硼对12Ni3CrMoV高强度钢焊接接头冷裂敏感性的影响

低碳调质高强度钢中添加硼对焊接冷裂敏感性的影响较少有人研究,并存在两种不同意见.本文对含硼量分别为0.005%,0.0014%,0.0028%,0.0035%的12Ni3CrMoV调质高强度钢焊接冷裂敏感性进行研究.试验结果表明:1.插销试验临界应力:含硼钢比无硼钢(含硼0.0005%)高;含硼钢中,临界应力按含硼量0.0014%,0.0028%,0.0035%的顺序递减.2.扫描电镜断口分析:无硼钢有沿晶断裂区、准介理断裂区和韧窝断裂区.含硼钢没有沿晶断裂区,只有准介理断裂区和韧窝断裂区.3.焊条未烘干时,无硼和含硼钢的插销临界应力都降低,无硼钢沿晶断裂区扩大,含硼钢仍无沿晶断裂区.4.硼在HAZ粗晶区中沿奥氏体晶界形成偏聚带,硼相主要沿奥氏体晶界呈不连续点状析出.含硼愈多,沿奥氏体晶界偏聚和硼相析出也愈多.5.C.D.Beachem提出的断口形貌发展过程示意图可以解释无硼钢断裂,不能完全解释含硼钢断裂过程.6.裂纹敏感性成分Pcm值表达式中,硼项系数为" 5"值得商榷.就本文钢材而言,硼项函数应为"负变数".本文对含硼钢延迟裂纹机理作了探讨.     

Structure of astacin and implications for activation of astacins and zinc-ligation of collagenases.

Astacin, a digestive zinc-endopeptidase from the crayfish Astacus astacus L., is the prototype for the 'astacin family', which includes mammalian metallo-endopeptidases and developmentally regulated proteins of man, fruitfly, frog and sea urchin. Here we report the X-ray crystal structure of astacin, which reveals a deep active-site cleft, with the zinc at its bottom ligated by three histidines, a water molecule and a more remote tyrosine. The third histidine (His 102) forms part of a consensus sequence, shared not only by the members of the astacin family, but also by otherwise sequentially unrelated proteinases, such as vertebrate collagenases. It may therefore represent the elusive 'third' zinc ligand in these enzymes. The amino terminus of astacin is buried forming an internal salt-bridge with Glu 103, adjacent to His 102. Astacin pro-forms extended at the N terminus, as observed for some 'latent' mammalian astacin homologues, did not exhibit this 'active' conformation, indicating an activation mechanism reminiscent of trypsin-like serine proteinases.     

血液的光学性质研究

本文用辐射输运理论方法去计算红细胞的光学特征量,并在此基础上提出检测血细胞数密度的理论实验方案,其结果与传统的方法一致。本文为开发一种血球数自动检测仪提供了理论基础和仪器结构原型。     

巷道底板上锚杆布置形式对预防底鼓效果的模拟研究

本文采用三个边界元模型对巷道底板上锚杆的不同布置形式对防治底鼓的效果进行了模拟研究。根据研究结果,提出采用在巷道底板上分期安装锚杆的方法,可有效地防治巷道底鼓。本文对巷道底鼓产生机理和防治措施的研究结果,具有一定的理论价值和应用参考价值。     

Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.