饱和一元醇物理化学性质的定量探讨

拓扑指数ｘｚ、路径数ｐ１和ｓ１、ｓ２是表征饱和一元醇分子大小、支化度、形状和羟基位置等结构特征的重要参量．本文提出计算饱和一元醇物理化学性质Ｐ的定量公式为：Ｐ＝ａ０＋ａ１ｐ１＋ａ２ｘ２／３ｚ＋ａ３ｓ１＋ａ４ｓ２式中ａ０、ａ１、ａ２、ａ３和ａ４为系数,对于某一物理化学性质为一定值．本文预测了含１０个碳原子以内的饱和一元醇的原子化热ΔＨａ、气相生成热ΔＨｇｔ、摩尔折射Ｒｍ、蒸发热ΔＨｖ、摩尔磁化率ＸＭ、液体密度Ｄ２０４、沸点Ｂ．Ｐ．、保留体积ｌｏｇＶｇ和分配系数ｌｏｇＰ等９项物理化学性质．     

脂肪醚物理化学性质的定量探讨

拓扑指数ｘｚ、路径数ｐ１和ｓ１、ｓ２等参量,是表征脂肪醚分子大小、支化度、形状和氧原子位置等结构特征的重要参量．本文提出计算脂肪醚物理化学性质Ｐ的定量公式Ｐ＝ａ０＋ａ１ｐ１＋ａ２ｘ２／３ｚ＋ａ３ｓ１＋ａ４ｓ２,预测了１０个碳原子以内的脂肪醚的Ｒｍ（ｃｍ３·ｍｏｌ－１）、Ｂ．Ｐ．（℃）、ｍ．ｐ．（℃）、ΔＨａ（ｋＪ·ｍｏｌ－１）、Ｄ２０４（ｇ·ｃｍ－３）和ｌｏｇｓ等６项物理化学性质     

La1+zBa2-zCu3Oy相的形成、固溶度及La对Ba的替代

对Ｌａ１＋ｚＢａ２－ｚＣｕ３Ｏｙ相的形成,固溶度和Ｌａ对Ｂａ的替代进行了系统研究,以期获得制备具有更高Ｔｃ的超导体的最佳条件。表明Ｌａ１＋ｚＢａ２－ｚＣｕ３Ｏｙ在空气中固溶度为０．２０－０．７０,Ｎ２中为０。在空气中合成Ｌａ１＋ｚＢａ２－ｚＣｕ３Ｏｙ时,Ｌａ能替代Ｂａ,但Ｂａ并不能替代Ｌａ,空气和Ｏ２有利于Ｌａ对Ｂａ的替代,但当在Ｎ２中合成Ｌａ１＋ｚＢａ２－ｚＣｕ３Ｏｙ时,Ｌａ对Ｂａ的替代受到抑制     

CaO—BaO—SiO2—TiO2系统溶胶涂液的制备和凝胶化过程

采用溶胶－凝胶工艺制备０．１ＣａＯ－０．１ＢａＯ－ＸＳｉＯ２－（０．８－Ｘ）ＴｉＯ２和ＹＣａＯ－（０．３－Ｙ）ＢａＯ－０．３ＳｉＯ２－０．４ＴｉＯ２（Ｘ＝０～０．５,Ｙ＝０～０．３摩尔分数）两组四元系统浸涂液。根据粘度变化和凝胶时间研究了组成、水和醋酸加入量对溶胶涂液稳定性的影响,得出了配制稳定期长的浸涂液的配比。利用红外光谱和Ｘ－射线衍射（ＸＲＤ）探讨溶胶形成过程和凝胶向玻璃态转变过程中的结构变化。结果表明：溶液中ＣＨ３ＣＯＯ－取代醇盐中的ＯＲ基团分别与Ｓｉ４＋和Ｔｉ４＋配位,形成反应活性不同于原醇盐的新的前驱体醇盐;经５００°Ｃ热处理后凝胶的红外光谱中出现由Ｔｉ—Ｏ—Ｓｉ伸缩振动所引起的吸收带。ＸＲＤ谱证实６０°Ｃ干凝胶中有醋酸盐晶体,５００°Ｃ热处理后,这种晶体消失,凝胶中生成Ｂａ２ＴｉＯ４晶相。     

