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cml相关的网络例句
与 cml 相关的网络例句 [注:此内容来源于网络,仅供参考]

Let L and P be Lie color algebras and let M be a graded module over P, the crossed modules which make M as their kernal and P as their cokernal are considered. It is shown that under a suitable equivalent relation, there is a bijection between the set of the equivalent classes CML and the homogeneous components of degree zero of H~3.

从交叉模的定义出发,对于给定的Lie color代数L,P以及阶化P模M,考虑所有以M为核、以P为余核的L的交叉模,在这些交叉模之间定义了一个等价关系,由此得到交叉模的等价类集CML,证明了CML与三维上同调群H~3的零次齐次部分之间存在一一对应,从而可以利用三维上同调群对Lie color代数的交叉模进行分类。

In the early 1990s, knowing that the constitutively activated kinase had a major role in CML, Druker approached scientists at what was then Ciba-Geigy with a proposal to find a small molecule that would inhibit the BCR-ABL tyrosine kinase activity.

在90年代早期,Druker认识到组成性活化的激酶在CML中的重要作用,并向当时的汽巴-嘉基药厂的科学家们提议寻找一种可抑制BCR-ABL酪氨酸激酶活性的小分子物质。

Fully Integrated Clock Recovery and Data Retiming Power Dissipation: 260mW with +3.3V Supply Clock Jitter Generation: 5mUIRMS Exceeds ANSI, ITU, and Bellcore SDH/SONET Jitter Specifications Differential Input Range: 50mVP-P to 1.6VP-P Single +3.3V Power Supply PLL Fast Track Mode Available Clock Output Can Be Disabled Input Data Rate: 2.488Gbps or 2.67Gbps Selectable Output Amplitude Tolerates 2000 Consecutive Identical Digits Loss-of-Lock Indicator Differential CML Data and Clock Outputs Operating Temperature Range:-40C to +85C

1第1页,本页显示记录1-5,共5条记录分1页显示完全集成的时钟恢复和数据重定时功耗:+3.3 V电源与时钟抖动产生:5mUIRMS超越美国ANSI,ITU和Bellcore实验室的SDH / SONET抖动规格差分输入范围:50mVP磷260mW至1.6VP - P的单+3.3 V供电锁相环快车道时钟输出模式下可用可以禁用输入数据速率:2.488Gbps或2.67Gbps可选输出振幅2000年连续容忍同位数丢失锁指示灯差分CML数据和时钟输出工作温度范围:-40℃至+85

The myeloproliferation degree in CML is more serious than CLL, there were cellular morphological changes in two types of leukemia, Gaucher cells were seen in CML.

骨髓增生度CML高于CLL,两类白血病细胞形态上有不同程度的改变,CML可见戈谢氏样细胞。

In advanced disease, their progressively anaplastic progeny ultimately maintain CML independently of the CML haematopoietic stem cell.

在进展期,它们不断退变的子代细胞最终维持了CML而不再依赖CML造血干细胞。

Allogenetic hemapoietic stem cell transplantation is considered to be the curative therapeutic method for CML.

异基因造血干细胞移植是CML的唯一根治方法,在CML慢性期移植可以获得较理想的疗效,但加速期及急变期移植的相关死亡率和移植后复发率明显升高。

Results The reticulin fibre proliferated in all specimen and most of them occured mega karyocytosis.The myelofibrosis was severer along with the progress of CML,while megakaryocyte counts didn′t change significantly.

结果 发现所有患者的骨髓组织均存在网硬蛋白纤维增多,且随CML进展其程度加重;大多数患者巨核细胞过度增生,在CML不同阶段中巨核细胞数比较未见显著差异。

I would like to take this opportunity to Thank very much Team Yokomo Japan and CML Distribution in the UK, I have had some great years with both, and could not of wished for nicer people to work with,special thanks to Tom, Masami, Umino Zapper, and Robert, at Yokomo and Jason, Mark, and Dave, at CML.

我愿借此机会非常感谢小组Yokomo日本和CML分布在英国,我有一些伟大的几年都,不能更好的希望人民一道,特别感谢汤姆,雅美,海野遥控,和罗伯特,在Yokomo和Jason ,标记,和Dave ,在慢性粒细胞白血病。

1、Cur inhibits K562 cells growth and induces cell apoptosis may be correlated with the down-regulation of p210~、inhibition of protein tyrosine phosphorylation and the signaling molecules such as p-Erk1/2、c-myc which are relevant with cell growth and apoptosis; 2、Cur synergizes STI571 to inhibit K562 cell growth and induce cell apoptosis may be correlated with the down-regulation of p210~、inhibition of protein tyrosine phosphorylation and the signaling molecules such as Hsp90、PKC which are relevant with cell growth and apoptosis; 3、Cur reverses the resistance of K562/G01 cells to STI571, and synergizes STI571 to inhibit K562/G01 cell growth and induce cell apoptosis; 4、Cur inhibits human originated CML CD34~+ cell growth、induces cell apoptosis, and enhances STI571 to down-regulate the expression of p210~, finally inhibit cell growth and induce cell apoptosis.

从以上实验结果我们得出如下结论: 1、Cur抑制K562细胞增殖、诱导细胞凋亡的作用可能与其下调p210~、蛋白酪氨酸磷酸化水平以及抑制下游p-Erk1/2、c-myc等信号分子有关; 2、Cur协同STI571抑制K562细胞增殖、诱导细胞凋亡的作用可能与其下调p210~、蛋白酪氨酸磷酸化水平以及抑制Hsp90和下游PKC等信号分子有关; 3、Cur可逆转K562/G01细胞对STI571的耐药性,并与STI571协同抑制K562/G01细胞增殖和诱导凋亡,其抑制K562/G01细胞增殖、诱导细胞凋亡的作用可能与其下调p210~、蛋白酪氨酸磷酸化水平以及抑制下游Procaspase-3和NF-κB等信号分子有关; 4、Cur可抑制来源于CML患者骨髓的CD34~+细胞的增殖并诱导其凋亡,还可协同STI571下调CML CD34~+细胞p210~表达,进而协同抑制细胞增殖、诱导细胞凋亡。

P210bcr/abl plays a central role in the pathophysiology of CML. The purpose of this study was to construct a cell line model that bcr/abl expression can be regulated by Tetoff inducingexpressionsystem. The fulllength b3a2 bcr/abl cDNA was subcloned into the pTRE2hyg expression vector to construct the pT2P210 plasmid.

CML是目前致病分子信号基础研究最为清楚的肿瘤之一,1960年Nowell和Hungerford在CML患者的白血病细胞中发现Ph染色体[1],1973年Rowley等[2]进一步应用染色体分带技术证明,Ph染色体是由9q34的abl基因和22q11 的 bcr 基因相互易位形成的 bcr/abl 融合基因。

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然而,正如其名字所指出的那样,CD盘不能写,也不能用任何方式改变其内容。

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