrhythmias leading to recurrent syncopes and sudden death. However, there is considerable variability in the clinical presentation, and potential severity is often difficult to evaluate. To analyze the relationship between phenotypes and underlying defects in KVLQT1, we investigated mutations in this gene in 20 RWS families originating from France. METHODS AND RESULTS: By PCR-SSCP analysis, 16 missense mutations were identified in KVLQT1, 11 of them being novel. Fifteen mutations, localized in the transmembrane domains S2-S3, S4-S5, P, and S6, were associated with a high percentage of symptomatic carriers (55 of 95, or 58%) and sudden deaths (23 of 95, or 24%). In contrast, a missense mutation, Arg555Cys, identified in the C-terminal domain in 3 families, was associated with a significantly less pronounced QT prolongation (459+/-33 ms, n=41, versus 480+/-32 ms, n=70, P=.0012), and significantly lower percentages of symptomatic carriers (7 of 44, or 16%, P<.001) and sudden deaths (2 of 44, or 5%, P<.01). Most of the cardiac events occurring in these 3 families were triggered by drugs known to affect ventricular repolarization. CONCLUSIONS: Our data show a wide KVLQT1 allelic heterogeneity among 20 families in which KVLQT1 causes RWS. We describe the first missense mutation in the C-terminal domain of KVLQT1, which is clearly associated with a fruste phenotype, which could be a favoring factor of acquired LQT syndrome.