汽轮机特殊结构轴承稳态性能分析和试验研究

本文对一种引进的特殊结构轴承进行了稳态性能研究。首先,建立了该轴承的数学模型,这一模型计及了偏心油楔油槽、瓦块惯性、轴颈轴向偏斜及紊流的影响;其次,采用二阶有限单元,求解了稳态数学模型并根据相似原理进行模拟试验,获得了稳态性能的计算和试验数据。     

性格行为特征与脑电特征间关系的研究

探讨性格行为特征和脑电特征之间的关系.在克莱佩林-内田测试(UK测试)过程中同时测量实验者的脑电,根据UK测试对实验者性格行为的3个特征即启动性、兴奋性和可变性的评价结果,分析对比不同性格行为特征的实验者的脑电数据,通过对比特定频段的脑电能量在UK测试过程中的分布情况,探讨实验者性格行为特征与脑电特征之间的关系.结果表明:实验者代表性格启动性的特征主要与UK测试上下半时开始时脑电β波的能量大小相关;代表性格可变性特征主要表现在UK测试过程中脑电β波能量的波动大小;代表性格兴奋性的特征则表现在脑电α波能量的大小和变化趋势.     

High frequency of homoplasmic mitochondrial DNA mutations in human tumors can be explained without selection

Researchers in several laboratories have reported a high frequency of homoplasmic mitochondrial DNA (mtDNA) mutations in human tumors. This observation has been interpreted to reflect a replicative advantage for mutated mtDNA copies, a growth advantage for a cell containing certain mtDNA mutations, and/or tumorigenic properties of mtDNA mutations. We consider another possibility-that the observed homoplasmy arose entirely by chance in tumor progenitor cells, without any physiological advantage or tumorigenic requirement. Through extensive computer modeling, we demonstrate that there is sufficient opportunity for a tumor progenitor cell to achieve homoplasmy through unbiased mtDNA replication and sorting during cell division. To test our model in vivo, we analyzed mtDNA homoplasmy in healthy human epithelial tissues and discovered that the model correctly predicts the considerable observed frequency of homoplasmic cells. Based on the available data on mitochondrial mutant fractions and cell division kinetics, we show that the predicted frequency of homoplasmy in tumor progenitor cells in the absence of selection is similar to the reported frequency of homoplasmic mutations in tumors. Although a role for other mechanisms is not excluded, random processes are sufficient to explain the incidence of homoplasmic mtDNA mutations in human tumors.     

Failure to confirm NOTCH4 association with schizophrenia in a large population-based sample from Scotland

The NOTCH4 gene was recently reported to be associated with schizophrenia based on TDT analysis of 80 British trios. The strongest evidence for association derived from two microsatellites. We genotyped both loci in a large sample of unrelated Scottish schizophrenics and controls, but failed to replicate the reported association, finding instead that each putative schizophrenia-associated allele had a somewhat lower frequency in schizophrenics than in controls.