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d-氨基葡萄糖    
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  d-glucosamine
    AIM: To investigate the role of c-jun N-terminal kinase (JNK) signaling pathway in the apoptosis of human eso-phageal cancer Eca-109 cells induced by the derivative of D-glucosamine ({2-(3-carboxy-1-oxopropyl)amino-2-deoxy-D-Glucose}, COPADG) and the possible mechanisms.
    目的:探讨c-Jun氨基末端激酶(JNK)信号通路在D-氨基葡萄糖衍生物2-(3-羧基-1-丙酰氨基)-2-脱氧-D-葡萄糖(COPADG)诱导人食管癌Eca-109细胞凋亡中的作用及机制.
短句来源
    Antitumor Effect of D-Glucosamine Hydrochloride in Mice
    D-氨基葡萄糖盐酸盐的抗肿瘤作用
短句来源
    Apoptosis in human esophageal cancer cell line Eca-109 induced by the derivative of D-glucosamine via JNK signaling pathway
    D-氨基葡萄糖衍生物通过JNK信号通路诱导Eca-109细胞凋亡
短句来源
  d-glucosamine
    AIM: To investigate the role of c-jun N-terminal kinase (JNK) signaling pathway in the apoptosis of human eso-phageal cancer Eca-109 cells induced by the derivative of D-glucosamine ({2-(3-carboxy-1-oxopropyl)amino-2-deoxy-D-Glucose}, COPADG) and the possible mechanisms.
    目的:探讨c-Jun氨基末端激酶(JNK)信号通路在D-氨基葡萄糖衍生物2-(3-羧基-1-丙酰氨基)-2-脱氧-D-葡萄糖(COPADG)诱导人食管癌Eca-109细胞凋亡中的作用及机制.
短句来源
    Antitumor Effect of D-Glucosamine Hydrochloride in Mice
    D-氨基葡萄糖盐酸盐的抗肿瘤作用
短句来源
    Apoptosis in human esophageal cancer cell line Eca-109 induced by the derivative of D-glucosamine via JNK signaling pathway
    D-氨基葡萄糖衍生物通过JNK信号通路诱导Eca-109细胞凋亡
短句来源
  amino-d-glucose
    Effect of amino-D-glucose derivative on proliferation of human gastric carcinoma cell line SGC-7901 in vitro
    D-氨基葡萄糖衍生物对人胃癌细胞系SGC-7901增生的影响
短句来源
    CONCLUSION: Amino-D-glucose derivative can induce SGC -7901 cell apoptosis, inhibit the cancer proliferation and downregulate expression of CD44 expression.
    结论:D-氨基葡萄糖衍生物通过诱导肿瘤细胞凋亡而抑制人胃癌SGC-7901细胞增生,同时还有下调CD44的作用.
短句来源
    RESULTS: Amino-D-glucose derivative inhibited SGC-7901 cell in a time- and dose-dependent manner.
    结果:D-氨基葡萄糖衍生物能明显抑制胃癌细胞的增长(P<0.01),MTT法显示抑制程度具有时间和剂量效应关系,统计组间比较差异有显著性(P<0.01);
短句来源
  d-aminoglucose
    The Effect of JNK Inhibitor on Caspase-3 Activation of the Human Esophageal Cancer Cell Line Eca-109 induced by the Derivative of D-aminoglucose
    JNK抑制剂对D-氨基葡萄糖衍生物诱导Eca-109细胞Caspase-3活化的影响
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  d-glucosamine
Transglycosylation reactions catalyzed by the enzyme produced N-acetyl-D-glucosamine and N-acetyl-D-galactosamine with respective yields of 38 and 46%.
      
fluorescens with respect to D-glucosamine-sensitized mice was 40-50 times lower than the toxicity of the classic endotoxins, LPSs of E.
      
It was shown that hemagglutination of luminous bacteria is inhibited by glucose, maltose, fructose, mannose, and N-acetyl-D-glucosamine.
      
The conversion of uridine diphosphate N-acetyl-D-glucosamine into uridine diphosphate N-acetyl-L-fucosamine was demonstrated with enzymes from cytoplasmic fraction of Salmonella arizonae O:59 cells in the presence of NAD+ (NADP+) and NADPH.
      
