复杂离子Tc~(16+)3p~6 3d~9,3p~5 3d~(10),3p~6 3d~8 4p组态原子参数的计算

用多组态自洽场方法,结合我们提出的半经验拟合公式,计算了高离化态类钻Tc~(16+)离子3p~63d~9,3p~53d~(10),3p~63d~84p组态的能级、波长和振子强度,并与实验符合得较好。     

类镍Pd~(19+)离子3d~94s,3d~94p,3d~94d组态原子参数的计算

用Cowan的多组态自洽场方法 ,结合我们提出的半经验公式 ,系统计算了高离化态类Pd19+离子 3d94s,3d94p ,3d9,3d94d组态的能级、波长和振子强度 ,并与实验进行比较     

类钴Y~(13+)离子3p~63d~9,3p~53d~(10),3p~63d~84p组态原子参数的计算

用多组态自治场方法，结合我们提出的半经验拟合公式，系统计算了高离化态类钴Ｙ１３＋离子３ｐ６３ｄ９，３ｐ５３ｄ１０，３ｐ６３ｄ８４ｐ组态的能级、波长和振子强度，并与实验符合得较好。     

RhXV离子4s~24p—4s4p~2、4s~24p—4s~24d和4s4p~2—4p~3跃迁能谱的预言

利用组态相互作用理论和参数外推方法,计算了RhXV离子4s~24p、4s~24d、4s4p~2和4p~3组态的能级以及4s~24p—4s4p~2、4s~24p—4s~24d和4s4p~2—4p~3跃迁的谱线波长和振子强度。4s~24p和4s4p~2组态的能级与已有实验结果符合很好,4s~24d和4p~3组态的能级以及4s~24p—4s~24d和4s4p~2—4p~3跃迁的波长和振子强度纯属理论预言结果。     

类钴Mo15+离子3p63d9,3p53d10,3p63d84p组态原子参数的计算

用多组态自洽场方法，结合我们提出的半经验拟合公式，计算了高离化态类钻Mo^15 离子3p^63d^9,3p^53d^10,3p^63d^34p组态的能级、波长和振子强度，并与实验符合得较好。     

高离化态类钴Ru^17＋离子3p^63d^9,3p^53d^10,3p^63d^84p光谱的计算

用多组态自洽场方法，结合我们提出的半经验拟合公式，计算了高离化态类钴Ru^17 离子3p^63d^9,3p^53d^10,3p^63d^84p组态的能级、波长和振子强度，并与实验符合得较好。     

类氖ArIX离子2s2p~63d和2s~22p~54f能级结构的组态相互作用计算

利用文献[7～11]给出的能谱观测数据,外推得到了AtⅨ离子2s2p~63d和2s~22p~54f组态的各径向积分参数。在组态相互作用理论下,用这些参数计算了ArⅨ离子各组态的能级及波函数分量,结果与有关实验数据符合得很好。     

高离化态类钴等电子序列原子参数的大规模计算

对Cowan程序包计算联接方式进行改进 ,从而实现大规模高离化态原子参数的计算 ,计算了高离化态类钴等电子序列 3p63d9,3p53d10 ,3p63d84p组态的能级、波长和振子强度 ,并与实验符合得较好     

Ce~(+48)类氖离子2p~5、3s、3p、3d能级能量和波长的相对论MCDF计算

本文用相对论多重组态Dirac—Fock方法得到了Ce~(+48)类氛离子的2p~5、3s、3p、3d组态的精细结构能级能量和跃迁波长值。     

类镍Mo14+离子3d94s,3d94p,3d94d组态原子参数的计算

用多组态自洽场方法 ,结合我们提出的半经验拟合公式 ,计算了高离化态类镍Mo14 + 离子 3d94s,3d94p ,3d94d组态的能级、波长和振子强度 ,并与实验符合得较好     

