模型校正在电子设备结构中的应用

为预测构件动态行为，用动力学有限元校正法建立某一航天用印刷电路板的动力学模型，用物理参数局部校正法导出物理意义明确的校正模型，用分步实验校正法提高模型的可靠度。结果表明，校正模型具有更大的适应性和可靠性。     

碘放射性核素在土壤－蔬菜系统中的转移系数

人工引入核电站排放的关键核素￣（１３１）Ｉ，采用γ能谱和总β计数两种方法确定核素在土壤－蔬菜系统中的转移系数。测得核素不同迁移时间、不同生长期的蔬菜、以及土壤中不同核素浓度等各种情况下的转移系数。给出转移系数的频数分布及变异性。γ能谱法测得的￣（１３１）Ｉ在广东土壤－蔬菜系统中转移系数的观察值范围为１．２８×１０￣（－２）～２．１０×１０￣（－１），几何平均值为５．０５×１０￣（－２），几何标准偏差为１．９６．实验中观察到蔬菜棵株大小、不同气候条件等因素对转移系数的影响。     

五峰垃圾填埋场渗滤液污染特征及处理系统

系统分析了五峰垃圾填埋场渗滤液中ＣＯＤ，ＢＯＤ＿５的季节变化特征，并对该填埋场的污水处理系统进行了研究和评价。     

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.