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增殖细胞
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  proliferative cells
    ? Results In the L-arginine group,the gastric mucosal cellular injury induced by GI/R was significantly alleviated,with the gastric mucosal injury area and apoptotic cells decreased and the proliferative cells increased(P<0.05).
    结果与GI/R组相比,L-arg组胃黏膜损伤明显减轻,胃黏膜损伤面积明显缩小,凋亡细胞减少,增殖细胞增加(P<0.05);
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    However,In the L-NAME group,the gastric mucosal cellular injury was significantly aggravated,showing increase of gastric mucosal injury area and number of apoptotic cells and decrease of proliferative cells(P<0.05). ?
    L-NAME组与GI/R组相比胃黏膜损伤明显加重,胃黏膜损伤面积明显增加,凋亡细胞增加,增殖细胞减少(P<0.05)。
短句来源
    The damaged gastric mucosa could initiate its repairing mechanism immediately through inhibiting cellular apoptosis and increasing the number of proliferative cells,which substitute the damaged cells gradually. The plerosis almost completes in three days after reperfusion showing a strong self-repair ability of gastric mucosa.
    然后胃黏膜启动自我修复机制,增殖细胞逐渐取代损伤细胞,3d左右就可基本修复,表明胃黏膜细胞具有很强的自我修复能力。
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  “增殖细胞”译为未确定词的双语例句
    In the L-NAME group,the results were the opposite: with the gastric mucosal cellular injury significantly aggravated and accompanied by increase of apoptotic cells,etc(P<0.05).
    L-NAME组与GI/R组相比胃黏膜凋亡细胞增加,增殖细胞减少,Bcl-2阳性细胞百分比和蛋白水平明显降低,Bax显著升高(P<0.05);
短句来源
    Methods: Using immunohistochemical staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) technique, we observed bcl-2 and bax protein expression and the change of gastric epithelial apoptotic index (AI) and proliferative index (PI) in HP-related gastritis (n=43 ).
    方法:采用免疫组织化学方法及脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记(TUNEL)技术,对HP阳性和HP阴性者胃粘膜上皮中增殖细胞,凋亡细胞进行原位观察和比较,同时检测 bc1-2/bax蛋白表达状态。
短句来源
    Objective To study the relationship between ling-term high-salt hot diet and chronic atrophic gastritis(CAG). The expression of apoptosis cells and proliferation cells were detected in the gastric mucosa of CAG rates induced by high-salt hot water.
    目的 研究热盐水灌胃导致的大鼠萎缩性胃炎胃粘膜组织中的凋亡细胞及增殖细胞表达状态 ,以探讨长期热咸饮食与慢性萎缩性胃炎发生的关系。
短句来源
    Conclusions Restenotic rate may be 67% in TIPS swine models. Restenotic tissues may be mainly composed of proliferated SMCs positively expressed anti-SMC-actin-α with strong ability of movement.
    结论猪TIPS模型中,再狭窄中主要为抗SMC-α阳性的平滑肌细胞增殖,细胞增殖迁移能力强;
短句来源
    Mild gastric mucosal injury was induced by ischemia alone. However,the injury worsened and reached the maximum at 1 h after reperfusion,almost simultaneously with the gastric mucosal cellular apoptosis increase and cellular proliferation decrease in gastric mucosa.
    结果发现,单纯缺血30min胃黏膜损伤较轻,再灌注后损伤逐渐加重,胃黏膜的凋亡细胞迅速增加,而增殖细胞迅速减少:至再灌注后1h达高峰;
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  proliferative cells
Monoclonal antibodies (McAb) to Ki-67, BrdU and OKT9 were used in APAAP technique for determining the proliferative cells of 46 myelodysplastic syndromes (MDS) with 16 serving as normal controls.
      
The ratio of CD8+ in proliferative cells was analyzed by flow cytometry.
      
CD8+ cells, accounting for a high proportion in proliferative cells, had a specific cytotoxicity to leukemia cells from which antigen peptides were prepared, suggesting that these CD8+ cells were CTLs specific to leukemia cells.
      
