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hepatitis b hb patients
相关语句
  相似匹配句对
     Ischaemia hepatitis
     缺血性肝炎
短句来源
     Hepatitis B Virus
     乙型肝炎病毒
短句来源
     HEPATITIS A
     A型肝炎
短句来源
     Hepatitis B vaccination.
     乙型肝炎疫苗免疫
短句来源
     (4) serious hepatitis.
     (4)部分重症肝炎。
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Objective:To study the associations of hepatitis B virus DNA ( HBV-DNA),cardiac troponin I(cTn I)and abnormal of electrocardiogram ( ECG) in hepatitis B ( HB) patients and to investigate the mechanism of myocardium hurt caused by HBV. Methods: Clinical data including Serum HBV-DNA,cTn I and abnormal of ECG in 36 cases of HB patients were collected and analyzed. . Results: Level of HBV-DNA in acute hepatitis was higher than that of chronic hepatitis....

Objective:To study the associations of hepatitis B virus DNA ( HBV-DNA),cardiac troponin I(cTn I)and abnormal of electrocardiogram ( ECG) in hepatitis B ( HB) patients and to investigate the mechanism of myocardium hurt caused by HBV. Methods: Clinical data including Serum HBV-DNA,cTn I and abnormal of ECG in 36 cases of HB patients were collected and analyzed. . Results: Level of HBV-DNA in acute hepatitis was higher than that of chronic hepatitis. The cTn I positive rate of different clinical types were different, total positive rate is 22. 2%( 8/36 ). Acute hepatitis is 50%(2 4). Inchronic hepatitis,sever is 25% (1/4) middle is 23. 4%(3/13) liver cirrhosis is 14. 2% (1/7) and mild is 12. 1 %(1/8). Positive rate in acute group was obviously higher than that of other groupst P<(>. 01). There were significant differences among chronic middle.sever and chronic mild, liver cirrhosis groups ( P<0. 01 ). but no difference between chronic mild and liver cirrhosis. chronic middle and sever, exist 36. 1 %(13/36) of HB had abnormal ECG. All four acute hepatitis patients had abnormal ECG. which was obviously higher than other groups(P<0. 01). Conclusion: 1 ) The positive rate of cTn 1 and abnormal of ECG is different. cTn I might be a sensitive and specific marker for estimating myocardium hurt caused by HBV:2 ) Myocardium hurt might he due to direct action of HBV in acute hepatitis,and auto-immune action caused by HBV in chronic hepatitis B.

目的:研究乙型肝炎(HB)病人血清乙型肝炎病毒脱氧核糖核酸(HBV-DNA)、肌钙蛋白Ⅰ(cTnⅠ)与心电图(ECG)改变三者的关系,探讨HBV对心肌损伤的机理。方法:收集36例HB的临床资料及ECG的变化,并检测血清HBV-DNA、cTn Ⅰ含量。结果:急性肝炎患者血清HBV-DNA含量明显高于慢性肝炎;各型肝炎cTn Ⅰ的阳性率不等,总阳性率为22.2%(8 36)。急性、慢性重度、慢性中度、肝硬化、慢性轻度的阳性率分别为50%(2/4)、25%(1/4)、23.4%(3、1 3)、14.2%、(1 7)、12.1%(1/8),急性肝炎明显高于其它各组(P<0.01)。慢性中度、莺度与慢性轻度、肝硬化之间也有显著差异(P<0.01)。慢性轻度与肝硬化之间、慢性中度与慢性重度之间无显著差异。HB病人ECG异常发生率为36.1%(13/36),4例急性肝炎患者均有过ECG改变,显著高于其它各组(P<0.01)。结论:1)cTn Ⅰ阳性与ECG异常表现并不一致,cTn Ⅰ可以作为判断HB心肌损伤的敏感和特异性指标;2)在HB急性期的心肌损伤可能是HBV直接作用,慢性HB心肌损伤是自身免疫作用的结果。

Objective To study the relationship between vascular endothelial growth factor (VEGF) expression and proliferation of hepatic blood vessel and fibrosis in hepatitis B (HB) patients. Methods The total RNA of VEGF was extracted from human liver tissues, and VEGF mRNA probe was acquired by RT-PCR. It was then labeled on hepatic tissues of 160 patients with HB and 10 healthy individuals (control group). Immunohistochemistry of VEGF was performed at the same time. Results The results...

