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新生儿接种乙型肝炎疫苗的远期效果观察陆建华,朱源荣,倪正平,黄飞,陈建国一、疫苗接种:我们对1984年12月至1985年12月出生的婴儿,按0、1、6全程免疫程序接种merck乙型肝炎疫苗。3岁时再随机分成0、5、10ug3个加强接种亚组。二、随访与... 相似文献
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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. 相似文献
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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. 相似文献
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乙型肝炎病毒感染与肝癌发生的31年随访研究 总被引:1,自引:0,他引:1
目的 研究乙型肝炎病毒(HBV)与肝癌发生的关系,评价HBsAg长期携带者发生肝癌的结局.方法 利用1976年建立的启东某社区15岁以上自然人群队列[血清筛检确定HBsAg、抗-HBs及丙氨酸转氨酶(ALT),并进行前瞻随访],该数据库与人群癌症登记资料、居民病伤死因资料链接核实,分析1977年1月至2007年12月12351名人群中肝癌等肿瘤的发生情况.结果 队列观察总人年数为355 305.0.HBsAg携带者中发生肝癌173例,发生率为361.55/10万;HBsAg非携带者发生肝癌95例,发生率为30.90/10万,两组比较RR=11.70(95%CI:9.06~15.19);其中男性和女性HBsAg携带者的RR值分别为12.30和10.46.两性各年龄组HBsAg携带者的肝癌发生率均高于非携带者.若以女性非携带者肝癌的发生率为1,则男性非携带者、女性携带者、男性携带者的RR值分别为3.07、10.46和37.76;该四组人群在31年中肝癌发生的累积率分别为0.86%、2.73%、10.22%和34.19%.非条件logistic回归模型分析显示性别(男性)、年龄、HBsAg、ALT为肝癌发生的显著影响因素,抗-HBs为保护因素.HBsAg携带与其他部位癌的发生未见有联系.结论 证实启东自然人群中HBsAg携带与肝癌发生的因果联系;针对HBV感染而采取干预措施是现场肝癌防治的重点. 相似文献
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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. 相似文献
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