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i型前胶原
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  type i procollagen
    Objective In order to screen the new serum index in diagnosing hepatic fibrosis, We analyzed the change regularity of serum type I procollagen (PCI) in patients with hepatic fibrosis.
    目的 :探讨肝纤维化时血清I型前胶原 (PCI)变化规律 ,为肝纤维化的诊断筛选新的血清学指标。
短句来源
    Carboxy Terminal Peptide of Type I Procollagen and Epidermal Growth Factor in Patients with Different Viral Hepatitis
    病毒性肝炎患者I型前胶原羧基端肽及表皮生长因子评价
短句来源
  procollagen i
    After 6 weeks of treatment, the rats were killed and liver samples were obtained for observing the histopathological changes and investigating content of hydroxyproline(HYP) , the mRNA levels of procollagen I (procol-I) and tissue inhibitor of metalloproteinase-1(TIMP-1).
    6周后,处死大鼠,取肝组织进行病理学观察并测定肝组织匀浆中的羟脯氨酸(HYP)含量,检测I型前胶原mRNA(procol-ImRNA)和组织金属蛋白酶抑制因子1mRNA(TIMP-1mRNA)的表达水平。
短句来源
    Objective To study the molecular mechanism of fibrosis in the patients with severe viral hepatitis by detecting the expressions of procollagen I mRNA and platelet-derived growth factor-1 (PDGF-1) mRNA and type Ⅰ ,Ⅳ collagen.
    目的 了解重症病毒性肝炎患者肝组织I型前胶原mRNA、血小板衍生生长因子-1(PDGF-1)mRNA及Ⅰ、Ⅳ型胶原蛋白的表达情况,探讨重症病毒性肝炎纤维化发生的分子机制。
短句来源
    After 6 weeks of treatment, the rats were killed and liver samples were obtained for observing the histopathological changes and investingating liver content of hydroxyproline(HYP), The mRNA levels of procollagen I (procol-I) and tissue inhibitor of metalloproteinase-1(TIMP-1). Serum biochemistry, including ALT, AST, TBIL, ALP, γ-GT as well as HA, LN were also analyzed.
    测定肝组织羟脯氨酸(HYP)含量。 检测I型前胶原(procol-I)mRNA和组织金属蛋白酶抑制因子I(TIMP-1)mRNA表达水平及血清透明质酸、层连蛋白、转氨酶、碱性磷酸酶、γ-谷氨酰转肽酶、胆红素水平。
短句来源
  “i型前胶原”译为未确定词的双语例句
    Results Human (α 1) Ⅲ procollagen mRNA expression in portal hypertensive patients were higher than control group(P<0.01), however, Human (α 1) I procollagen mRNA expression in portal hypertensive patients shows a non-significant difference pattern with control group(P>0.05).
    结果门脉高压症时脾静脉壁 (α1)Ⅲ型前胶原mRNA表达明显增高 (P <0 .0 1) ,但门脉高压症病人脾静脉壁 (α1)I型前胶原mRNA表达与非门脉高压症病人相比差异无显著性意义 (P >0 .0 5 )。
短句来源
    Study the Change Regularity of serum PCI in Patients with Hepatic Fibrosis
    肝纤维化时血清I型前胶原变化规律探讨
短句来源
    Methods The specimens of liver tissues in 20 cases of severe viral hepatitis and 6 cases without liver disease were detected for procollagen Ⅰ mRNA and PDGF-1 mRNA by situ hybridization, and for type Ⅰ , Ⅳcollagen by immunohistochemical staining. The total collagen was detected by Sirius red staining.
    方法 将重症病毒性肝炎肝组织标本20例,非肝病患者肝组织6例,用原位杂交法检测肝组织I型前胶原和PDGF-1 mRNA的表达,用免疫组化法观察肝组织Ⅰ、Ⅳ型胶原蛋白的沉积、分布和含量,用天狼红染色观察肝组织总的胶原含量。
短句来源
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  type i procollagen
Targeted inhibition of type I procollagen synthesis by antisense DNA oligonucleotides
      
Antisense DNA oligonucleotides directed against specific sequences within α1(I) and α2(I) mRNA of type I procollagen were complexed to a cell-specific carrier, and screened for their effectiveness in reducing α1(I) and α2(I) mRNA levels.
      
