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glioma相关的网络例句

查询词典 glioma

与 glioma 相关的网络例句 [注:此内容来源于网络,仅供参考]

Result:The monoclonal antibody H12 against human glioma which the hybridizing cell secretions can consociate specifically with human glioma.

结果:该杂交瘤细胞株分泌抗人脑胶质瘤细胞单克隆抗体H12具有与脑胶质瘤细胞特异性结合的特性。

Mdr-l gene and its D-gp expression might be in association wi th the MDR of glioma cells.Verapamil, erythromycin and dihydropyridine could rev erse MDR of glioma cells.

mdrl基因及其P-gp蛋白的表达与胶质瘤细胞产生的MDR有关;异搏定、红霉素和潘生丁对胶质瘤细胞MDR有逆转作用。

Objective: To investigate the relationship between glioma and PGE2 and to find the possibility of indomethacin curing glioma.

目的:探讨脑胶质瘤与PGE2之间的内在联系,找出消炎痛类药物作为胶质瘤辅助治疗的可能性。

Rat glioma cell C6 was infected by the deficiency recombinant retrovirus (named C6TK). The sensitivity of C6TK cells to GCV or ACV increased 450 or 10 times than that of C6 cells respectively. Rat C6 glioma model was successfully built, and SD rats inoculated intracerebrally C6TK cells had normal gliomas. The average survival periods of the rats were about 15 days. However, after treated with ACV, the growth of C6TK tumors obviously regressed, and the survival periods extended to 57.8±8.1 days, especially in rats injected with mixed PA317TK and C6 cells or in situ PA317TK cells, which the tumors nearly disappeared after ACV administration and the survival periods extended to over 120 or 71.4±36.1 days respectively, P<0.001.

结果:构建了带有HSV-tk基因的反转录病毒载体GINaTK,应用脂质体转移方法将GINaTK导入反转录病毒包装细胞PA317,成为产病毒细胞PA317TK,用带有HSV-tk基因的复制缺陷型反转录病毒感染C6细胞,命名为C6TK细胞,对GCV和ACV的敏感性分别高于亲本450倍和10倍;成功地建立了大鼠脑胶质瘤模型,并证实转染细胞C6TK的成瘤效应未改变,存活期约为15天;而经ACV治疗后,含有C6TK细胞的肿瘤生长明显被抑制,大鼠生存期延长为57.8±8.07天,尤其是采用PA317TK细胞混和治疗组和原位治疗组,肿瘤基本消失,大鼠生存期显著延长,混和治疗组存活120天以上,原位治疗组存活至71.4±36.1天。t检验,P值均小于0.001。

Results: GINaTK retroviral vector containing HSV-tk was constructed and transduced into PA317 retrovirus packaging cell by lipofectin (named PA317TK). Rat glioma cell C6 was infected by the deficiency recombinant retrovirus (named C6TK). The sensitivity of C6TK cells to GCV or ACV increased 450 or 10 times than that of C6 cells respectively. Rat C6 glioma model was successfully built, and SD rats inoculated intracerebrally C6TK cells had normal gliomas. The average survival periods of the rats were about 15 days. However, after treated with ACV, the growth of C6TK tumors obviously regressed, and the survival periods extended to 57.8±8.1 days, especially in rats injected with mixed PA317TK and C6 cells or in situ PA317TK cells, which the tumors nearly disappeared after ACV administration and the survival periods extended to over 120 or 71.4±36.1 days respectively, P <0.001.