Objective To study the relationship between vascular endothelial growth factor (VEGF) expression and proliferation of hepatic blood vessel and fibrosis in hepatitis B (HB) patients. Methods The total RNA of VEGF was extracted from human liver tissues, and VEGF mRNA probe was acquired by RT-PCR. It was then labeled on hepatic tissues of 160 patients with HB and 10 healthy individuals (control group). Immunohistochemistry of VEGF was performed at the same time. Results The results of hybridization in situ showed that VEGF mRNA was negative in the control group. While in the HB groups, VEGF mRNA was located in the hepatic sinusoids, Disse′s space and hepatocyte cytoplast around the dilated sinusoids. Immunohistochemistry showed that VEGF was expressed in three patterns: the cytoplasm, sinusoid membrane, and sinusoidal endothelium. The expression strength and distribution range of VEGF were closely related with the grading and staging of HB, hepatic vascular inflammation, destruction, obstruction, proliferation and fibrosis. There was remarkable difference between different liver pathological changes (P<0.01). Conclusion Up-expression of VEGF in liver tissues of HB can promote hepatic vascular proliferation and liver sinusoidal capillarization.

目的研究血管内皮生长因子(VEGF)表达与乙型肝炎(HB)肝血管增生及肝纤维化的关系。方法从人肝组织提取VEGF总RNA,经RTPCR扩增取得VEGFmRNA基因探针,对160例HB肝组织(HB组)及10例正常肝组织(对照组)的VEGFmRNA作了定位观察,同时对VEGF表达变化进行了检测。结果原位杂交显示,对照组VEGFmRNA阴性。HB组VEGFmRNA定位于肝窦、狄氏腔及扩张的肝窦周围肝细胞胞质;而VEGF则有胞质、膜窦、窦内皮3种形态,其表达强度、分布范围与HB分级分期、肝血管炎症、破坏、阻塞、增生及纤维化呈同步关系,不同肝病变之间差异显著(P<0.01)。结论肝组织VEGF表达增强可促进肝血管生成及肝窦毛细血管化。

Objective To assess the association of polymorphisms of human leucocyte antigen (HLA) -DRB1 and -DQA1 region allele with outcomes of hepatitis B virus(HBV) infection in Han population of north China. Methods A total of 207 chronic hepatitis B(HB) patients,212 chronic asymptomatic HBV carriers (HBV carrier),and 148 self-limited HBV infection were recruited to examine the association between gene polymorphisms and outcomes of HBV infection. Polymerase chain reaction-sequence...

Objective To assess the association of polymorphisms of human leucocyte antigen (HLA) -DRB1 and -DQA1 region allele with outcomes of hepatitis B virus(HBV) infection in Han population of north China. Methods A total of 207 chronic hepatitis B(HB) patients,212 chronic asymptomatic HBV carriers (HBV carrier),and 148 self-limited HBV infection were recruited to examine the association between gene polymorphisms and outcomes of HBV infection. Polymerase chain reaction-sequence specific primers (PCR-SSP) technique was used to genotype HLA-DRB1 and HLA-DQA1 loci. Results The frequency of HLA-DQA1*0301 in chronic HB patients (14.81%) was significantly lower than those in HBV carriers (25.24%) and self-limited HBV infection subjects (25.00%) (P_ c =0.002; P_ c =0.007). The frequency of HLA-DQA1*0102 in self-limited HBV infection subjects (8.78%) was significantly higher than those in chronic HB patients (2.18%) and HBV carriers (1.89%) (P_ c =0.000; P_ c =0.000). In addition,the frequency of HLA-DQA1*0302 in self-limited HBV infection subjects (4.05%) was significantly lower than that in chronic HB patients (11.41%) (P_ c =0.005). HLA-DQA1*0302 was demonstrated to be risk factors of chronic HBV (OR=3.913,P=0.0006),while HLA-DQA1*0102 and HLA-DQA1*0301 to be protective factors against chronic HBV (OR=0.200,P=0.0004; OR=0.258,P=0.0000) after age,sex,smoking and drinking were adjusted by logistic regression analysis. There were positive interactions between drinking and HLA-DQA1*0102 interaction index (Ⅱ)=1.49or HLA-DQA1*0302 (Ⅱ=12.12). There were negative interactions between drinking and HLA-DQA1*0301 (Ⅱ=0.78) Conclusions The subjects with HLA-DQA1*0302 allele have an increased risk to chronic HB infection compared with other subjects without this allele,while HLA-DQA1*0301 and HLA-DQA1*0102 are associated with HBV clearence. Gene-environment interaction can affect the outcomes of HBV infection.