Relative resistance of a strain to the hyperacute or high-dose mode of death is not necessarily correlated with resistance to the midlethal mode, which is believed to be the result of damage to the proliferative cells of the midgut.
      
Using novel inferential procedures, we estimate the generation-time distribution and the offspring distribution of proliferative cells, and the waiting-time distribution of resting cells.
      
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This study was attempted to have an understanding of relationship between Helicobacter pylori (Hp) and proliferation as well as apoptosis of gastric epithelid cells,and between cell proliferation and apoptosis.Endoscopic mucosal biopsies were taken in 72 cases with chronic gastritis.With Hp positive (n=46) biopsies were repeated after Hp eradication;in cases of Hp negative (n=26) specimens from the some sites obtaimed.Terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) technique and proliferative cell nuclear antigen (PCNA) immunohistochemical staining were applied for investigation.Results showed that:(1)Hp infection did induce cell proliferation and apoptosis in paralle;(2)Hp infected mucosa demonstrated very high apoptotic and PCNA labelling indices,which declined after therapy.It is supposed that Hp induced cell apoptosis may be a tigger factor for cell hyperproliferation,resulting in carcinogenesis....

This study was attempted to have an understanding of relationship between Helicobacter pylori (Hp) and proliferation as well as apoptosis of gastric epithelid cells,and between cell proliferation and apoptosis.Endoscopic mucosal biopsies were taken in 72 cases with chronic gastritis.With Hp positive (n=46) biopsies were repeated after Hp eradication;in cases of Hp negative (n=26) specimens from the some sites obtaimed.Terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) technique and proliferative cell nuclear antigen (PCNA) immunohistochemical staining were applied for investigation.Results showed that:(1)Hp infection did induce cell proliferation and apoptosis in paralle;(2)Hp infected mucosa demonstrated very high apoptotic and PCNA labelling indices,which declined after therapy.It is supposed that Hp induced cell apoptosis may be a tigger factor for cell hyperproliferation,resulting in carcinogenesis.

为研究幽门螺杆菌(Hp)感染对胃粘膜上皮细胞增殖和凋亡的影响,探讨胃粘膜上皮细胞增殖与细胞凋亡之间的关系,采用脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记(TUNEL)技术、增殖细胞核抗原(PCNA)免疫组织化学染色对Hp阳性患者Hp根除前后及Hp阴性者胃粘膜上皮中增殖细胞、凋亡细胞进行原位观察和比较。结果Hp阳性患者胃粘膜细胞增殖指数、凋亡指数均显著增加,Hp根除后,上述指标均显著降低,而Hp仍为阳性者上述指标则无显著性变化。胃粘膜细胞增殖指数与凋亡指数呈显著正相关。提示Hp诱导胃粘膜上皮细胞凋亡可能是刺激胃粘膜上皮细胞过度增殖的机制之一,使胃粘膜的不稳定性增加,从而增加患胃癌的危险性。

AIM To investigate whether Helicobacter pylori (Hp) infection has any effects on the gastric epithelial cell proliferation and apoptosis,as well as its role in the pathogenesis of gastric ulcer. METHODS Endoscopic gastric mucosal biopsies were taken from 1 group (10 cases) of normal subjects (NS) and 4 groups (10 cases for each group) of patients with gastric ulcer (GU) and chronic superficial gastritis (CSG) with or without Hp infection. Apoptosis cells in gastric mucosa were quantitated by terminal...

AIM To investigate whether Helicobacter pylori (Hp) infection has any effects on the gastric epithelial cell proliferation and apoptosis,as well as its role in the pathogenesis of gastric ulcer. METHODS Endoscopic gastric mucosal biopsies were taken from 1 group (10 cases) of normal subjects (NS) and 4 groups (10 cases for each group) of patients with gastric ulcer (GU) and chronic superficial gastritis (CSG) with or without Hp infection. Apoptosis cells in gastric mucosa were quantitated by terminal deoxynucleatidyl transferase mediated dUTP nick and labelling (Tunel method) and proliferation cells by immunohistochemical staining (LSAB method) for proliferating cell nuclear antigen (PCNA). RESULTS Apoptosis index (AI) of the patients in Hp positive GU group was much higher than that of the patients in Hp negative GU group ( P <0 05), but there was no significant difference in PCNA labelling indices (PCNA LI) between the two groups ( P >0 05). AI and PCNA LI of the patients in Hp positive CSG group were significantly higher than those of the patients in Hp negative CSG group ( P <0 05). AI/PCNA LI ratio of the patients in Hp positive GU group was 1 541, and this ratio was much higher than those in other groups ( P <0 05). CONCLUSION Hp infection might induce apoptosis of gastric epithelial cells, and this effects might lead to the imbalance of the AI/PCNA LI ratio and ultimately promote the development of gastric ulcer.

