乙型肝炎病毒感染标志物与肝癌关系的前瞻研究

目的:探讨患者携带乙型肝炎表面抗原(HBsAg)与发生肝癌的关系.方法:在肝癌高发的启东地区,对515例20～60岁男性HBsAg携带者作乙型肝炎病毒感染标志物HBsAg、HBsAb、HBeAg、HBeAb、HBcAb(HBVM 1、2、3、4、5)检测,进行连续20年的队列研究.结果:队列发生肝癌111例,肝癌发生率为1 340.90/10万人年,肝癌发生中位年龄为43岁,平均生存期为1年3个月,41-50岁年龄组的肝癌发生率高于其他年龄组(P＜0.05).队列HBVM以15、135、145为主要模式,分别占队列的38.83%(200/515)、15.92%(82/515)、44.08%(227/515),此3种模式的肝癌发生率分别为1 433.69/10万人年、2 284.71/10万人年、984.10/10万人年,135模式显著高于145模式(P＜0.01).肝癌中15、135、145模式分别占39.64%(44/111)、23.42%(26/111)、35.14%(39/111),15模式显著多于135模式(P＜0.01).肝硬化死亡率分别为195.50/10万人年、966.61/10万人年和277.57/10万人年,135模式显著高于15、145模式(P＜0.01).结论:HBsAg携带者是发生肝癌的高危人群,对其进行定期随访,能早期发现肝癌患者,给予早期治疗后可延长肝癌患者生存期.HBV复制程度与肝癌发生有关,通过抗病毒治疗等手段可能会延缓或解除肝癌的发生.     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.     

乙肝疫苗母-婴阻断失败者病毒全基因变异分析

Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants.     

外伤性白内障后房型人工晶体植入

作者自1988年开展后房型人工晶体植入术。本文报告了近期外伤性白内障后房型人工晶体植入4例4眼,最大年龄32岁.最小年龄12岁.均男性。术后视力恢复均良好.最佳的达1.2.文中探讨了手术适应症,手术方法及并发症的处理.并认为后房型人工晶体植入应用于外伤性白内障手术可以给患者恢复良好的视力.有利于立体视功能的恢复,使患者重返工作岗位为四化多作贡献。     

我国肝癌发病趋势及展望

原发性肝细胞癌(下称肝癌)是世界上最常见的恶性肿瘤之一.据报道,肝癌发病位居全球所有恶性肿瘤发病的第6位,而肝癌死亡则居第3位.     

S100A4蛋白在肝癌组织中的表达及临床意义

目的:探讨SIOOA4蛋白在肝细胞癌、肝硬化、癌旁组织及正常肝组织中的表达及临床意义.方法:用组织芯片技术结合免疫组织化学法检测S100A4蛋白在肝癌相关组织中的表达差异,采用统计学方法分析其表达差异的临床意义.结果:免疫组织化学检测发现,S100A4蛋白在人原发性肝细胞癌、硬化肝组织、癌旁肝组织中表达较高,在正常肝组织中表达则很低,表达阳性率分别为70.2%、54.4%、41.7%和0.0%;统计学分析结果表明,S100A4蛋白表达影响肝癌患者的术后生存期,低表达患者的生存期比高表达患者延长.结论:S100A4蛋白在肝癌及相关组织中的表达率依次为,肝细胞癌＞癌旁肝＞肝硬化＞正常肝,在非微血管侵袭肝癌患者中S100A4阳性表达可明显降低其术后生存率.     

小儿后房人工晶状体植入临床观察

随着现代显微手术的开展和后房型人工晶状体植入术的普及 ,为少年儿童白内障的治疗和视力的复明开辟了广阔的前景。现将我院儿童白内障摘出后房型人工晶状体植入的总结报告如下。临床资料(一 )一般资料 :1989年 5月至 2 0 0 1年 5月 ,共施行儿童白内障摘出和人工晶状体植入术 3 8例 46眼。男 2 5例 ,女 13例。年龄最小 10月 ,最大 14岁。其中先天性白内障 14例 2 2眼 ,外伤性白内障 2 4例 2 4眼。外伤性白内障 2 0眼一期植入后房型人工晶状体 ,4眼二期植入后房型人工晶状体 ;先天性白内障中 2 0眼一期植入后房型人工晶状体 ,2眼 (均为双眼白…     

肿瘤高发现场工作评估问题探讨

阐述了肿瘤高发现场工作评估的重要性,探讨了评估的主要形式、评估内容、评估方法、评估原则等,对开展评估工作具有重要参考价值.     

启东乙肝疫苗干预研究随访人群中慢性乙肝、肝硬化患病的危险因素分析

目的 探索启东乙型肝炎疫苗(以下简称乙肝疫苗)干预研究人群患慢性乙型肝炎(以下简称慢乙肝)、肝硬化的危险因素.方法 采用分层随机抽样方法,于2013年1月～10月,在启东乙肝疫苗干预研究随访人群中抽取研究对象进行面对面问卷调查,调查内容包括人口社会学资料、个人及家族成员慢乙肝、肝硬化及肝癌史等;同时进行谷丙转氨酶(alanine aminotransferase,ALT)、乙型肝炎病毒(hepatitis B virus,HBV)感染血清学标志物检测及肝脏彩色超声检查.使用多因素Logistic回归分析乙肝疫苗干预研究随访人群罹患慢乙肝、肝硬化的危险因素.结果 疫苗组慢性乙型肝炎及肝硬化患病率均低于对照组;慢性乙型肝炎患者中男性、有肝癌家族史、新生儿期未接种乙肝疫苗和出生于1986年以前四个因素,调整后的0R(95％ CI)值分别为:3.60(2.04～6.34)、2.47(1.25 ～4.88)、2.68(1.57 ～4.56)和1.72(1.02～2.89).肝硬化患者中男性因素,调整后的0R(95％ CI)值为6.89(2.02 ～23.43).结论 启东新生儿接种乙肝疫苗能降低青年期罹患慢乙肝、肝硬化的风险,男性、肝癌家族史及出生于1986以前为慢性乙型肝炎的危险因素,男性亦为肝硬化的危险因素.