非异构的

In this thesis, two classes nonquaternary Cholinesterase Reactivators (1,2,4-oxadiazole and a -ketothio Hydroximic Acids derivatives ) and some clinical therapy used reactivators added to almost 40 cases have been caculated by using Comparative Molecular Field Analysis,ab initio and molecular mechanism methods. The characteristics of the molecular orbitals and the quantitative structure-activity relationship have been investigated.

本文利用比较分子力场法，量子化学从头算法，分子力学及计算化学回归分析等方法，对1，2，4-oxadiazole类非季铵肟胆碱酯酶复能剂，α—酮硫代异羟肟酸酯复能剂及部分现临床使用的复能剂，近40个化合物进行了计算，分析和研究了其电子结构和几何结构特征，建立了定量构效关系方程，得到了以下一些有意义的结果。

Majority of acute leukemias in infant, either acute lymphoblastic leukemia or acute myeloblastic leukemia, posses a chromosomal translocation affecting the 11q23 chromosome region which specifically inoles the mixed-lineage leukemia gene.1-3 Most pediatric leukemias with MLL rearrangement clearly hae a remarkably short latency.1,4 MLL gene rearrangement is also associated with secondary leukemias of patients preiously treated with the topoisomerase II inhibitors.4 The latency of these secondary leukemias is similarly ery short.4 Of note, the concordance rate of leukemia with MLL rearrangement in infant monozygotic twins approximates to 100%,1,4 and identical breakpoint in the MLL gene was shared in these pairs of identical twin infants with concordant ALL.1,4 Moreoer, the unique and clonotypic MLL fusion gene was detectable in neonatal blood spots for Guthrie cards from non-twined indiiduals who subsequently deeloped ALL.1,4 These obserations indicate not only that MLL fusion is generated in utero but also that MLL fusion proteins could be capable of inducing leukemic transformation with few, if any, secondary mutations.2,3,4 Greaes et al speculate that an MLL fusion protein somehow promotes rapid transition to full-blown disease in patients ia ery rapid clonal expansion, genetic instability, or inhibition of DNA damage repair.4 In general, for clonal expansion of malignancies, tumor cells often hae acquired strategies that escape immune sureillance of the hosts.5,6 Immune escape mechanisms also contribute to the failure of graft-ersus-leukemia effect after allogeneic hematopoietic stem cell transplantation.7 Therefore, leukemia cells could acquire some immune escape mechanisms during leukemogenesis.

绪论 绝大多数的婴儿白血病，不管是急性淋巴性白血病或是急性骨髓性白血病，在染色体11q23部位有染色体易位的情况；这个部位的染色体易位牵连了混合谱系白血病基因。大多数具有MLL基因重排的儿童白血病潜伏期明显短很多。MLL基因重排也和经拓扑异构酶II抑制剂治疗后的继发性白血病有关。这些继发性白血病的潜伏期类似地都非常的短。很重要的是，单卵双胞胎婴儿同时患有或同时免于MLL基因重排阳性的白血病的一致性接近100%；并且同样患有ALL的同卵双胞胎的MLL基因的断裂点是一致的。而且，这种独特的克隆特异性的MLL融合基因能够从那些得ALL的非双生个体出生时的血斑标本中检测到。这些发现表明MLL融合基因产生在胎儿还在子宫的是后，而且MLL融合蛋白能过和其他的基因突变一起诱导白血病的产生。Greaes 等推测MLL融合蛋白在某种情况下同过快速克隆增殖，遗传的不稳定性或是DNA损伤修复的抑制促使疾病迅速地全面爆发。恶性肿瘤细胞的克隆增殖通常已经获得了逃避机体免疫监视的能力。免疫逃避机制也归因于异体外周血干细胞移植后移植物抗白血病作用的失效。所以，白血病细胞在白血病的产生过程中可能获得了某些免疫逃脱机制。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。