Osteocalcin, a biochemical marker for osteoblast activity, and the carboxy-terminal propeptide of type I procollagen (PICP), a marker of collagen formation, were slightly but not significantly higher in gastrectomy-treated patients.
      
Simultaneously, circulating carboxyterminal propeptide of type I procollagen (PICP) was released in the perfusion medium (threefold versus C).
      
Gene expression of type I procollagen was significantly greater in Group MH than in Group MC at 7?days postoperatively and was also significantly greater in Group AH than in Group AC at 28?days (P?>amp;lt;?0.05).
      
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  procollagen i
Procollagen Iα2 (COL1A2) mRNA levels were quantitated by (a) northern blot analysis and (b) reverse transcriptase polymerase chain reaction.
      
Active transforming growth factor-β1 activates the procollagen I promoter in patients with acute lung injury
      
Experimental tissue expansion induces changes in expression of procollagen I and III messenger RNA
      
Dermal procollagen I and procollagen III gene expression in response to tissue expansion was investigated by dot-blot analysis using digoxigenin-labeled RNA probes complementary to either human procollagen-al (I) mRNA or procollagen-a1 (III) mRNA.
      
In response to the trauma of surgery, procollagen I and III mRNA transcriptions were found to be decreased significantly within the first few days after implantation.
      
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Background/Aims: To study the effects of taurine on proliferation and collagen gene expression of rat lipocytes and hepatocytes in vitro. Methods: Rat lipocytes and hepatocytes were isolated and cultured, cell proliferation and collagen syntheses were assessed by mesuring the incorporation of 3H-TdR and 3H-proline: type Ⅰ and type Ⅲ procollagen mRXA levels were determinded by in situ hybridization technique. Results: Taurine (5-80mmol/L) markedly inhibited lipocyte. hepatocyte proliferation and collagen syntheses...

Background/Aims: To study the effects of taurine on proliferation and collagen gene expression of rat lipocytes and hepatocytes in vitro. Methods: Rat lipocytes and hepatocytes were isolated and cultured, cell proliferation and collagen syntheses were assessed by mesuring the incorporation of 3H-TdR and 3H-proline: type Ⅰ and type Ⅲ procollagen mRXA levels were determinded by in situ hybridization technique. Results: Taurine (5-80mmol/L) markedly inhibited lipocyte. hepatocyte proliferation and collagen syntheses in a dose- and time-dependent manner. 20mmol L taurine significantly suppressed the type Ⅰ and type Ⅲ procollagen mRNA expression. Conclusions: Taurine has an antifibrotic effect and it could be of clinical significance and prospective for application in liver fibrosis.

目的:研究牛磺酸对大鼠贮脂细胞、肝细胞增殖及胶原基因表达的影响,为应用牛磺酸防治肝纤维化提供实验依据。方法:分离、培养大鼠贮脂细咆和肝细胞:采用~3H-胸腺嘧啶和~3H-脯氨酸掺入测定细胞增殖及胶原合成:用原位杂交检测I、Ⅲ型前胶原mRNA含量:结果:在5~80mmol/L浓度范围内。牛磺酸能显著抑制贮脂细咆、肝细胞的增殖及胶原合成,并呈时间、剂量依赖性关系:20mmol/L牛磺酸可显著抑制I、Ⅲ型前胶原mRNA的表达。结论:牛磺酸在体外具有抗肝纤维化作用,其对于防治肝纤维化可能有一定的临床意义和应用前景。

Background Aims: To observe the effect of glycyrrhetinic acid on proliferation, expression of procollagen type I Ⅲ procollagen mRNA and desposition of collagen type I Ⅲ in fibrotic liver of rat. Methods: The liver fibrosis model of rat was induced by CCl4. The rats was classified as normal control group, model control group and glycyrrhetinic acid treated group. Each group contained early, middle, late stage subgroup. After using drugs for 2, 6 and 9 weeks, the rats were killed respectivly. The Ito cells were...