兰道定理中的一个新上界

对在单位园盘Ｄ中正则的函数ｆ（ｚ）＝ａ０＋ａ１ｚ＋…,且ｆ（ｚ）≠０,１,证明了｜ａ１｜≤２｜ａ２｜｜ｌｏｇ｜ａ０｜｜＋Ａ－Ｍ｜ｌｏｇ｜ａ０｜｜＋Ａ－４πＫ１１＋｜ａ０｜Ｋ｜ａ０｜１＋｜ａ０｜［］｛｝,其中Ａ是海曼常数,Ｍ是绝对常数．     

荞麦组织培养中的植株再生

用荞麦无菌苗的幼茎和幼叶作外植体分别接种在ＭＳ补加不同激素组合的培养基上培养获得再生植株。实验结果表明,适宜诱导愈伤组织的激素组合为２．４－Ｄ４．０ｍｇ／Ｌ＋ＫＴ０．２ｍｇ／Ｌ,适宜愈伤组织生长的激素组合为２．４－Ｄ１．０ｍｇ／Ｌ＋ＫＴ１．０ｍｇ／Ｌ。诱导芽的较适宜的组合为６－ＢＡ３．０ｍｇ／Ｌ＋ＩＡＡ０．１ｍｇ／Ｌ,不定芽接种到含ＭＳ＋ＩＢＡ２．０ｍｇ／Ｌ＋ＫＴ０．１ｍｇ／Ｌ的ＭＳ培养基上就能生     

▽n(G)={1}的有限群

设Ｇ满足标题的条件。１、若ｎ＝４,则下述结论之一成立;;（１）Ｇ可解;;（２）Ｇ≌Ａ~５;;（３）Ｇ≌ＰＳＬ（２,１３）;;（４）Ｇ≌ＰＳＬ（２,ｐ）,满足ｐ＝４ｐ１＋１＝６ｐ２－１,这里ｐ１≥４３,ｐ２≥２９;;（５）Ｇ≌ＰＳＬ（２,ｐ）,满足ｐ＝６ｐ１＋１＝４ｐ２—１,这里ｐ１≥７,ｐ２≥１１;;２、若ｎ＝５且Ｇ与ＰＳＬ（２,ｐ）无关,则下述结论之一成立：（１）Ｇ可解;;（２）Ｇ≌ＰＳＬ（２,２~３）;;（３）Ｇ≌ＰＳＬ（２,３~３）;;３、设３　π（Ｇ）,８≤ｎ≤２ｐ＋１．若对任ｑ＜ｐ,Ｇ与Ｓｚ（２~ｑ）无关,则Ｇ可解。     

钴与噻唑偶氮间苯二胺类试剂配合物溶液平衡的研究

以２－（４,５－二甲基－２－噻唑偶氮）－５－二甲氨基苯胺为代表,应用分光光度法研究了噻唑偶氮间苯二胺类试剂与钴配合物的溶液平衡．结果表明,该配合物在溶液中存在着四种质子化型体ＣｏＲ２Ｈ３＋３,ＣｏＲ２Ｈ２＋２,ＣｏＲ２Ｈ＋和ＣｏＲ２,它们之间存在着三级离解平衡,测定其离解常数分别为ｐＫａ１＝－４．６４,ｐＫａ２＝０．６８,ｐＫａ３＝４．６２．其中ＣｏＲ２Ｈ２＋２具有较高的摩尔吸光系数,且能在较宽的酸度范围内存在,是适宜于分析应用的型体     

2′－6′－二乙胺基萤烷的合成及晶体结构研究

利用Ｘ－射线衍射分析测定了标题化合物的晶体结构．Ｃ２４Ｈ２０ＮＯ３Ｃｌ属单斜晶系，空间群Ｐ２１／ｎ，Ｍｒ＝４０５．８８，ａ＝１１．６２５（３），ｂ＝１３．８４４（３），ｃ＝２２．６４３（４）×１０－１０ｍ，β＝９４．８０（２）°，Ｖ＝２０１５．（１）×１０－３０ｍ３，Ｚ＝４，Ｆ（０００）＝８４８，Ｄｃ＝１．３３ｇ／ｃｍ３，Ｒ＝０．０８４和Ｒｗ＝０．０９６．含有氧的六圆环为半椅式构象，五圆环和它相邻的苯环几乎共面．Ｃ（１４）与Ｏ（１），Ｃ（２１）与Ｏ（１）为典型的Ｓｐ２－Ｓｐ２键，使相邻两个苯环之间产生了共轭     

