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cisplatin相关的网络例句

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与 cisplatin 相关的网络例句 [注:此内容来源于网络,仅供参考]

We further evaluated the synergistic cytotoxicity of TRAIL in combination with actinomycin D, cisplatin and paclitaxel in A549 cell lines in vitro and in vivo.

本实验选择了人肺腺癌A549细胞瘤株作为我们实验研究的对象,通过TRAIL对人肺腺癌A549细胞诱导凋亡研究,在A549的荷瘤裸鼠的动物模型上研究了其体内的抗肿瘤活性,并进一步研究了TRAIL与化疗药物放线菌素D(actinomycin D,Act D)、紫杉醇和顺铂(cisplatin,CDDP)的联合作用对人肺腺癌A549细胞的体外协同抗肿瘤活性,通过化疗药物协同增强TRAIL抗肿瘤活性作用机制的初步研究,为降低临床化疗药的用药量,减轻其对机体的不良反应提供一定的理论基础。

All patients had locally advanced squamous cell carcinoma of the oral cavity, oropharynx, larynx, or hypopharynx, and were randomized to either radiation therapy once daily or radiation therapy once daily combined with three courses of high-dose cisplatin chemotherapy.

所有的病人都患有局限性晚期的口腔、喉部、咽部或者喉咽部的鳞壮上皮癌。这些病人被随机给予每日一次放射治疗或者在每日一次放射治疗的基础上加用三个疗程的cisplatin化疗。

This paper investigated the protective effect of carnosine on cisplatin-induced acute nephrotoxicity in KM mice and the possible plausible mechanism.

研究肌肽对顺铂(cisplatin, CDDP)所致小鼠体内急性肾损伤的保护作用,并探讨可能的机制。

Whether cisplatin induced Bcl-xL deamidation may be inhibited by NAC, remains to be determined.

是否cisplatin引发的Bcl-xL 去胺基化,可能受到NAC抑制,仍待进一步证实。

In addition, ectopic expression of deamidation forms of Bcl-xL sensitized the SKOV3-ip1 cells to cisplatin to a level equivalent to that caused by overexpression of E1A.

因此,由实验结果可以推论诱导Bcl-xL去胺基化对於E1A所调控增加卵巢癌细胞SKOV3-ip1对cisplatin的敏感性扮演著一个重要的角色。

Recent studies showed that deamidation of Bcl-xL, an anti-apoptotic protein, regulates cellular response to DNA damage. This Bcl-xL deamidation induced by cisplatin appears to be mediated by p53 and Rb.

目前有研究显示在DNA损伤下,抗死蛋白Bcl-xL的去胺基化可调控细胞反应,而在抑癌基因p53和Rb 突变的癌细胞中也发现抗癌药物cisplatin的处理会导致Bcl-xL 的去胺基化。

Previously study shows that Bcl-xL deamidation is induced in response to cisplatin treatment in the absence of Rb, and Bcl-xL deamidatioon alters its antiapoptosis function.

之前的研究更显示在无Rb的细胞中当Bcl-xL 受到抗癌药物 cisplatin 刺激发生去胺基化后,会失去其原有抗细胞凋亡的功能。

It is known that adenovirus E1A inactivates Rb normal function by directly binding to Rb. Thus, we reason if E1A blocks the normal function of Rb, it may lead to cisplatin-induced deamidation of Bcl-xL and sensitize the p53-null ovarian cancer cell, SKOV3-ip1 cells, to cisplatin.

过去已知腺病毒E1A会藉由与Rb结合而抑制它的正常功能;因此我们推论若E1A抑制Rb的正常功能之下,cisplatin的处理应该可以导致Bcl-xL 的去胺基化并且使没有p53的卵巢癌细胞SKOV3-ip1对cisplatin较敏感。

When E1A mutant containing CR2 domain deletion expressed in ovarian cancer cells that contain wild type Rb, we detected low E2F activity. Also, Bcl-xL deamidation was suppressed and the cells were survived under cisplatin treatment in E1A mutant transfected cells.

故当E1A mutant (CR2 domain deletion)在含wild type Rb的卵巢癌细胞中表现时,我们侦测到E2F活性较低且Bcl-xL去胺基化现象被抑制,这使得细胞对抗癌药物 cisplatin具有些微抗性,存活率上升。

The 3 different regimens consisted of gemcitabine and cisplatin, carboplatin and paclitaxel, and docetaxel and cisplatin. Although this was not a direct head-to-head comparison, the "data derived from this series of embedded trials strongly suggest that commonly used platinum-based doublets produced similar results," the editorial comments."What modest differences exist are likely a result of unrecognized biologic differences in the treated populations and are probably of little clinical relevance."J Natl Cancer Inst.

这三种化学治疗药物包括gemicitabine、cisplatin、carboplatin与paclitazel、docetaxel与carboplatin;虽然这不是直接的比较,这些数据来自这一连串的研究暗指以铂金类药物为基础的比较出现类似结果;存在于之间微小的差异可能是接受治疗的病患中,未能侦测到的生物差异,且在临床上的相关性可能是不高的。

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