目的探讨中国北方汉族人群白细胞抗原(HLA)DRB1及DQA1区等位基因多态性与乙型肝炎病毒(HBV)感染不同结局的关系,分析基因—环境交互在慢性乙肝发生中的作用。方法采用病例—对照研究(慢性乙肝患者207人,HBV携带者212人,自限性HBV感染者148人)方法,比较3组人群检测的HLA等位基因频率并应用交互相乘模型分析基因—环境交互作用。结果慢性乙肝组HLA-DQA1*0301等位基因频率(14·81%)显著低于HBV携带组(25·24%)和自限性HBV感染组(25·00%)(Pc=0·002;Pc=0·007);自限性HBV感染组HLA-DQA1*0102等位基因频率(8·78%)显著高于HBV携带组(1·89%)和慢性乙肝组(2·18%)(Pc=0·000;Pc=0·000);自限性HBV感染组HLA-DQA1*0302等位基因频率(4·05%)显著低于慢性乙肝组(11·41%)(Pc=0·005)。经多元logistic回归分析调整年龄、性别、吸烟和饮酒的混杂效应后,HLA-DQA1*0302仍是发展为慢性乙肝的危险因素(OR=3·913,P=0·0006),HLA-DQA1*0102和HLA-DQ...

目的探讨中国北方汉族人群白细胞抗原(HLA)DRB1及DQA1区等位基因多态性与乙型肝炎病毒(HBV)感染不同结局的关系,分析基因—环境交互在慢性乙肝发生中的作用。方法采用病例—对照研究(慢性乙肝患者207人,HBV携带者212人,自限性HBV感染者148人)方法,比较3组人群检测的HLA等位基因频率并应用交互相乘模型分析基因—环境交互作用。结果慢性乙肝组HLA-DQA1*0301等位基因频率(14·81%)显著低于HBV携带组(25·24%)和自限性HBV感染组(25·00%)(Pc=0·002;Pc=0·007);自限性HBV感染组HLA-DQA1*0102等位基因频率(8·78%)显著高于HBV携带组(1·89%)和慢性乙肝组(2·18%)(Pc=0·000;Pc=0·000);自限性HBV感染组HLA-DQA1*0302等位基因频率(4·05%)显著低于慢性乙肝组(11·41%)(Pc=0·005)。经多元logistic回归分析调整年龄、性别、吸烟和饮酒的混杂效应后,HLA-DQA1*0302仍是发展为慢性乙肝的危险因素(OR=3·913,P=0·0006),HLA-DQA1*0102和HLA-DQA1*0301是HBV感染后的保护因素(OR=0·200,P=0·0004;OR=0·258,P=0·0000)。饮酒与HLA-DQA1*0102[交互指数(Ⅱ)=1·49]、HLA-DQA1*0302(Ⅱ=12·12)在慢性乙肝的发生中可能存在正交互作用,与DQA1*0301存在负交互作用(Ⅱ=0·78)。结论携带HLA-DQA1*0302等位基因者感染HBV后可能增加慢性乙肝发生的风险,而携带HLA-DQA1*0301和HLA-DQA1*0102者可能降低慢性乙肝发生的风险;基因—环境交互作用可能影响HBV感染的结局。

 
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