The conversion of uridine diphosphate N-acetyl-D-glucosamine into uridine diphosphate N-acetyl-L-fucosamine was demonstrated with enzymes from cytoplasmic fraction of Salmonella arizonae O:59 cells in the presence of NAD+ (NADP+) and NADPH.
      
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  d-glucosamine
Transglycosylation reactions catalyzed by the enzyme produced N-acetyl-D-glucosamine and N-acetyl-D-galactosamine with respective yields of 38 and 46%.
      
fluorescens with respect to D-glucosamine-sensitized mice was 40-50 times lower than the toxicity of the classic endotoxins, LPSs of E.
      
It was shown that hemagglutination of luminous bacteria is inhibited by glucose, maltose, fructose, mannose, and N-acetyl-D-glucosamine.
      
The conversion of uridine diphosphate N-acetyl-D-glucosamine into uridine diphosphate N-acetyl-L-fucosamine was demonstrated with enzymes from cytoplasmic fraction of Salmonella arizonae O:59 cells in the presence of NAD+ (NADP+) and NADPH.
      
The conversion of uridine diphosphate N-acetyl-D-glucosamine into uridine diphosphate N-acetyl-L-fucosamine was demonstrated with enzymes from cytoplasmic fraction of Salmonella arizonae O:59 cells in the presence of NAD+ (NADP+) and NADPH.
      
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  其他


Objective To evaluate Amifostin's effect on protecting kidney from cisplatinum (DDP) injury and its adverse reactions and safety.Methods 193 Patients were divided into two groups randomly: 102 in group A (treatment group) and 91 in group B (control group). Indexes such as blood routine, blood calcium, liver function, blood urea nitrogen (BUN), cretinine (C), and urinary N-acetyl-beta-D-glucosaminidase (NAG)/C and micro-albumin (MAB/C) were monitored at different intervals before or after treatment.Results...

Objective To evaluate Amifostin's effect on protecting kidney from cisplatinum (DDP) injury and its adverse reactions and safety.Methods 193 Patients were divided into two groups randomly: 102 in group A (treatment group) and 91 in group B (control group). Indexes such as blood routine, blood calcium, liver function, blood urea nitrogen (BUN), cretinine (C), and urinary N-acetyl-beta-D-glucosaminidase (NAG)/C and micro-albumin (MAB/C) were monitored at different intervals before or after treatment.Results In the two courses of treatment in both groups, the deviation (D) values of MAB/C before treatment and on D2 in group A were lower than those in grop B ( P <0.05), so were those before treatment and on D4, D6, D10 and D14 ( P <0.01). The D-values of NAG/C before treatment and on D4, D6, D10 and D14 in the first course of group A were obviously lower than those on the corresponding days in group B ( P <0.01), so were those before treatment and on D2, D4, D6, D10 and D14 in the second course ( P <0.01).Conclusion The reduction of MAB/C and NAG/C by Amifostin in group A demonstrates that: Amifostin is able to effectively protect the renal function, regardless of the type of tumor. In contrast with group B, Amifostin in group A shows no protection for tumor in lung cancer and ovarian cancer. The main side effects of Amifostin are mild hypotension, nausea, vomiting and hypocalcemia in some patients.

目的 观察阿米福汀 (amifostin)保护肾脏免受顺铂 (DDP)损害的疗效及药物不良反应和安全性。方法  193例恶性肿瘤患者随机分为化疗加阿米福汀组 (观察组 )和单纯化疗组 (对照组 ) ,观察组 10 2例 ,对照组 91例。观察组和对照组患者于疗前和疗后不同时期分别测定其血象、血钙、肝功能、血尿素氮 (BUN)、肌酐 (Cr)、尿N 乙酰 β D 氨基葡萄糖苷酶与肌酐比值 (NAG/C)和尿微量白蛋白与肌酐的比值 (MAB/C)。结果 观察组 2个疗程的第 2天 ,其MAB/C与疗前的差值低于对照组第2天的MAB/C与疗前的差值 ,经统计学检验 ,P <0 .0 5。观察组 2个疗程的第 4,6 ,10 ,14天的MAB/C与疗前的差值明显低于对照组的对应点与疗前的差值 ,经统计学检验 ,P <0 .0 1。观察组第 1个疗程第 4,6 ,10天及第 2个疗程的第 2 ,4,6 ,10 ,14天的NAG/C与疗前的差值明显低于对照组的对应各点与疗前的差值 ,经统计学检验 ,P <0 .0 1;观察组第 1个疗程第 2天和第 14天的NAG/C与疗前的差值亦低于对照组 ,经统计学检验 ,P <0...