结果:构建了带有HSV-tk基因的反转录病毒载体GINaTK,应用脂质体转移方法将GINaTK导入反转录病毒包装细胞PA317,成为产病毒细胞PA317TK,用带有HSV-tk基因的复制缺陷型反转录病毒感染C6细胞,命名为C6TK细胞,对GCV和ACV的敏感性分别高于亲本450倍和10倍;成功地建立了大鼠脑胶质瘤模型,并证实转染细胞C6TK的成瘤效应未改变,存活期约为15天;而经ACV治疗后,含有C6TK细胞的肿瘤生长明显被抑制,大鼠生存期延长为57.8±8.07天,尤其是采用PA317TK细胞混和治疗组和原位治疗组,肿瘤基本消失,大鼠生存期显著延长,混和治疗组存活120天以上,原位治疗组存活至71.4±36.1天。t检验,P值均小于0.001。

Methods DCs were prepared from peripherad blood mononuclear induce d with gra-nulocyt e/macrophage colony-stimulating factor and interleukin-4. Apoptosis of glioma cells were induced with γ-radiation. We design these experiment groups including (1) coculture of DCs and apoptotic glioma cells and T cells,(2) coculture of DCs and U937 cells and T cells,(3) coculture of DCs and cultured glioma cell and T cells,(4) coculture of Des and T cell.

用粒-巨噬细胞集落刺激因子加白介素-4(IL-4)从人外周血分化、诱导DCs、γ-射线在体外诱导培养的人脑胶质瘤细胞凋亡,将DCs、T淋巴细胞和凋亡胶质瘤细胞共培养,同时设计不同类型肿瘤细胞(U937及培养胶质瘤细胞)作对照,分离、富集DCs、T淋巴细胞进行免疫应答及肿瘤细胞杀伤试验。

Results:Three important MRI feat ures of brain stem gliomas were found:①enlargement of brain stem contour.Using different sequences and planes the precise tumor location could be obtained.Sagittal scan could well display the early stage of brain stem glioma,the tectal glioma and cervicomedullary junction glioma.

结果:MRI表现有以下3个特征:①肿瘤使脑干的外形增大,通过不同序列和断面显示肿瘤的精确部位,矢状面对于显示胶质瘤的早期改变、顶盖部位及延髓颈髓联合部位的胶质瘤具有独特作用。

The glioma's invasive tissue is the recurring source of glioma in clinical treatment, even after resecting glioma.

在胶质瘤治疗的过程中,即使肿瘤组织自身被切除,浸润组织则是胶质瘤复发的根源。

Neural stem cells have a strong self-renew mechanism and it can transform after a little break. Neural stem cells have a long term survival, which mean that it has more probability of wrong copy than mature cells. These cells are formed glioma stem cells in the end. The genes who adjust neural stem cells can express in glioma stem cells, which hold out glioma stem cells from neural stem cells. There is another presume that glioma stem cells come from differentiated cells. Through the gene break of these cells, they can obtain characteristics of stem cells, then form glioma stem cells.

神经干细胞具有很强的自我更新机制,获得较少突变即有可能恶性转化,而且干细胞存活时间较长,这意味着干细胞比成熟细胞发生细胞复制的错误几率更大,因外界环境的刺激而发生突变的机会更多,最终形成脑胶质瘤干细胞,同时调节神经干细胞增殖和自我更新的基因在脑胶质瘤的脑胶质瘤干细胞中也表达,这也是支持神经干细胞是脑胶质瘤干细胞来源的;也有推测认为它可能起源于已分化的细胞,由这些细胞突变发生去分化得来,并通过基因突变而获得了干细胞自我更新的特性,从而形成脑胶质瘤干细胞。

Statistical data of TF grading scores showed that its expression was not significantly related to the size and location of glioma, sex, and age of patients, but closely related to the glioma gradings and microvessel quantity of the tumor.VEGF was found in gliomas of all gradings and its expression was significantly enhanced with the increase of glioma gradings.

TF分级计数统计结果显示其表达与肿瘤的大小、部位及患者性别、发病年龄等临床因素无显著相关性,但与肿瘤的分级及肿瘤微血管数量密切相关。2、VEGF在各级胶质细胞瘤组织中均有表达,随着肿瘤组织学分级的增加,VEGF的表达明显增强。

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每逢看到沃林顿那刚毅的脸,那乌黑、忧郁的眼睛,她便会相信,他一定作过不幸的爱情的受害者。

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