充液航天器试验的三维数值分析

对自旋充液航天器地面气浮台试验的动力学特性进行了分析和计算。以刚体系统的动量矩定理和流体运动的基本方程为基础，考虑液体晃动、涡旋、重力、离心力及Ｃｏｒｉｏｌｉｓ力等因素的影响，并运用Ｐｆｅｉｆｆｅｒ推广的关于流体均匀涡旋运动的理论，导出了液体晃动的边值问题和流固耦合旋转系统运动的联立微分方程组。运用边界元方法求解了重力场中部分充液偏置贮箱内液体晃动的三维边值问题，并将系统运动的联立微分方程组交换后化为广义特征值问题来求解。从而求得液体晃动的能量耗散率和系统的章动时间常数。     

粗网节块内功率的重构

粗网节块程序如ＮＧＦＭ、ＳＩＭＵＬＡＴＥ等只能给出平均功率。而反应堆设计中更关心的是堆芯内燃料元件的功率分布。本文讨论了获得堆内元件功率分布的重构方法。双二次多项式用于快群中子通量展开，与双曲函数项结合的双二次多项式用于热群中子通量密度展开。研究了２１项和１３项展开法，并与ＣＩＴＡＴＩＯＮ细网格计算进行比较。结果表明，本文中研制的２１项方法程序ＲＥＣＯＮ比ＳＩＭＵＬＡＴＥ－３ＮＥＭＯ程序中所用的１３项方法精确得多，在外围区域更明显。     

弹簧纵波的理论和实验研究

通过对弹簧振动特性的分析,建立了弹簧纵波方程—简谐波方程.得到了弹簧上纵波传播速度与弹簧参量间的理论关系,并从实验上进行了验证.     

铁系元素冠醚配合物的研究——Ⅶ 硝酸铁与4''''-碘苯并-15-冠-5固态配合物的合成及性质

硝酸铁(水合物)与4'-碘苯并-15-冠-5反应形成固态配合物.进行了元素分析及摩尔电导测定,考察了红外光谱、紫外光谱,并作了热重和差热及 X-射线粉末衍射分析.证明该配合物中 Fe(NO_3)_3与配体之比为1:2,为不含结晶水的固态夹心配合物.     

Calcium/calmodulin-dependent protein kinase II increases glutamate and noradrenaline release from synaptosomes

A variety of evidence indicates that calcium-dependent protein phosphorylation modulates the release of neurotransmitter from nerve terminals. For instance, the injection of rat calcium/calmodulin-dependent protein kinase II (Ca2+/CaM-dependent PK II) into the preterminal digit of the squid giant synapse leads to an increase in the release of a so-far unidentified neurotransmitter induced by presynaptic depolarization. But until now, it has not been demonstrated that Ca2+/CaM-dependent PK II can also regulate neurotransmitter release in the vertebrate nervous system. Here we report that the introduction of Ca2+/CaM-dependent PK II, autoactivated by thiophosphorylation, into rat brain synaptosomes (isolated nerve terminals) increases the initial rate of induced release of two neurotransmitters, glutamate and noradrenaline. We also show that introduction of a selective peptidergic inhibitor of Ca2+/CaM-dependent PK II inhibits the initial rate of induced glutamate release. These results support the hypothesis that activation of Ca2+/CaM-dependent PK II in the nerve terminal removes a constraint on neurotransmitter release.     

A binding site for the T-cell co-receptor CD8 on the alpha 3 domain of HLA-A2

Adhesion measurements between CD8 and 48 point mutants of HLA-A2.1 show that the CD8 alpha-chain binds to the alpha 3 domain of HLA-A2.1. Three clusters of alpha 3 residues contribute to the binding, with an exposed, negatively charged loop (residues 223-229) playing a dominant role. CD8 binding correlates with cytotoxic T-cell recognition and sensitivity to inhibition by anti-CD8 antibodies. Impaired alloreactive T-cell recognition of an HLA-A2.1 mutant with reduced affinity for CD8 is not restored by functional CD8 binding sites on an antigenically irrelevant class I molecule. Therefore, complexes of CD8 and the T-cell receptor bound to the same class I major histocompatibility complex molecule seem to be necessary for T-cell activation.     

New Sivapithecus humeri from Pakistan and the relationship of Sivapithecus and Pongo

New humeri of two species of the Miocene hominoid Sivapithecus are described from near Chinji in Pakistan from between approximately 9 and 11 Myr ago. Sivapithecus, a middle and late Miocene hominoid from Turkey and Indo-Pakistan, is overall unlike any living hominoid, although facial-palatal similarities to the extant orangoutan, Pongo, have been used to support a hypothesis of close relationship. Living hominoids have postcranial similarities assumed to be shared derived, among them features of the proximal humerus. However, the new Sivapithecus proximal humeri differ from those of living hominoids, supporting an alternative hypothesis in which Sivapithecus and Pongo are not closely related. It is not clear how to choose between these incompatible hypotheses.     

Genetic mapping of chronic childhood-onset spinal muscular atrophy to chromosome 5q11.2-13.3

SPINAL muscular atrophy (SMA) describes a group of heritable degenerative diseases that selectively affect the alpha-motor neuron. Childhood-onset SMAs rank second in frequency to cystic fibrosis among autosomal recessive disorders, and are the leading cause of heritable infant mortality. Predictions that genetic heterogeneity underlies the differences between types of SMA, together with the aggressive nature of the most-severe infantile form, make linkage analysis of SMA potentially complex. We have now analysed 13 clinically heterogeneous SMA families. We find that 'chronic' childhood-onset SMA (including intermediate SMA or SMA type II, and Kugelberg-Welander or SMA type III) is genetically homogeneous, mapping to chromosomal region 5q11.2-13.3.