目的 观察阿米福汀 (amifostin)保护肾脏免受顺铂 (DDP)损害的疗效及药物不良反应和安全性。方法  193例恶性肿瘤患者随机分为化疗加阿米福汀组 (观察组 )和单纯化疗组 (对照组 ) ,观察组 10 2例 ,对照组 91例。观察组和对照组患者于疗前和疗后不同时期分别测定其血象、血钙、肝功能、血尿素氮 (BUN)、肌酐 (Cr)、尿N 乙酰 β D 氨基葡萄糖苷酶与肌酐比值 (NAG/C)和尿微量白蛋白与肌酐的比值 (MAB/C)。结果 观察组 2个疗程的第 2天 ,其MAB/C与疗前的差值低于对照组第2天的MAB/C与疗前的差值 ,经统计学检验 ,P <0 .0 5。观察组 2个疗程的第 4,6 ,10 ,14天的MAB/C与疗前的差值明显低于对照组的对应点与疗前的差值 ,经统计学检验 ,P <0 .0 1。观察组第 1个疗程第 4,6 ,10天及第 2个疗程的第 2 ,4,6 ,10 ,14天的NAG/C与疗前的差值明显低于对照组的对应各点与疗前的差值 ,经统计学检验 ,P <0 .0 1;观察组第 1个疗程第 2天和第 14天的NAG/C与疗前的差值亦低于对照组 ,经统计学检验 ,P <0 .0 5。结论 阿米福汀可以明显降低观察组的MAC/C及NAG/C的量 ,表明阿米福汀对患者的肾脏功能有明显的保护作用 ,不受肿瘤类型的限制。对肺癌和卵巢癌的化疗疗效统计 ,与对照组比较 ,阿米福汀对观察组肿瘤无保护作用 (P

AIM: To study the antit umor effect of D-Glucosamine·HCl(D-GlcN·HCl) in tumor-bearing mice by ig route. MET HOD:Weight of tumor,peripheral leckocyte count,WBC /RBC ratio of marr ow cell an d body weight were used as index which was observed to evaluate the antitumor ef fect of D- GlcN·HCl. RESULT: The results showed that tumor inhibitory r ate of D-GlcN·HCl(20,10 mg/kg) on S 180 reached 66 .7% and 57.1% respectively. It could obviously prolong the survival days of mice with Heps. Surviva l p rolong rate...

AIM: To study the antit umor effect of D-Glucosamine·HCl(D-GlcN·HCl) in tumor-bearing mice by ig route. MET HOD:Weight of tumor,peripheral leckocyte count,WBC /RBC ratio of marr ow cell an d body weight were used as index which was observed to evaluate the antitumor ef fect of D- GlcN·HCl. RESULT: The results showed that tumor inhibitory r ate of D-GlcN·HCl(20,10 mg/kg) on S 180 reached 66 .7% and 57.1% respectively. It could obviously prolong the survival days of mice with Heps. Surviva l p rolong rate of Heps-bearing mice reached 208.2% and 133.7% respectively by i g D- GlcN·HCl(20,10 mg/kg). It also had good inhibitory action of on the tumor wei ght of the mice with EC and had no inhibitory effect on peripheral leukocyte,WB C/RBC ratio of bone marrow and weights of tumor-bearing mice. CONCLUS IO N: This study showed that the inhibitory effect of D-GlcN·HCl on S 180 ,Heps and EC in mice was remarkable, and it had no obvious inhib itory a ction on peripheral leukocyte,WBC/RBC ratio of bone marrow and weights of tumor -bearing mice.

