ZnWo_4:C_r~(3+)的吸收光谱研究

本文通过对ZnWo_4:Cr~(3+)晶体的光学吸收谱的观测资料的分析,假定C_r~(3+)杂质的有效晶场为八面体结构变形后的D_4~※晶场.采用O_h点群表象准对角型简化强场方案,导出了d~3-D_4~※强场能量矩阵.首次计算了ZnWo_4:C_r~(3+)的自旋允许谱精细结构.理论计算结果与实验吻合较好.     

Tetanus and botulinum-B neurotoxins block neurotransmitter release by proteolytic cleavage of synaptobrevin.

Clostridial neurotoxins, including tetanus toxin and the seven serotypes of botulinum toxin (A-G), are produced as single chains and cleaved to generate toxins with two chains joined by a single disulphide bond (Fig. 1). The heavy chain (M(r) 100,000 (100K)) is responsible for specific binding to neuronal cells and cell penetration of the light chain (50K), which blocks neurotransmitter release. Several lines of evidence have recently suggested that clostridial neurotoxins could be zinc endopeptidases. Here we show that tetanus and botulinum toxins serotype B are zinc endopeptidases, the activation of which requires reduction of the interchain disulphide bond. The protease activity is localized on the light chain and is specific for synaptobrevin, an integral membrane protein of small synaptic vesicles. The rat synaptobrevin-2 isoform is cleaved by both neurotoxins at the same single site, the peptide bond Gln 76-Phe 77, but the isoform synaptobrevin-1, which has a valine at the corresponding position, is not cleaved. The blocking of neurotransmitter release of Aplysia neurons injected with tetanus toxin or botulinum toxins serotype B is substantially delayed by peptides containing the synaptobrevin-2 cleavage site. These results indicate that tetanus and botulinum B neurotoxins block neurotransmitter release by cleaving synaptobrevin-2, a protein that, on the basis of our results, seems to play a key part in neurotransmitter release.     

影响南方红豆杉种子萌发因素的研究

研究了南方红豆杉种胚的发育状况、外种皮的结构以及种子各部分抑制物质相对活性．结果表明种子形态成熟时,种胚基本成熟,离体培养可以生长成苗;外种皮的不透气性和胚乳中的某些抑制物质可能是抑制南方红豆杉种子萌发的因素,但ＡＢＡ不是萌发的抑制因素．     

Experimental detection of alpha-particles from the radioactive decay of natural bismuth

The only naturally occurring isotope of bismuth, 209Bi, is commonly regarded as the heaviest stable isotope. But like most other heavy nuclei abundant in nature and characterized by an exceptionally long lifetime, it is metastable with respect to alpha-decay. However, the decay usually evades observation because the nuclear structure of 209Bi gives rise to an extremely low decay probability and, moreover, generates low-energy alpha-particles difficult to detect. Indeed, dedicated experiments attempting to record the alpha-decay of 209Bi in nuclear emulsions failed. However, scintillating bolometers operated at temperatures below 100 mK offer improved detection efficiency and sensitivity, whereas a broad palette of targets could be available. Here we report the successful use of this method for the unambiguous detection of 209Bi alpha-decay in bismuth germanate detectors cooled to 20 mK. We measure an energy release of 3,137 +/- 1 (statistical) +/- 2 (systematic) keV and a half-life of (1.9 +/- 0.2) x 10(19) yr, which are in agreement with expected values.     

SCO UNIX系统下Oracle数据库的自动备份

论述了数据库系统备份的重要性，井详细讨论了SCO UNIX下0racle数据库系统自动备份的几种实现方法。     

Protection of telomeres through independent control of ATM and ATR by TRF2 and POT1