目的观察Hp感染对胃溃疡(GU)患者胃粘膜上皮细胞增殖与凋亡的影响,进而对溃疡发生机制进行探讨.方法标本取自内镜下胃粘膜活检,细胞凋亡检测采用Tunel方法,细胞增殖检测采用免疫组化LSAB方法测定增殖细胞核抗原(PCNA).结果GUHp+患者细胞凋亡指数(AI)明显高于Hp-患者(P<005),但比较两者的增殖细胞指数(PCNALI),无显著性差异(P>005);慢性浅表性胃炎Hp+患者AI,PCNALI明显高于Hp-患者(P<005),GUHp+患者的AI/PCNALI比值为1541,明显高于其他各组(P<005).结论Hp感染能诱导GU患者胃粘膜上皮细胞凋亡增加,出现细胞凋亡与细胞增殖平衡失调,促进溃疡形成

Objective: To investigate the bcl-2 and bax protein expression and its association with apoptosis and cell proliferation in Helicobacter pylori(HP) related gastritis. Methods: Using immunohistochemical staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) technique, we observed bcl-2 and bax protein expression and the change of gastric epithelial apoptotic index (AI) and proliferative index (PI) in HP-related gastritis (n=43 ). Results: AI and PI in HP positive gastritis...

Objective: To investigate the bcl-2 and bax protein expression and its association with apoptosis and cell proliferation in Helicobacter pylori(HP) related gastritis. Methods: Using immunohistochemical staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) technique, we observed bcl-2 and bax protein expression and the change of gastric epithelial apoptotic index (AI) and proliferative index (PI) in HP-related gastritis (n=43 ). Results: AI and PI in HP positive gastritis were significantly higher than that in HP negative gastritis (P < 0. 01). The positive rate of bax protein expression in HP positive gastritis was significantly higher than that in HP negative gastritis (P < 0. 01 ), whereas the positive rate of bcl-2 protein expression was similar in both groups (P > 0.05 ). In HP positive gasitritis, the percentage of apoptotic cells in the bcl-2 negative group was higher than that in the bcl-2 positive group, the percentage of apoptotic cells in the bax negative group was lower than that in the bax positive group (P < 0. 01 ). Conclusions: HP may be involved in the induction of the apoptosis and proliferation of gastric epithelial cells. The bcl-2 may inhibit apoptosis and the bax may promote apoptosis in HP positive gastritis.

目的:探讨幽门螺杆菌HP引起胃粘膜上皮细胞凋亡和增殖改变及HP致癌作用的可能机制。方法:采用免疫组织化学方法及脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记(TUNEL)技术,对HP阳性和HP阴性者胃粘膜上皮中增殖细胞,凋亡细胞进行原位观察和比较,同时检测 bc1-2/bax蛋白表达状态。结果: HP阳性者胃粘膜上皮细胞增殖指数和凋亡指数显著高于HP阴性者(P<0.01)。bax蛋白表达阳性率在HP阳性组较HP阴性组升高显著( P< 0. 01),而 bcl-2蛋白表达阳性率两组差异不显著( P> 0. 05)。在 HP阳性慢性胃炎中, bcl-2蛋白表达阳性组细胞凋亡指数显著低于阴性组(P<0.01)。bax蛋白表达阳性组细胞凋亡指数显著高于阴性组(P<0.01)。结论:HP可诱导胃粘膜上皮细胞凋亡和过度增殖,bcl-2蛋白低表达和bax蛋白高表达参与此调节机制,推测认为HP在胃癌的发生过程中可能有重要意义。

 
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