目的 :研究D 氨基葡萄糖盐酸盐灌胃给药 (ig)对荷瘤小鼠的抗肿瘤作用 ,考察该药对荷瘤小鼠的白细胞生成和体重有无抑制作用。方法 :采用抗移植性肿瘤实验方法 ,检测受试药物对荷瘤小鼠的瘤重、生命延长率、外周血白细胞总数、骨髓粒细胞与红细胞比值及体重的影响。结果 :D 氨基葡萄糖盐酸盐 2 0 ,10mg/kg连续给药 10d对小鼠移植肉瘤 180 (S1 80 )的肿瘤抑制率分别为 66 7%和 57 1% ;对肝癌腹水瘤 (Heps)小鼠的生命延长率分别为 2 0 8 2 %和 13 3 7% ;该药 2 0mg/kg对小鼠移植的艾氏腹水实体瘤 (EC)瘤重有显著抑制 (P <0 0 5)作用 ,10mg/kg也有一定的抑制作用 ,但与对照组比较无显著差异。高、低剂量对该模型小鼠外周血白细胞、骨髓粒细胞与红细胞比值无明显抑制作用。该药对荷瘤小鼠体重无明显影响。结论 :D 氨基葡萄糖对小鼠移植肉瘤 180 (S1 80 )、肝癌腹水瘤 (Heps)、EC腹水实体瘤有显著的抑制作用 ,该抑瘤作用属首次发现。但该药对EC腹水实体瘤小鼠白细胞生成和荷瘤小鼠体重无明显抑制作用。

AIM: To study the in vitro inhibitory effect of amino-D-glu-cose derivative on the proliferation of the gastric carcinoma cell line SGC-7901. METHODS: Cell growth was measured by MTT colorimet-ric assay. DNA content was detected by flow cytometer (FCM). The morphological changes of apoptotic cells were evaluated by transmission electronic microscopy. CD44 expression was analyzed by immunohistochemistry. RESULTS: Amino-D-glucose derivative inhibited SGC-7901 cell in a time- and dose-dependent manner. After treatment,...

AIM: To study the in vitro inhibitory effect of amino-D-glu-cose derivative on the proliferation of the gastric carcinoma cell line SGC-7901. METHODS: Cell growth was measured by MTT colorimet-ric assay. DNA content was detected by flow cytometer (FCM). The morphological changes of apoptotic cells were evaluated by transmission electronic microscopy. CD44 expression was analyzed by immunohistochemistry. RESULTS: Amino-D-glucose derivative inhibited SGC-7901 cell in a time- and dose-dependent manner. After treatment, apoptosis peak was demonstrated by FCM, and apoptotic morphological changes were observed under microscope. Immunohistochemist and image analysis showed that expression of CD44 was downregulated (216.5±7.0 vs 190.0±14.2, P= 0.000). CONCLUSION: Amino-D-glucose derivative can induce SGC -7901 cell apoptosis, inhibit the cancer proliferation and downregulate expression of CD44 expression.

目的:观察D-氨基葡萄糖衍生物体外对人胃癌SGC- 7901细胞增生的影响,探讨其可能作用机制. 方法:采用MTT法,筛选药物作用最佳浓度.用流式细胞仪分析诱导凋亡前后的细胞DNA含量,透射电镜观察凋亡细胞的超微结构.免疫组化测定CD44表达. 结果:D-氨基葡萄糖衍生物能明显抑制胃癌细胞的增长(P<0.01),MTT法显示抑制程度具有时间和剂量效应关系,统计组间比较差异有显著性(P<0.01);流式细胞仪分析可见亚二倍体(Sub-G1)凋亡峰;电镜观察到凋亡细胞的典型变化,免疫组化及光密度检测示CD44表达下降(216.5±7.0 vs 190.0±14.2,P=0.000). 结论:D-氨基葡萄糖衍生物通过诱导肿瘤细胞凋亡而抑制人胃癌SGC-7901细胞增生,同时还有下调CD44的作用.

 
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