不同酸掺杂对聚苯胺导电性能的影响

采用元素分析、Ｘ射线光电子谱（ＸＰＳ）以及直流电导率σｄｃ（Ｔ）与温度关系等方法对三种聚苯胺ＰＡＮＩ－ＨＣｌ,ＰＡＮＩ－Ｈ２ＳＯ４和ＰＡＮＩ－Ｈ３ＰＯ４进行了研究．在Ｃｌ（２ｐ）谱中,可以分辨四个二重态的自旋轨道裂分偶极子Ｃｌ（２ｐ１／２）和Ｃｌ（２ｐ３／２）．Ｓ（２ｐ）－ｃｏｒｅ－ｌｅｖｅｌ谱显示了二重态自旋轨道的裂分偶极子Ｓ（２ｐ１／２）和Ｓ（２ｐ３／２）,而Ｐ（２ｐ）－ｃｏｒｅ－ｌｅｖｅｌ谱仅在结合能为１３４．０３ｅＶ时显示单一的峰值．室温时ＰＡＮＩ－ＨＣｌ和ＰＡＮＩ－Ｈ２ＳＯ４的σｄｃ比ＰＡＮＩ－Ｈ３ＰＯ４的σｄｃ高数倍．ＰＡＮＩ样品的导电性与温度的关系表明它们是半导体,而且符合准一维的变程跳跃（Ｑ１Ｄ－ＶＲＨ）模型     

Synthesis and Fluorescence Spectra of Triazolylcoumarin Fluorescent Dyes

Much attention is devoted to fluorescent dyes especially those with potential in versatile applications. Reactions under "click" conditions between nonfluorescent 3 - azidocoumarins and terminal alkynes produced 3 -(1, 2, 3- triazol- 1 - yl)cournarins, a novel type of fluorescent dyes with intense fluorescence. The structures of the new coumarins were characterized by 1H NMR, MS, and IR spectra. Fluorescence spectra measurement demonstrated excellent fluorescence performance of the triazolylcoumarins and this click reaction is a promising candidate for bioconjugation and bioimaging applications since both azide and alkynes are quite inert to biological systems.     

两类具有失约现象的预约系统的性能比较

给出了关于具有失约现象的预约排队模型S(2,)/M/1和S(3,p)/M/1的系统性能的进一步讨论,应用仿真方法对两个模型进行深入探讨并给出详尽的数值性能分析以及两个模型的比对效果.同时,分别比较了两类临界值并量化了失约现象对顾客平均等待时间和系统损耗的影响.     

原子电四极矩E2光谱跃迁几率的算符形式和多电子效应研究

利用多组态Dinac-Fock广义扩展平均能级（MCDF－EAL）方法系统地计算了铍LiI3d→2s,3p→2p,碳CIII2s3d1D2→2s21so,2p21S0,钙C I功43枯1D2→4s21So,钛TiIII3d23p→323F,3d4s3D→3d23F,铜CuII 3d94s1D2→3d10 1S0,锌ZnI 4s4d1D2→4s2 1s0和铯CsI 5d→6s等电四极矩E2光谱跃迁的能级间隔,跃迁几率和振子强度,计算中考虑了重要的核的有限体积效应,Breit修正和QED修正,所得结果和最近的实验数据及其它理论计算进行了比较。     

S4+离子3s2-3s3p和S5+离子3s-3p电子碰撞激发截面

利用全相对论扭曲波电子碰撞激发计算程序REIE06,系统计算了阈值附近不同入射电子能量下S~(4+)离子基态3s~(21)S_0到激发态3s3p ~3P_(0,1,2)~1P_1和S~(5+)离子基态3s ~2S_(1/2)到激发态3p ~2P_(1/2)~2P_(2/3)精细结构能级的碰撞截面,在两种关联模型下,分析了组态相互作用对碰撞截面的影响.目前的计算结果与Wallbank实验值~([14])相比,得到很好的一致性.     

具有给定共轭类长的有限非可解群

设G是有限非可解群且Z(G)=1.如果G的非中心共轭类长为pq,p r2,qr2,那么G同构于5次交错群A5;如果G的非中心共轭类长为15,5p,15p,5p2,3p3,那么G同构于5次对称群S5.     

