女性HBsAg携带者HBV五项标志物分析

<正> 本文对青壮年女性HBsAg携带者分别进行了为期5年和9年的随访观察,并对其HBV五项标志物的检出模式进行分析。 1 资料与方法 1.1对象:1985年及1989年临产妇共2253例。于产前采集血清检测HBsAg(R—PHA法),凡HBsAg≥1:8刘为阳性。于1994年底对HBsAg阳性者再次进行HBV五项标志物检测,分别称作5年组     

颈交感神经阻滞对放烧复合伤小鼠死亡率的影响及其可能的作用途径

背景:颈交感神经阻滞促进机体神经-内分泌-免疫系统等稳态的恢复,其能否抑制创伤后应激紊乱导致的内稳态失衡仍不明确。目的:观察颈交感神经阻滞对放烧复合伤小鼠死亡率的影响,探讨颈交感神经阻滞可否成为严重创伤后续损害简单有效的治疗手段。设计:随机分组设计,动物对照实验。单位:解放军广州军区广州总医院麻醉科。材料:实验于2004-02/2005-07在解放军第三军医大学复合伤研究所完成。选择昆明小鼠160只,随机抽签法分为对照组80只(仅对动物给予放烧复合伤,颈部注射生理盐水0.3mL)和颈交感神经阻滞组80只(对动物给予放烧复合伤,伤后给予颈交感神经阻滞,1次/d,连续14d)。方法:动物致伤方法:①放射损伤:60Coγ射线5Gy,照射距离1.5m,吸收剂量率(5.17～5.33)mGy/s,全身一次均匀照射。②烧伤:放射损伤后给予20g/L凝固汽油涂于背部燃烧8s造成15%总体表面积Ⅲ度烧伤(病理切片证实)。颈交感神经阻滞方法:对大鼠进行双侧颈交感神经阻滞,注射5g/L利多卡因0.2mL,注射后5min观察小鼠是否出现类似于霍纳综合征症状。主要观察指标:观察两组动物伤后2,5,7,10,15,20,30d死亡率及伤后7,14,21d外周血红细胞、白细胞、血小板计数的变化,另观察颈交感神经阻滞对放烧复合伤后3,6,14d血清肿瘤坏死因子α、白细胞介素1β、白细胞介素6的影响。结果:纳入动物160只,均进入结果分析。①与对照组比较,颈交感神经阻滞治疗使放烧复合伤后5,7,10,15,20,30d的死亡率显著降低犤对照组各时相点累计死亡率分别为8%,22%,32%,54%,74%,82%,90%;颈交感神经阻滞组分别为8%,14%,16%,22%,28%,34%,56%犦。②颈交感神经阻滞组伤后7,14,21d的血红细胞计数、血小板计数及白细胞计数与对照组比较显著增加犤以21d为例,血红细胞计数分别为23.21×1012L-1,14.58×1012L-1;血小板计数分别为16.87×1011L-1,12.57×1011L-1;白细胞计数分别为20.65×109L-1,14.58×109L-1犦。③颈交感神经阻滞组伤后3,6,14d的血清炎性细胞因子肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平与对照组比较显著下降犤以14d为例,肿瘤坏死因子α分别为189,365ng/L;白细胞介素1β分别为14,23ng/L;白细胞介素6分别为70,132ng/L犦。结论:颈交感神经阻滞显著降低放烧复合伤动物的死亡率,是治疗严重创伤简单而有效的手段;颈交感神经阻滞降低放烧复合伤动物死亡率的机制可能是通过促进造血功能的恢复、抑制过度的炎性反应而实现的。     

揭开学生力不从心之谜

笔者在心理咨询中常常与来访的学生和家长说，对于上进心很强，学习成绩忧秀的学生不急需我们的帮助．对于完全没有上进要求．学习又很差的学生不在我们的帮助范围：而对于有一定的上进愿望，但总是处于心有余而力不足的状态，学习成绩落后或明显退步的学生我们可以考虑从专业的心理领域给予一些有效的支持和处理。     

糖尿病伴发抑郁症中医证治体会

糖尿病伴发抑郁症临床并不罕见,笔者从事糖尿病临床工作多年,深刻体会到中医学对此有丰富的治疗经验,只要掌握诊断本病的技巧,并把握好用药指征,对本病的治疗确能获得满意效果。1明确诊断本病属中医学情志致病的范畴,其中包括郁证、痞证、梅核气、百合病等多种综合性疾病。现代医学对本病的诊断概念十分明确:即糖尿病患者心境低落持续2周以上,诊断本病就成立。概念虽如此明确,而确诊并非如此容易,临床医师常会忽略或不能识别糖尿病患者同时伴有抑郁障碍,视抑郁症而不见的现象屡见不鲜,其原因是抑郁症有其隐闭性,抑郁症患者主诉症状时往往不…     

肝癌高发区HBsAg阳性青少年血清透明质酸、Ⅳ型胶原检测结果分析

目的肝癌高发区HBsAg阳性及阴性青少年血清透明质酸(HA)、Ⅳ型胶原(Ⅳ-C)水平比较分析.方法 用放免法测定144例16岁和19岁HBsAg阳性及阴性青少年血清HA、Ⅳ-C.结果 HA和Ⅳ-C在16岁阳性组及16岁阴性组中的异常率和均值都无显著差异.但19岁阳性组HA的异常率(68.2%)和均值[(105.0±41.3)ng/ml]明显高于19岁阴性组[27.3%和(58±21.5)ng/ml];19岁阳性组和阴性组的Ⅳ-C异常率和均值无显著差异.结论 HA可作为初步反映年龄大于16岁青年的肝纤维化随访检测指标之一.     

拿什么拯救你我的爱情

小敏坐在心理咨询中心的沙发上,无奈地把头埋在手里。只有在这里,她才能放松自己一直绷紧的神经,让自己宣泄出那焦虑、痛苦、怨恨交织在一起的复杂感受。小敏是一个理性而又坚强的女孩,在咨询中虽     

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.     

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.