对"矛盾"、"对立"范畴的再认识

韩非的“矛盾”富言属于逻辑矛盾。他的“矛盾”思想则是非此即彼、非彼即此,二者必居其一。这种仅仅在对立两极中的思维方法并非完全正确。哲学上的辩证关系,借用“矛盾”、“对立”范畴来表述,也不十分恰当,因为矛与盾不是对立的双方,而辩证关系也应包括对立统一、鼎立统一、多立统一。所以我们必须确立立体矛盾观,即对立面-中介-对立面,或正中反矛盾论,或同异反分析法。     

位移连续变更与极限状态函数的连续生成

基于我国《建筑结构设计统一标准》的极限状态设计原则,结构物不允许出现影响正常使用的外观变形,提出了刚架结构位移连续变更方法·用数值分析与递推公式相结合的方法,实现连续变更结构的变形极限状态函数的连续生成·重分析不必重新形成结构刚度矩阵,不必反复求逆矩阵,使得识别系统主要失效模式的方法得以简化,有效地提高了计算时效,并为刚度可靠性分析提供了新方法·算例验证了方法的正确性及实用性·     

Mutations in Rab3a alter circadian period and homeostatic response to sleep loss in the mouse

Rab3a is the most abundant Rab (ras-associated binding) protein in the brain and has a regulatory role in synaptic vesicle trafficking. Mice with a targeted loss-of-function mutation in Rab3a have defects in Ca(2+)-dependent synaptic transmission: the number of vesicles released in response to an action potential is greater than in wildtype mice, resulting in greater synaptic depression and the abolishment of CA3 mossy-fiber long term potentiation. The effect of these changes on behavior is unknown. In a screen for mouse mutants with abnormal rest-activity and sleep patterns, we identified a semidominant mutation, called earlybird, that shortens the circadian period of locomotor activity. Sequence analysis of Rab3a identified a point mutation in the conserved amino acid (Asp77Gly) within the GTP-binding domain of this protein in earlybird mutants, resulting in significantly reduced levels of Rab3a protein. Phenotypic assessment of earlybird mice and a null allele of Rab3a revealed anomalies in circadian period and sleep homeostasis, providing evidence that Rab3a-mediated synaptic transmission is involved in these behaviors.     

Increased proliferation of B cells and auto-immunity in mice lacking protein kinase Cdelta

Protein kinase C (PKC), which comprises 11 closely related isoforms, has been implicated in a wide variety of cellular processes, such as growth, differentiation, secretion, apoptosis and tumour development. Among the PKC isotypes, PKC-delta is unique in that its overexpression results in inhibition of cell growth. Here we show that mice that lack PKC-delta exhibit expansion of the B-lymphocyte population with the formation of numerous germinal centres in the absence of stimulation. The rate of proliferation in response to stimulation was greater for B cells from PKC-delta-deficient mice than for those from wild-type mice. Adoptive transfer experiments suggested that the hyperproliferation phenotype is B-cell autonomous. Production of interleukin-6 was markedly increased in B cells of PKC-delta-null mice as a result of an increase in the DNA-binding activity of NF-IL6. Furthermore, the PKC-delta-deficient mice contain circulating autoreactive antibodies and display immune-complex-type glomerulonephritis, as well as lymphocyte infiltration in many organs. These results suggest that PKC-delta has an indispensable function in negative regulation of B-cell proliferation, and is particularly important for the establishment of B-cell tolerance.     

基于AutoCAD2000的服装样片自由放码技术

论述了服装样片放码技术原理,以及AutoCAD2000样片的输入、输出与放码之间的关系;阐述了以AutoCAD为平台,采用VisualC 6.0和ObjectARX2000编程开发服装样片自由放码应用程序的设计思想,可提高执行效率,同时具有直接读取数字化仪和屏幕打板并用的优势。设计的应用程序,模仿了“画顺”的设计思想,重点使用了AutoCAD2000基本类库AcDb中的AcDbCurve类、LWPOLYLINE实体和addVertexAt()函数,并基于图形数据库扩展记录进行放码数据存储。给出了已成功运用到实践中的程序框图和源程序代码节选。     

试论原子相互结合的根本原因

在教材和教学中讲到原子相结合的原因时 ,应强调元素的原子倾向于能量最低 ,结构稳定 ,而不能仅用“八隅律”来解释。     

基于PEEC方法的平面电路EMC问题分析

提出了基于部分元等效电路（PEEC）方法求解印制板电路电磁兼容问题的新方法,即将印制板电路的辐射问题分为两步：（1）用部分元等效电路的方法确定印制板导体上的场源（电流）分布;（2）将所有电流元的辐射场进行叠加求总的辐射场。文中对上述方法进行了分析,在此基础上通过一个对称电路和一个非对称电路的辐射场计算,提出了一些工程设计中减小辐射的设计准则。     

明胶-十二烷基硫酸钠复配体系表面活性的研究

对明胶－十二烷基硫酸钠(SDS)复配体系,研究了SDS浓度、明胶浓度、明胶种类及分子量对其表面活性的影响。实验结果表明,随着SDS浓度的增加,体系的表面张力降低,并在其变化曲线中有一“平台”区域,同时体系的乳化力增大,其乳化力顺序为纯SDS溶液>水解皮明胶－SDS>水解骨明胶－SDS>骨明胶－SDS>皮明胶－SDS体系;各体系的起泡力及其稳定性亦随之增大。而明胶浓度的增加导致了各明胶－SDS体系表面张力的增大,且明胶浓度对大分子明胶体系的影响较之小分子明胶体系要大;明胶浓度的增加降低了体系的泡沫稳定性;但明胶浓度及其种类、分子量对体系的乳化力影响不大。     

中共从"革命党"变为执政党的首要理论基石:生产力标准

作为中国共产党第三代领导集体和江泽民总书记在理论上的最重大建树之一,"三个代表"也是把邓小平同志关于生产力标准的理论发挥应用于党建领域的结果,它形成了中共从"革命党"变为执政党的首要理论基石,也是目前中共一切理论的逻辑出发点.本文力求从八个方面说明这个逻辑出发点何以成立.     

Glycine binding primes NMDA receptor internalization

NMDA (N-methyl-d-aspartate) receptors (NMDARs) are a principal subtype of excitatory ligand-gated ion channel with prominent roles in physiological and disease processes in the central nervous system. Recognition that glycine potentiates NMDAR-mediated currents as well as being a requisite co-agonist of the NMDAR subtype of 'glutamate' receptor profoundly changed our understanding of chemical synaptic communication in the central nervous system. The binding of both glycine and glutamate is necessary to cause opening of the NMDAR conductance pore. Although binding of either agonist alone is insufficient to cause current flow through the channel, we report here that stimulation of the glycine site initiates signalling through the NMDAR complex, priming the receptors for clathrin-dependent endocytosis. Glycine binding alone does not cause the receptor to be endocytosed; this requires both glycine and glutamate site activation of NMDARs. The priming effect of glycine is mimicked by the NMDAR glycine site agonist d-serine, and is blocked by competitive glycine site antagonists. Synaptic as well as extrasynaptic NMDARs are primed for internalization by glycine site stimulation. Our results demonstrate transmembrane signal transduction through activating the glycine site of NMDARs, and elucidate a model for modulating cell-cell communication in the central nervous system.