Identification of a G1-type cyclin puc1+ in the fission yeast Schizosaccharomyces pombe

In rapidly growing cells of the budding yeast Saccharomyces cerevisiae, the cell cycle is regulated chiefly at Start, just before the G1-S boundary, whereas in the fission yeast Schizosaccharomyces pombe, the cycle is predominantly regulated at G2-M. Both control points are present in both yeasts, and both require the p34cdc2 protein kinase. At G2-M, p34cdc2 kinase activity in S. pombe requires a B-type cyclin in a complex with p34cdc2; this complex is the same as MPF (maturation promoting factor). The p34cdc2 activity at the G1-S transition in S. cerevisiae may be regulated by a similar cyclin complex, using one of the products of a new class of cyclin genes (CLN1, CLN2 and WHI1 (DAF1/CLN3)). At least one is required for progression through the G1-S phase, and deletion of all three leads to G1 arrest. WHI1 was isolated as a dominant allele causing budding yeast cells to divide at a reduced size and was later independently identified as DAF1, a dominant allele of which rendered the cells refractory to the G1-arrest induced by the mating pheromone alpha-factor. The dominant alleles are truncations thought to yield proteins of increased stability, and the cells are accelerated through G1. Without WHI1 function, the cells are hypersensitive to alpha-factor, enlarged and delayed in G1. Heretofore, this G1-class of cyclins has not been identified in other organisms. We have isolated a G1-type cyclin gene called puc1+ from S. pombe, using a functional assay in S. cerevisiae. Expression of puc1+ in S. pombe indicates that it has a cyclin-like role in the fission yeast distinct from the role of the B-type mitotic cyclin.     

FeS2-H2O系综合平衡电势-pH图及其应用

根据综合平衡原理,建立和讨论了一种新型的ＦｅＳ２－Ｈ２Ｏ系电势－ｐＨ图及该体系中溶液态物质的浓度分布函数单质硫只有较小的稳定区且依赖于溶液中含硫物种总浓度Ｃｔ（Ｓ）和Ｈ２Ｓ气体的分压大小,当Ｃｔ（Ｓ）固定时,分压小于某临界值后单质硫的稳定区将消失Ｆｅ２Ｏ３（Ｓ）和ＦｅＳ２（Ｓ）的稳定区均很大,Ｆｅ２Ｏ３的稳定性与溶液中含铁总浓度Ｃｔ（Ｆｅ）有关,而ＦｅＳ２的稳定性与Ｃｔ（Ｓ）、Ｃｔ（Ｆｅ）及Ｈ２Ｓ气体的分压均有关图３,表３,参４     

D8p的连通3度Cayley有向图的正规性

称有限群G的Cayley（有向）图X是正规的,如果G的右正则表示R（G）正规于图X的全自同构群Aut（X）.该文主要研究8p阶二面体群G∶=D8p=〈a,b a4p=b2=1,b-1ab=a-1〉的连通3度Cayley有向图X∶=Cay（G,S）的正规性.并证明：（1）若p=2时,Cayley（有向）图X不正规当且仅当S~{b,a,a5}和S~{b,ba,bak}（k=3,4,5,6）.（2）若p为奇素数,Cayley（有向）图X不正规当且仅当S~{b,a,a2p＋1}和S~{b,ba,bak}（k=2p,2p＋1）.     

Chk1 prevents abnormal mitosis of S-phase HeLa cells containing DNA damage

To explore effects of DNA damage on cell-cycle progression in p53-deficient tumor cells, synchronized HeLa cells at G1, S and G2/M phases were treated with methyl methanesulfnate （MMS）. The results showed that the MMS treatment resulted in the cell-cycle arrest or delay in all 3 phases, while the S-phase cells were the most sensitive to MMS. Further studies demonstrated that ATM-Chk2 and p38 MAPK signaling pathways were activated in all 3 phases when the cells were treated with MMS; whereas Chk1 was activated only in S phase under the drug treatment, indicating that Chk1 specifically participated in S-phase checkpoints. To analyze the role of Chk1 in S-phase checkpoints, we administered a specific Chk1 inhibitor, UCN-01, to the S-phase cells. The results showed that the S-phase cells treated with MMS＋UCN-01 could enter aberrant mitosis without finishing DNA replication, indicating that Chk1 mainly functions in the DNA damage checkpoint rather than in the replication checkpoint. In addition, MMS treatment alone inhibited the accumulation of cyclin B1, a key component of M-phase CDK-cyclin complex, in the S-phase cells, whereas the inhibition of Chk1 activation resulted in the accumulation of cyclin B1 in the MMS-treated S-phase cells. This observation further supports the view that DNA-damaged S-phase cells enter abnormal mitosis when Chk1 activation is inhibited. Our results demonstrate that Chk1 is a specific kinase that plays an important role in the MMS-induced S-phase DNA damage checkpoint. As p53 is not involved in this process, Chk1 may be a potential target for p53-deficient tumor therapy.