When telomeres are rendered dysfunctional through replicative attrition of the telomeric DNA or by inhibition of shelterin, cells show the hallmarks of ataxia telangiectasia mutated (ATM) kinase signalling. In addition, dysfunctional telomeres might induce an ATM-independent pathway, such as ataxia telangiectasia and Rad3-related (ATR) kinase signalling, as indicated by the phosphorylation of the ATR target CHK1 in senescent cells and the response of ATM-deficient cells to telomere dysfunction. However, because telomere attrition is accompanied by secondary DNA damage, it has remained unclear whether there is an ATM-independent pathway for the detection of damaged telomeres. Here we show that damaged mammalian telomeres can activate both ATM and ATR and address the mechanism by which the shelterin complex represses these two important DNA damage signalling pathways. We analysed the telomere damage response on depletion of either or both of the shelterin proteins telomeric repeat binding factor 2 (TRF2) and protection of telomeres 1 (POT1) from cells lacking ATM and/or ATR kinase signalling. The data indicate that TRF2 and POT1 act independently to repress these two DNA damage response pathways. TRF2 represses ATM, whereas POT1 prevents activation of ATR. Unexpectedly, we found that either ATM or ATR signalling is required for efficient non-homologous end-joining of dysfunctional telomeres. The results reveal how mammalian telomeres use multiple mechanisms to avoid DNA damage surveillance and provide an explanation for the induction of replicative senescence and genome instability by shortened telomeres.     

原子及轨道电亲性：新能量标度及其相关分析

应用原子的平均电离能来近似度量电亲性或电负性。所提出的电亲性新标度XLL与总电离能U除以原子价壳层电子数目N即平均电离能B成正比，进一步地从原子总电离能T或平均电离能B可确定其价与杂化轨道电亲性。它们虽支接从基态自由原子计算得到，却与从热化学数据得到的鲍林电负性颇为一致，因而计算上避免了其经验性，也可方便地计算惰性元素的电亲性，应用上同样具有广适性，并已显示出其优越性和独到处。     

Abelson murine leukaemia virus transformation involves loss of epidermal growth factor-binding sites

Malignant transformation by mammalian RNA sarcoma viruses has previously been shown to involve a reduction in receptor sites for a well characterized 6,000-molecular weight (MW) growth-promoting substance, designated epidermal growth factor (EGF). Although Abelson murine leukaemia virus (AbLV) resembles sarcoma viruses in its ability to transform embryo fibroblasts in cell culture, AbLV induces a rapid B-cell lymphoid leukaemia rather than fibrosarcomas in vivo. The major translational product of AbLV is a highly phosphorylated polyprotein of MW 120,000 which exhibits an associated tyrosine-specific protein kinase activity and probable transforming function. We show here that AbLV transformation resembles transformation by RNA sarcoma viruses with respect to the abolition of EGF-binding sites. EGF binding is restored to control levels following loss of polyprotein expression in morphological revertants of AbLV-transformed clones and remains uninfluenced in cell lines infected with transformation-defective (td) AbLV mutants encoding polyproteins deficient in protein kinase activity. These findings indicate that AbLV transformation involves a polyprotein-associated, tyrosine-specific protein kinase activity which mediates its effect through a mechanism resulting directly or indirectly in the abolition of EGF-binding sites.     

线虫动物门、腹毛动物门及轮虫动物门间的系统学研究

用支序分析方法对线虫动物门、腹毛动物门和轮虫动物门三者之间的系统学进行了分析，结论是三者为一单系群，其中腹毛动物门和轮虫动物门为一对姐妹群，线虫动物门则是三者的共同祖先较早地分出的另一支。由此我们认为，应将这三者合并为一新门合胞体动物门（Syncytia)，原来各门分别降为线虫纲、腹毛纲和轮虫纲；原腔动物门这一分类阶元应予废弃。     

Real-space imaging of an orbital Kondo resonance on the Cr(001) surface

The Kondo effect is usually connected with the interaction between a localized spin moment and itinerant electrons. This interaction leads to the formation of a narrow resonance at the Fermi level, which is called the Abrikosov-Suhl or Kondo resonance. Scanning tunnelling microscopy is an ideal technique for real-space investigations of complicated electronic structures and many-body phenomena, such as the formation of the Kondo resonance or d-wave pairing in high-T(c) superconductors. Theory has predicted that similar, Kondo-like many-electron resonances are possible for scattering centres with orbital instead of spin degrees of freedom--the quadruple momenta in uranium-based compounds or two-level systems in metallic glasses are examples of such 'pseudo-Kondo' scattering centres. Here we present evidence for the orbital Kondo resonance on a transition-metal surface. Investigations of an atomically clean Cr(001) surface at low temperature using scanning tunnelling microscopy reveal a very narrow resonance at 26 meV above the Fermi level, and enable us to visualize the orbital character of the corresponding state. The experimental data, together with many-body calculations, demonstrate that the observed resonance is an orbital Kondo resonance formed by two degenerate d(xz), d(yz) surface states.