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胶质细胞瘤

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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。

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。

In this study, RT-PCR and Western Blotting were performed to quantify the regulation of endogenic nerve growth factor expression in neuroglia cells by HCMV infection. The results showed that basal, endogenous NGF expression in U251 was unchanged during early HCMV infection.

本研究采用RT-PCR和Western Blotting技术,检测正常培养和感染HCMV的神经胶质瘤(U251)细胞NGF的表达,探讨人巨细胞病毒对神经胶质瘤细胞内源性神经生长因子表达的影响。

Radiosensitive genes of gliomas and apoptosis, cell cycle transformation,DNA damage induced by irradiation and DNA repair promoted by them are suggested to be associated with glioma radiosensitivity.

脑胶质瘤内在的放射敏感性基因及其引起的细胞凋亡、细胞周期的变化和放射线导致的DNA损伤修复等,都与脑胶质瘤的放射敏感性密切相关。

Ribonuclease inhibitor has no inhibitory effect on the growth of cultured glioma cells in vitro, whereas it has significant inhibitor effect on the growth of glioma in vivo.

RNasin体外对培养的胶质瘤细胞生长无抑制作用,而体内对胶质瘤瘤体的生长有明显抑制作用。

CIK cells are highly efficient cytolytic effector cells which have a stronger significant suppression against growth of glioma in vitro and in vivo.

CIK细胞是一种新型和高效的免疫活性细胞,具有较强的体内外抑制胶质瘤生长的作用,有可能用于临床上脑胶质瘤的过继性免疫治疗。

Postoperative pathological results revealed that 79 cases (86.8%) were low-grade gliomas, 4 cavernous hemangiomas, 4 anaplastic astrocytomas, 2 gliosis, 1 arteriovenous malformation, and 1 gliosarcoma.

术后病理结果示低级别胶质瘤79例(86.8%),海绵状血管瘤4例,间变性星形细胞瘤4例,神经胶质增生2例,动静脉畸形1例,胶质肉瘤1例。

RESULTS A variable degree of vascular hyalinization and glioma intercellular with enhanced tenascin immunostaining was observed.Expression of tenascin and cell proliferation in gliomas correlated positively with each other and increased with the degree of tumor malignancy.

结果 胶质瘤与其增生血管内皮细胞均表达Tenascin,Tenascin基因表达与肿瘤细胞增殖指数呈显著正相关,随胶质瘤恶性程度提高,Tenascin和Ki-67表达均增强。

Objective To investiga te the ability of dendritic cells ac quiring antigen from apoptotic glioma cells and inducing CTLs activati on.

目的 观察树突状细胞从凋亡脑胶质瘤细胞获取抗原后,体外诱导抗肿瘤免疫应答及对胶质瘤细胞的特异性免疫杀伤效果。

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