混凝土材料的拓扑学特征及分形特征的评价

在分析比较了拓扑空间、分形空间以及拓扑维数、分形维数的基础上，用拓扑学和分形理论评价了混凝土材料的超细掺合料颗粒特征、粗集料表面特征、混凝土断裂表面和水泥石断裂表面特征以及混凝土孔隙显微结构等特征；研究表明对于超细硅灰、轻集料、卵石以及水泥石断裂表面可以用拓扑学的理论进行抽象化处理，对于超细粉煤灰、碎石、混凝土断裂表面以及孔隙显微结构等几何特征，采用分形理论是十分有效的，其分形维数大于它的拓扑维数，小于它的空间维数，符合相应的自然规律。     

简化的牛顿—拉夫逊潮流计算法

提出了一种利用简化潮流雅可比矩阵来缩短牛顿－拉夫逊潮流计算收敛时间的方法，并通过算例验证了其有效性。     

一种绘制P-V曲线的快速方法

回顾了电压稳定的基本概念 ,提出了一种静态等值的新方法 ;同时提出了利用该方法的静态等值结果 ,快速绘制P V、Q V曲线的方法。数字仿真结果表明 ,该方法与实际潮流计算绘制的P V、Q V曲线在上半支和鼻形点附近均吻合得很好 ,从而验证了该方法的有效性。     

测定Ni-Al合金XRD相组成用纯NiAl3的制备工艺

传统的萃取工艺难以制得高纯度的NiAl3相,将这种NiAl3相与等量α-Al混合后测得的K值有较大的误差,仅适用于测量精度要求不高的情况。为了用XRD准确测定Ni-Al合金的相组成,作用萃取和平衡凝固两种方法对NiAl3相K值测定时使用的纯相制备工艺进行了实验研究。研究证实,熔融合金以小于2K／h的冷却速度缓慢凝固至固相线以下,可得到α-Al与NiAl3两相的质量比接近于1的相组成,用比试样测得的K值经修正后可用于未知试样中NiAl3相的精确测定。     

Megavoltage imaging with low Z targets: implementation and characterization of an investigational system

The poor quality of stereotactic radiotherapy portal images is a limiting factor in precise image registration. To alleviate this problem, a low atomic number (Z) target was implemented on our Siemens MXE linear accelerator. This investigational system was used to assess the performance of various target materials by filming an aluminum contrast object. Beryllium, carbon and conventional target materials were studied. The bremsstrahlung spectra of these materials were simulated using Monte Carlo techniques. These spectra were used to calculate the dependence of narrow beam contrast on phantom thickness for verification of the data measured from film. A Monte Carlo simulation of the beryllium spectrum in a wide beam geometry was used to evaluate the effect of phantom-to-film distance on contrast. Although the same degree of contrast improvement with distance was not realized in practice, the improvement in image quality rivaled that achieved using a scatter reduction grid. A comparison of conventional localization images of the head and neck of an anthropomorphic phantom with images produced with a beryllium or carbon target and a mammography film and screen system supports earlier suggestions that the technique is clinically useful.     

Lack of effect of a selective vasopressin V1A receptor antagonist SR 49,059, on potentiation by vasopressin of adrenoceptor-mediated pressor responses in the rat mesenteric arterial bed

The vasopressin receptor subtype involved in the enhancement by vasopressin of adrenoceptor-mediated vasoconstriction was investigated in rat isolated perfused mesenteric arteries. [Arg8]vasopressin (1-10 nM) dose-dependently increased the perfusion pressure and enhanced the pressor response to the adrenoceptor agonist methoxamine (40 nmol) or electrical stimulation of periarterial nerves (16 Hz), at the concentration of 10 nM of [Arg8]vasopressin up to 4 and 3 fold, respectively. During prolonged exposure (45 min) the direct vasoconstrictor effect of [Arg8]vasopressin (10 nM) rapidly declined whereas the potentiation of methoxamine-induced vasoconstriction was maintained. The selective vasopressin V1A receptor antagonist SR 49,059 (1-3 nM) and the non-selective V1A/B and oxytocin receptor antagonist [deamino-Pen1,Tyr(Me)2,Arg8]vasopressin (15-45 nM) inhibited the direct vasoconstrictor action of [Arg8]vasopressin but had no effect on the enhancement of the pressor response to methoxamine or electrical stimulation. The V1B receptor agonist [deamino-Cys1,beta-(3-pyridyl)-D-Ala2,Arg8]vasopressin (100-1000 nM) and the V2 receptor agonist [deamino-Cys1,D-Arg8]vasopressin (1-10 nM) were devoid of any pressor activity and did not potentiate methoxamine-evoked vasoconstriction. In contrast, [1-triglycyl,Lys8]vasopressin (100 - 1000 nM) potentiated the methoxamine responses without per se inducing vasoconstriction. In arteries precontracted with methoxamine (7.5 microM) pressor responses to [Arg8]vasopressin (3-10 nM) were not inhibited by a dose of SR 49,059 (3 nM) which abolished the peptide's vasoconstrictor effect under control conditions. These data show that the direct vasoconstrictor effect of [Arg8]vasopressin is mediated by V1A receptors while the enhancement of adrenoceptor-mediated pressor responses is insensitive to V1A, V1B, and oxytocin receptor antagonists and is not mimicked by selective agonists of V1B and V2 receptors. In conclusion, an unusual interaction of vasopressin with V1A receptors, or even the existence of a novel receptor subtype, has to be considered.     

Solution structure of the heparin-binding domain of vascular endothelial growth factor

Tricorn protease was previously described as the core enzyme of a modular proteolytic system displaying multicatalytic activity. Here we elucidate the mode of cooperation between Tricorn and its interacting factors, and we identify two additional factors, F2 and F3, closely related aminopeptidases of 89 kDa. In conjunction with these three factors, Tricorn degrades oligopeptides in a sequential manner, yielding free amino acids. We have been able to reconstitute a proteolytic pathway comprising the proteasome, Tricorn, and its interacting factors, F1, F2, and F3, which converts proteins efficiently into amino acids. Therefore, it is quite likely that Tricorn also acts in vivo downstream of the proteasome and, in cooperation with its interacting factors, completes protein catabolic pathways.     

Computerized documentation for a rural nursing intervention project

Complex traits are generally taken to be under the influence of multiple genes, which may interact with each other to confer susceptibility to disease. Statistical methods in current use for localizing such genes essentially work under single-gene models, either implicitly or explicitly. In genomic screens for complex disease genes, some of the marker loci must be in tight linkage with disease susceptibility genes. We developed a general multi-locus approach to identify sets of such marker loci. Our approach focuses on affected sib pair data and employs a nonparametric pattern recognition technique using artificial neural networks. This technique analyzes all markers simultaneously in order to detect patterns of locus interactions. When applied to previously published sib pair data on type I diabetes, our approach finds the same genes as in the published report in addition to some new loci. For a specific two-locus model of inheritance, the power of our approach is higher than that of the currently used analysis standard.