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作 者:黄力毅[1] 玉艳红[1] 宣伟军[2] 吴继周[1] 黄璐[1]
机构地区:[1]广西医科大学第一附属医院,广西南宁530021 [2]广西中医学院,广西南宁530001
出 处:《中华医院感染学杂志》2007年第11期1321-1324,共4页Chinese Journal of Nosocomiology
基 金:广西科学基金项目(桂科自0339050);广西卫生厅课题(桂卫Z2004127)
摘 要:目的探讨慢性肝病患者乙型肝炎病毒C基因启动子变异(HBV BCP)与血清白细胞介素10(IL-10)、12(IL-12)、肿瘤坏死因子α(TNF-α)、γ-干扰素(IFN-γ)及病毒含量(HBV DNA)的关系。方法采用PCR微板核酸杂交结合ELISA检测显示技术,对176例HBV慢性感染者(慢性乙型病毒性肝炎轻、中、重度,肝炎肝硬化,慢性重型肝炎和原发性肝癌)血清进行检测HBV BCP区核苷酸(nt)1762碱基A→T和1764碱基G→A联合突变;采用双抗体夹心ELISA检测技术,检测患者血清细胞因子(IL-10、IL-12、TNF-α和IFN-γ)水平。结果HBVBCP变异阳性组、阴性组间对细胞因子(IL-10、IL-12、TNF-α和IFN-γ)及HBV DNA复制水平的影响差异有统计学意义(P<0.05),BCP变异阳性组的血清IL-10(80.96±30.86vs72.11±24.19 mg/L)I、L-12(41.33±15.10vs35.98±14.47 mg/L)、TNF-α(56.04±27.05vs38.01±10.49 mg/L)、IFN-γ(19.81±12.29vs16.55±8.99mg/L)和HBV DNA(108.2478±0.9826vs105.8876±1.4822拷贝/ml)的水平明显高于BCP变异阴性组。结论HBV BCP变异可导致血清IL-10I、L-12、TNF-α、IFN-γ和病毒复制水平增高。OBJECTIVE To study the correlation of hepalitis B virus (HBV)basic core promoter (BCP) mutation with the interleukins (IL-10,IL-12), tumor necrosis factor (TNF)-α, interferon (IFN)-γ, as well as HBV DNA contents in patients with chronic hepatitis B virus infection. METHODS (1) Project subject: 176 patients [chronic hepatitis B with mild, moderate and severe degree; liver cirrhosis, chronic fulminant and hepatocellular carcinoma (HCC)] with chronic hepatitis B virus infection were studied. (2) Project methods: (I) The A to T mutation at nucleotide 1762 and G to A mutation at nucleotide 1734 were determined by the method of polymerase chain reaction (PCR) microplate hybridization ELISA in these patients. ② The serum cytokines(IL-10, IL-12, TNF-α and IFN-γ) of these patients were measured by specific-ELISA. RESULTS The serum levels of cytokinesCIL-10 (80.96ff=30.86 vs 72.11±24.19 mg/L), IL-12(41.33±15.10 vs 35.98±14.47 mg/L), TNF-α(56.04ff=27.05 vs 38.01 ±=10.49 mg/L), IFN-γ(19.81±12.29 vs 16. 155±8.99 mg/L)and HBV DNA contents (108. 2478 ± 0. 9826 vs 105. 8876±1. 4822copies/ml) in BCP mutant group were significantly higher than that in non-mutant group (P〈0.05). CONCLUSIONS The mutants in HBV BCP might enhance the serum levels of cytokines (IL-10, IL-12, TNF-a and IFN-α), which could lead to the replication of HBV DNA.
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