3p^3阶群之构造

在有限群理论中,确定n阶群的构造是一个分类问题。本文试图确定3p~3(p是奇素数,且p≠3)阶群的构造,即证明下面的定理: 令p是一个素数,则3p~3(p≠3)阶群有 (1)7种类型,当p≠1(mod3)。 (2)19种类型,当p=1(mod3)。     

p63在胃癌组织中的表达

目的:探讨抑癌基因p53蛋白家族成员p63蛋白在胃癌及癌旁组织中的表达情况.方法:回顾性分析41例胃癌及37例癌旁组织,利用组织微阵列技术,构建88点组织阵列,并采用免疫组织化学技术S-P法检测该阵列中p63蛋白在胃癌及其癌旁组织中表达情况.结果:①p63蛋白定位于细胞核,呈弥漫分布的棕黄色颗粒;②胃癌组织中,p63蛋白表达于核大间变细胞中;p63蛋白在高分化型胃癌中阳性表达率为5.9%,在低分化型胃癌中的阳性表达率为41.7%,两者比较差异有统计学意义(P<0.05);③p63蛋白在胃癌癌旁组织中无表达,在胃癌中的阳性表达率为24.4%,两者比较差异有统计学意义(P<0.05).结论:①p63蛋白的高表达可能参与了胃癌的发生;②p63与胃癌的分化程度有关,并可能参与了胃癌细胞的分化.     

二次域Q_p(d~(1/2))上的复值乘法特征

以复值乘法特征为象征定义了一对Riesz变换 ,研究了经典理论在p adic场合的对应 .这是在二次域上构造共轭温度系的基础 ,也是早先一维理论的继续 .作为Riesz变换的一个应用 ,对Qp(d)上的一类分布建立了微商理论 .     

三角晶场中3d^3离子精细光谱结构和局域结构的关系

目的研究三角晶场中3d3离子光谱精细结构和晶体局域结构之间的关系。方法利用自旋哈密顿理论,采用对角化能量矩阵的方法。结果计算了YAG：Cr3＋晶体的光谱精细结构和键角之间的关系。结论三角晶场中3d3离子基态能级分裂对晶格局域结构变化非常敏感,而其它激发态能级对晶格局域结构不很敏感。     

p63 protects the female germ line during meiotic arrest

Meiosis in the female germ line of mammals is distinguished by a prolonged arrest in prophase of meiosis I between homologous chromosome recombination and ovulation. How DNA damage is detected in these arrested oocytes is poorly understood, but it is variably thought to involve p53, a central tumour suppressor in mammals. While the function of p53 in monitoring the genome of somatic cells is clear, a consensus for the importance of p53 for germ line integrity has yet to emerge. Here we show that the p53 homologue p63 (refs 5, 6), and specifically the TAp63 isoform, is constitutively expressed in female germ cells during meiotic arrest and is essential in a process of DNA damage-induced oocyte death not involving p53. We also show that DNA damage induces both the phosphorylation of p63 and its binding to p53 cognate DNA sites and that these events are linked to oocyte death. Our data support a model whereby p63 is the primordial member of the p53 family and acts in a conserved process of monitoring the integrity of the female germ line, whereas the functions of p53 are restricted to vertebrate somatic cells for tumour suppression. These findings have implications for understanding female germ line fidelity, the regulation of fertility and the evolution of tumour suppressor mechanisms.     

具有4p~3阶自同构群的有限幂零群

通过有限群的自同构群的阶来研究该有限群,得出满足一些给定条件的有限群G的结构.文中假设G幂零时给出满足方程|Aut(G)|=4p~3(P为奇素数)的G的构造。     

p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development

The p63 gene, a homologue of the tumour-suppressor p53, is highly expressed in the basal or progenitor layers of many epithelial tissues. Here we report that mice homozygous for a disrupted p63 gene have major defects in their limb, craniofacial and epithelial development. p63 is expressed in the ectodermal surfaces of the limb buds, branchial arches and epidermal appendages, which are all sites of reciprocal signalling that direct morphogenetic patterning of the underlying mesoderm. The limb truncations are due to a failure to maintain the apical ectodermal ridge, a stratified epithelium, essential for limb development. The embryonic epidermis of p63-/- mice undergoes an unusual process of non-regenerative differentiation, culminating in a striking absence of all squamous epithelia and their derivatives, including mammary, lacrymal and salivary glands. Taken together, our results indicate that p63 is critical for maintaining the progenitor-cell populations that are necessary to sustain epithelial development and morphogenesis.