Background Aims: To observe the effect of glycyrrhetinic acid on proliferation, expression of procollagen type I Ⅲ procollagen mRNA and desposition of collagen type I Ⅲ in fibrotic liver of rat. Methods: The liver fibrosis model of rat was induced by CCl4. The rats was classified as normal control group, model control group and glycyrrhetinic acid treated group. Each group contained early, middle, late stage subgroup. After using drugs for 2, 6 and 9 weeks, the rats were killed respectivly. The Ito cells were isolated from liver and cultured in DMEM medium. The effect of glycyrrhetinic acid on proliferation and collagen synthesis of Ito cells were determined with H-TDR. H-proline incoperating test After culturing two weeks, total RNA of Ito cells were etracted. The cDNA of procollagen typeI Ⅲ and interstitial collagenase were labeled using Dig High Primer technique. The level of procollagen type I Ⅲ and interstitial collagenase mRNA were measured by Northern blot. Desposition of collagen type I Ⅲ in fibrotic liver was evaluated with Dot blot. Results: At 4h, 24h, 48h, glycyrrhetinic acid inhibited the intake of H-TDR. H-prolme by Ito cells significantly. The inhibition rate was 15% , 21%,31%, respectively. When the concentration of glycyrrhetinic acid ≥0.125μg/ml, the intake of H-prohne by Ito cells was inhibited obviously. Only the concentration of glycyrrhetinic acid≥0.25μg ml. it showed inhibition to H-TDR The level of procollagen type I Ⅲ mRNA in glycyrrhetinic acid treated group was significantly lower than model controle group in all stage of fibrosis. At 2. 6 week groups, the desposition of collagen type I Ⅲ in glycyrrhetinic acid treated group was decreased significantly than model control group. No difference was found in 9 week groups. There was no difference in expression of collagenase mRNA between glycyrrhetinic acid treated group and model control group. Conclusions: Glycyrrhetimc acid inhibited the proliferation and collagen synthesis of Ito cells. Downregulated expression of procollagen type I Ⅲ mRNA and reduced desposition of collagen type I Ⅲ in fibrosis liver There was no effect of collagenase

目的:观察甘草酸对鼠肝纤维化时Ito。细胞增殖和IⅢ型前胶原mRNA表达和肝脏胶原沉积的影响。方法:以CCl_4复制肝纤维化模型,动物分组为止常对照组,模型对照组及甘草酸治疗组三个大组,各组又包括早(2周),中(6周)。晚(9周)期组,分别于用药后第2、6、9周处死动物,分离提取肝Ito细胞,培养两周后提取总RNA,以DIG High-Prlmer去标记IⅢ型前胶析和间质胶原酶cDNA探针,Northern杂交分析IⅢ型前胶原和间质胶原酶mRNA表达.鼠肝IⅢ型胶原沉积用Dot blot测定,用~3H-TDR~3H-脯氨酸观察甘草酸对培养的Ito细胞增殖和胶原合成的影响 结果,甘草酸对Ito细胞H-TDR和H-脯氨酸的掺入在4h、24h、48h与空白对照比呈明显抑制作用(P<0.05),其抑制率分别为15%、21%、31%,在甘草酸浓度≤0.125μg/ml时,对Ito细胞~3H-TDR掺入抑制不明显,而≥0.25μg/ml时呈现明显抑制作用(P<0.05),对H脯氨酸掺入,在甘草酸浓度≥0.125μg/ml时,则出现明显抑制作用(P<0.05),且随浓度增加而抑制作用加强。在鼠肝纤维化早、中、晚各期,模型对...

