建立人微小病毒B19的PCR检测方法

人微小病毒Ｂ１９是微小病毒科中唯一能感染人的病毒。能够提供Ｂ１９抗原的病毒体外培养系统尚未建成，因此限制了血清学实验的开发和普及。为此作者建立起Ｂ１９病毒的ＰＣＲ检测方法。设计引物在表达外壳蛋白ＶＰ１基因区，扩增长度为４００ｂｐ。     

手术治疗Danis-Weber B型踝关节骨折

目的：探讨Danis-Weber B型踝关节骨折的手术治疗及围手术期处理方法.方法：本组41例Danis-Weber B型踝关节骨折,男28例,女13例;年龄18～70岁,平均37岁.所有患者均采用切开复位内固定治疗,手术标准是直视下解剖复位,且围手术期进行规范的处理方案.应用改良Baird和Jackson评分系统评定其疗效.结果：全部病例均获得随访,随访时间4～58个月,平均17个月.根据Baird和Jackson评分系统,优24例,良11例,可6例,优良率为85.4%.结论：Danis-WeberB型踝关节骨折手术治疗中,满意的骨折复位、稳定的内固定及恰当的围手术期治疗对提高复位质量,改善远期疗效具有较显著的临床意义.     

mPer2对小鼠B16黑色素瘤细胞增殖作用的影响

目的:研究mPer2对小鼠黑色素瘤细胞B16增殖作用的影响。方法:将构建好的mPer2全长表达质粒(pcDNA3.1-mPer2)转染入小鼠黑色素瘤细胞B16中,并以pcDNA3.1空质粒转染为对照,通过平板克隆形成实验和MTT法检测两组细胞的增殖情况。结果:平板克隆形成实验和MTT法检测结果均显示Period2转染组小鼠黑色素瘤细胞B16较空质粒对照组明显降低。结论:mPer2的高表达能显著性的抑制小鼠黑色素瘤细胞B16的生长。     

不同原料制备乙型肝炎病毒特异性转移因子的研究

目的　为临床治疗乙肝提供一种安全、有效的免疫调节剂。方法　用组织匀浆、反复冻融破碎细胞、透析灭活和过滤除菌等技术 ,获得乙型肝炎病毒特异性转移因子 (HBV STF) ;用Lowry法测多肽含量 ;用苔黑酚显色法测定核糖核酸 (RNA)含量 ,用氨基酸分析仪分析测定HBV STF的水解氨基酸总含量。结果　来源于HbsAg阳性胎盘和HbsAg阳性血液的多肽含量分别为 0 4 9± 0 0 14和 0 2 9± 0 0 13(P <0 0 1) ,RNA含量分别为 0 34± 0 0 10和 0 2 2± 0 0 0 8(P <0 0 1)氨基酸总含量为 198 6± 1 5 6 2和 12 3 4± 1 5 2 1(P <0 0 1)。结论　用HbsAg阳性胎盘制备的乙型肝炎病毒特异性转移因子质量优于HbsAg阳性血液。     

卡维地洛对高血压大鼠主动脉的保护作用

目的 :研究卡维地洛对核因子 κB(NF κB)、单核细胞趋化蛋白 1(MCP 1)在自发性高血压大鼠 (SHR)大血管中表达的影响 ,探讨其对血管保护的机制。方法 :18只雄性 12周龄SHR随机分为阳性组 ,卡维地洛组 ( 30mg/kg·d) ,美托洛尔组 ( 50mg/kg·d) ,灌喂 8周 ;另选同龄雄性WistarKyoto大鼠为阴性组 (n =6 )。用免疫组化法测各组主动脉NF κB、MCP 1的表达 ,ELISA法测血清MCP 1含量。结果 :与阴性组比较 ,阳性组主动脉组织中NF κB、MCP 1表达增加 (P<0 .0 1) ,且两者正相关 (r=0 .72 8,P <0 .0 1) ;血清MCP 1含量升高 1.6 4(P <0 .0 1)。 8周后 ,治疗组之间血压无明显差异 (P >0 .0 5) ,但卡维地洛更显著抑制NF -κB、MCP 1表达 (P <0 .0 5)。结论 :卡维地洛可能独立于降压外抑制NF κB的活化来调控MCP 1表达。     

