生血作用

In the SD rats with acute liver failure, the different levels of serum endotoxin are existed and the level of cell factors diversification inflammation progressional reactions can be induced, and SMD can regulate the level of cell factors to treat the disease.

急性肝衰竭状态下，可存在不同程度的内毒素血症，并引起细胞因子水平变化的炎症级联反应，生脉散通过调节细胞因子水平起到治疗作用。

Objective To observe the effect of raw rhubarb and its effect on levels of plasmal IL-6,IL-8 in patients with sepsis.

目的 观察生大黄对脓毒血症患者的治疗作用及对血浆 IL-6、 IL-8的影响。

Tissue factor, a receptor on the cell surface of factor VII as well as a coactive factor to activate factor VII, plays an essential role in hemostasis through the activation of the intrinsic and extrinsic coagulation pathways simultaneously.

组织因子(Tissue factor，TF)既是Ⅶ因子在细胞表面的受体，又是激活Ⅶ因子的辅助因子，它可同时启动内外两条凝血途径，在生理性止血中起重要作用。

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。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。