目的:观察甘草酸对鼠肝纤维化时Ito。细胞增殖和IⅢ型前胶原mRNA表达和肝脏胶原沉积的影响。方法:以CCl_4复制肝纤维化模型,动物分组为止常对照组,模型对照组及甘草酸治疗组三个大组,各组又包括早(2周),中(6周)。晚(9周)期组,分别于用药后第2、6、9周处死动物,分离提取肝Ito细胞,培养两周后提取总RNA,以DIG High-Prlmer去标记IⅢ型前胶析和间质胶原酶cDNA探针,Northern杂交分析IⅢ型前胶原和间质胶原酶mRNA表达.鼠肝IⅢ型胶原沉积用Dot blot测定,用~3H-TDR~3H-脯氨酸观察甘草酸对培养的Ito细胞增殖和胶原合成的影响 结果,甘草酸对Ito细胞H-TDR和H-脯氨酸的掺入在4h、24h、48h与空白对照比呈明显抑制作用(P<0.05),其抑制率分别为15%、21%、31%,在甘草酸浓度≤0.125μg/ml时,对Ito细胞~3H-TDR掺入抑制不明显,而≥0.25μg/ml时呈现明显抑制作用(P<0.05),对H脯氨酸掺入,在甘草酸浓度≥0.125μg/ml时,则出现明显抑制作用(P<0.05),且随浓度增加而抑制作用加强。在鼠肝纤维化早、中、晚各期,模型对照组Ito细胞IⅢ型前胶原mRNA表达均高于正常对照组(P<0.05),甘草酸组各期Ito细胞IⅢ型前胶原mRNA表达与模型对照组比均显著降低(P<0.05).Ito细胞间质胶原酶mRNA表达.在早、中期模型对照组均高于正常对照组(P<0.05

Objective In order to screen the new serum index in diagnosing hepatic fibrosis, We analyzed the change regularity of serum type I procollagen (PCI) in patients with hepatic fibrosis. Methods It was done examining the specimens of hepatic biopsy by H E staining, and measuring serum PCI by radioimmunoimaging. Results Serum PCI is 79±14μg/L in I stage of fibrosis ,88±18μg/L in Ⅱ stage, 118±32μg/L in Ⅲ stage, and 129±31μg/L in Ⅳ stage. There is statistical difference between Ⅲ and Ⅳstage of fibrosis group and...

Objective In order to screen the new serum index in diagnosing hepatic fibrosis, We analyzed the change regularity of serum type I procollagen (PCI) in patients with hepatic fibrosis. Methods It was done examining the specimens of hepatic biopsy by H E staining, and measuring serum PCI by radioimmunoimaging. Results Serum PCI is 79±14μg/L in I stage of fibrosis ,88±18μg/L in Ⅱ stage, 118±32μg/L in Ⅲ stage, and 129±31μg/L in Ⅳ stage. There is statistical difference between Ⅲ and Ⅳstage of fibrosis group and healthy control group (P<0.05, P<0.01). Conclusion The results demonstrate that serum PCI levels markedly elevate in Ⅲ and Ⅳ stage of fibrosis, and serum PCI has an important value in differentiating cirrhosis from fibrosis.

目的 :探讨肝纤维化时血清I型前胶原 (PCI)变化规律 ,为肝纤维化的诊断筛选新的血清学指标。方法 :30例肝纤维化均经肝活检确诊 (H E染色 ,显微镜下分期 ) ,应用放免法测定血清PCI浓度。结果 :肝纤维化I和Ⅱ期PCI各为 79± 14μg/L、88± 18μg/L ,18例中阳性 4例 (2 2 2 % ) ;Ⅲ和Ⅳ期PCI分别为 118± 32 μg/L和 12 9±31μg/L ,12例中 11例阳性 (91 7% )。和正常人相比 ,肝纤维化Ⅰ和Ⅱ期PCI无差异 ,Ⅲ和Ⅳ期有显著性差异 (P <0 .0 5 ,P <0 .0 1)。结论 :PCI在肝纤维化早期升高不明显 ,晚期有显著增加 ,对是否演变成肝硬化有重要预测价值。

 
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