前S1蛋白在HBV指标中的重要意义

前S1蛋白是HBV衣壳蛋白的一部分，存在于大分子表面抗原蛋白之中，它是乙肝早期诊断的敏感指标，也反映了乙肝病毒的复制和乙肝病情的活动。本文研究显示，162例非乙肝病人血清中前S1蛋白全部阴性；311例乙肝患者中，前S1蛋白阳性率为38．9％，其中急性乙肝93．8％，慢性活动性肝炎51．2％，在乙肝二对半检测模式中，大三阳中该指标阳性率87．1％，小三阳为32．1％。以HBV DNA检测为标准，前S1蛋白的灵敏度为94．1％等，假阴性5．9％，总符合率93．9％。     

Ectopic T cell receptor expression causes B cell immunodeficiency in transgenic mice

Mice expressing transgenic T cell receptors (TCR) are used to explore important questions in immunity. However, transgene expression may have unexpected effects. We previously reported a B cell immunodeficiency, comprising decreased B cell numbers and diminished antibody responses, in mice that express a transgenic TCR specific for nicotinic acetylcholine receptor; the mice were generated using cassette vectors designed specifically for transgenic TCR expression [see Kouskoff et al. J. Immunol. Methods 1995. 180: 273-280]. We now show data suggesting that this defect is due to the expression and accumulation of TCR alpha and beta chains inside B cells and induction of an endoplasmic reticulum stress response, causing apoptosis at the pre B-I and later B cell stage. Thus, inappropriate transgene expression can profoundly affect B cells, leading to a previously undescribed mechanism of immunodeficiency.     

A phenotypic study of B lymphocyte subpopulations in human bone marrow.

The regulatory mechanisms that monitor the size of the peripheral B cell pool and determine cell death or survival are poorly understood. In rodents B lymphopoiesis is maintained at a high rate throughout adult life, and under resting conditions there is little recruitment into the long-lived peripheral pool; it therefore follows that most newly formed B lymphocytes have a very short lifespan. The maturation stages of B lymphopoiesis in humans and in experimental mammals appear to be similar. We have determined the phenotype of sIgM- and sIgD-expressing cells from normal adult human bone-marrow and peripheral blood by dual immunofluorescence with an extensive panel of monoclonal antibodies representative of major B cell clusters, in order to identify antigenic differences that may play a regulatory role. Antibodies of the CD21, CD22 and CD9 clusters, the unclustered restricted B antibody 7-F-7 and anti-IgD were reactive with different proportions of sIgM+ cells in blood and bone marrow; 29.5% (range 5-60%) of sIgM+ cells in marrow were sIgD- and most of these cells were also CD21- and CD22-, thus defining a unique marrow population. However, newly formed and mature re-circulating cells comprising the sIgM+sIgD+ population could not be distinguished by the panel of antibodies.     

银杏内酯B对体外培养乳鼠心肌细胞氧化损伤的保护作用

目的探讨银杏内酯B对体外培养乳鼠心肌细胞氧化损伤的保护作用及其机制.方法利用低浓度过氧化氢诱导原代培养乳鼠心肌细胞氧化损伤为模型,通过电镜观察细胞超微结构,以及培养介质中LDH活力,MDA含量,心肌细胞内Na -K -ATPase,GSH-PX活力的改变,来评价银杏内酯B对心肌细胞的保护作用,并探讨其机制.结果过氧化氢对心肌细胞有显著的损伤作用.银杏内酯B可使培养介质中的LDH和MDA水平显著下降,细胞内Na -K -ATPase,GSH-PX活力显著提高,同时细胞超微结构得到改普.结论银杏内酯B对过氧化氢致心肌细胞损伤有保护作用,机理与其抑制脂质过氧化和提高细胞内钠钾泵活力的作用有关.     

Decreased perforin and granzyme B expression in senescent HIV-1-specific cytotoxic T lymphocytes

Cytotoxic T lymphocyte (CTL) senescence may be an important mechanism of immune failure in HIV-1 infection. We find that senescence of HIV-1-specific CTL clones causes loss of killing activity, preventable by transduction with telomerase. Furthermore, senescence is associated with reduced expression of the effector molecules granzyme and perforin, suggesting CTL "exhaustion" can result in hypofunction. These results agree with other studies showing that HIV-1-specific CTL exhibit abnormal phenotypes in vivo, and suggest the possibility that chronic turnover is an important mechanism of antiviral failure in HIV-1 infection.