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Methods The article applied the orthogonal design to find out the optimum proportion of the rutin, soybean isoflavone and curcumin. The free radical DPPH scaving ratio was used as evaluating standard of orthogonol design and the hominal liver cancer cell SMMU-7721 was used in MTT trial to evaluate the inhibitory ability of the compound. Results The optimum proportion of rutin-soybean isoflavone-curcumin 2:3:7 was achieved.

选取3种天然植物抗氧化物质芦丁、大豆异黄酮、姜黄素,利用正交试验设计选择合适配方,以自由基DPPH的清除率作为正交试验评价标准,并利用人肝肿瘤细胞SMMU-7721进行四甲基偶氮唑盐试验来考察配方体外试验对肿瘤细胞的抑制作用。

The clinical features included peripheral lymphadenopathy and skin lesions, recurrent fever was very common. the pathological features included partial lymphomatous involvement of lymph node, sheets of analplastic large cells infiltrated the sinuses and paracortices, immunohistochemical cd30 was strongly positive. the prognosis was comparative well.

结果:间变性大细胞性淋巴瘤占小儿非霍奇金淋巴瘤的12.8%,临床表现主要是外周淋巴结肿大及皮肤损害,长期反复发热常见,病理特征为淋巴结部分受累,成片异形大细胞侵犯淋巴窦及副皮质区,免疫组化cd30强阳性,预后相对较好。

The leaf in the Karst area was isolateral and had closely arranged mesophyllous cells.

在显微结构方面:岩溶区生长的扇叶铁线蕨的叶片具有旱生植物叶片特点,即叶片为等面叶,叶肉细胞排列较为紧密以及叶片维管组织发达等:而非岩溶区生长的扇叶铁线蕨的叶片为异面叶,特点为叶肉细胞排列相对疏松,维管组织不发达。

Then the bFGF was replaced by transforming growth factor-β1 (TGF-β1 10 μg·L-1) for next three weeks. Results Some spindle MSCs turned into round or elliptic shape and secreted metachromatic matrix with Toluidine blue.

结果:细胞形态由纺锤形变为圆形或椭圆形,细胞分泌了大量的甲苯胺蓝异染的基质,形成了类软骨陷窝。

Primary cultured chondrocytes are poly-angle, cytoplasm-rich, and their nuclei are either round or oval with clear necleole. Metachromatic and alcian blue positive staining in primary cultured chondrocytes was observed. Intercellular matrix was anti-collagen type Ⅱ staining but not anti-collagen type Ⅰ staining by IHC assay.

原代培养软骨细胞呈多角型,胞质丰富,胞核成圆形或椭圆型,核仁清楚,甲苯胺蓝呈异染性,阿尔新蓝8Gx 染色阳性,细胞外基质Ⅱ型胶原免疫组化染色阳性,Ⅰ型胶原染色阴性。

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。

Glucosinolates and myrosinase are present in the vacuoles and in the de finite protosome in intact cell and tissues respectively. but when tissues and c ells are damaged, myrosinase will release and hydrolyze glucosinolates to genera te degraded products, such as isothiocyanates and so on.

在完整的植物中,硫代葡萄糖苷存在于细胞的液泡中,葡萄糖硫苷酶存在于特定的蛋白体中,两者相互分离,但当组织和细胞受到损伤时,葡萄糖硫苷酶就会被释放出来,葡萄糖硫苷酶将硫代葡萄糖苷水解,产生异硫代氰酸盐等降解产物。

There are four kind of isoforms of endothelin in human and other mammals named ET-1, ET-2, ET-3 and ET-β, which are slightly different in construction and pharmacological effect. In human beings, ET-1 is the dominative subtypes. ET-1 remains in blood at a low level about 5ng per liter on physical state. It is synthesized, stored, released and metabolized locally. The half-life of ET-1 is about 1 hour. ET-1 is the most potent vasoconstrictive factor till now, and it is more functional in vein than in artery. In vascular bed, there are two kind of ET receptors. Type A mainly located in smooth muscle cells, whereas type B in endothelial cells. The latter can stimulate intimal hyperplasia via a parasecretion way and activate some oncogenes such as c-fos and c-myc and then enhance their expression. These alterations result in constriction of blood vessels, thus the SMC steps into proliferate state from silent state.

人及哺乳动物体内有四种结构及药理学性质略有差异的异物体,分别为ET-1、ET-2、ET-3、ET-β,而在人主要是ET-1,在生理条件下,ET-1在血浆中含量较低,约为5ng〓,故ET-1不是一个循环激素,而是局部合成释放,局部起作用的活性物质,半衰期约1小时,ET-1是目前已知的最强的血管收缩剂,对静脉的作用比动脉强,在血管床,ET受体有A、B两型,A型主要分布在平滑肌细胞,B型主要分布在内皮细胞,它可以通过旁分泌途径刺激内膜增生,具有有丝分裂原效应,可以激活某些癌基因如C-fos、C-myc使其表达增强引起血管收缩,使静止期SMC进入增殖期,还可以通过信号传导途径,与bFGF、GTF-β、PDGF等生长因子协同作用,起共有丝分裂原作用。

Additional 5 Balb/c and 5 B6 mice were implanted peritoneally with hybridoma cell-containing diffuse chamber.

目的 观察自制细胞扩散匣的免疫隔离作用及匣内异基因瘤细胞的在体生长情况。

"The increased levels of apoptosis in the midbrain and pronephric kidney we observe suggest that atrazine may cause tissue malformation by inducing ectopic programmed cell death, either directly or indirectly through a mechanism that has not been identified," wrote the researchers.

&提高水平的细胞凋亡的脑和肾pronephric我们观察表明,莠去津可能会导致畸形组织异位诱导细胞程序化死亡,直接或间接地通过一种机制,还没有确定,&研究人员写道。

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