国内丙型肝炎病毒感染与肝细胞癌关系的19个病例对照研究的 Meta 分析

本文对国内１９个有关丙型肝炎病毒（ＨＣＶ）感染与肝细胞癌（ＨＣＣ）关系的病例对照研究进行Ｍｅｔａ分析。经齐性检验表明，１９个研究中有１７个研究结果是一致的。对此１７个研究结果加权合并，累积ＨＣＣ病例１５７７例，ＨＣＶ感染率为２３．０％，累积对照１９８０例，ＨＣＶ感染率为４．０％；合并ＯＲ值为６．７。结果表明，国内ＨＣＶ感染与ＨＣＣ关系密切，ＨＣＶ感染是ＨＣＣ发生的一个危险因素。     

高脂血症患者C—反应蛋白含量的变化及氟伐他汀对它的影响

OBJECTIVE: To observe the changes of C-reactive protein (CRP) level and its relationship with blood lipids, and the effects of fluvastatin on CRP and the lipids in patients with hyperlipidemia. METHODS: Serum levels of cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C) and lipoprotein(a)[Lp(a)] were measured by enzyme assay, and plasma CRP level by immunonephelometry before and after fluvastatin treatment (20 mg/d for 4 weeks) in patients with hyperlipidemia. RESULTS: CRP levels were above normal in 90.3% hyperlipidemia cases in spite of the various accompanying diseases. Fluvastatin treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL (-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01), and also brought down Lp(a) concentration (-13.81%). CRP levels was very effectively reduced after the treatment (-15.92%, P<0.001). No association between basal CRP levels and basal lipids and Lp(a) concentrations was observed. Positive correlation of CRP, however, was observed after fluvastatin treatment with TC/HDL (r=0.62, P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations were noted between CRP and HDL (r=-0.288, P=0.023). CONCLUSION: CRP levels increases markedly in patients with hyperlipidemia, a fact that is independent of the accompanying diseases. In addition to modulating blood lipid levels, fluvastatin also reduces CRP level, the latter possibly serving as an independent predictive factor for atherosclerotic cardiovascular diseases and also as an indicator for estimating the effectiveness of the treatment.     

利培酮对氯氮平血浓度影响的研究

目的　了解利培酮对氯氮平血浓度的影响及二药合用的疗效与不良反应。方法　对 5 0例原服用氯氮平治疗的难治性精神分裂症患者合并利培酮治疗 ,分别于合并治疗前及后 1月、2月、3月测定氯氮平血浓度 ,同时评定PANSS ,TESS量表。结果　合用利培酮后 ,氯氮平血浓度无明显升高 ,PANSS评分明显降低(P <0 .0 1) ,TESS评分有所增加。结论　利培酮对氯氮平血浓度无明显影响 ,二药合用能增加疗效 ,不良反应有所增加。     

静脉输液回血问题研究

在静脉输液操作中常常遇到许多静脉输液穿刺成功后无回血情况。由于一次性输液管壁弹性差、管腔内径小，又因液体静压及重力的作用，容易造成回血不畅。尤其是老年人、婴幼儿、休克和脱水病人，因穿刺后无回血无法判断穿刺是否成功，而反复穿刺。这样既增加了病人痛苦，又增加了护士工作量。利用负压原理和局部血管扩张法，[第一段]     

Neurodegeneration in the Central Nervous System of apoE-Deficient Mice

Apolipoprotein E (apoE) is involved in the development and regeneration of the central nervous system (CNS). ApoE may also be necessary to maintain the integrity of the synapto-dendritic complexity. We analyzed the synaptic alterations in the CNS of apoE-deficient (knockout) mice during the aging process. In apoE-deficient homozygous mice, there was an age-dependent 15 to 40% loss of synaptophysin-immunoreactive nerve terminals and microtubule-associated protein 2-immunoreactive dendrites in the neocortex and hippocampus, when compared to controls. Dendritic alterations were observed as early as 4 months of age. Ultrastructural analysis revealed extensive dendritic vacuolization and disruption of the endomembrane system and cytoskeleton in apoE-deficient homozygous mice. Further immunocytochemical studies of the neuronal cytoskeleton showed that in apoE-deficient mice there was a decrease in the immunoreactivity of α and β tubulin (but not kinesin) in the cell bodies and processes. These results support the contention that apoE might play an important role in maintaining the stability of the synapto-dendritic apparatus and that altered or deficient functioning of this molecule could underlie the synaptic and cytoskeletal alterations in Alzheimer's disease.     

高浓度氨基酸对肿瘤细胞体外增殖的影响

本研究首先采用Hanks溶液作为介质,观察了不同氨基酸浓度(1～5mmol/L)对艾氏腹水癌细胞、瓦克癌肉瘤256细胞体外增殖的影响,然后以含有平衡氨基酸组成的Eagle最低必需培养基作为介质进一步观察了不同氨基酸浓度的增加对艾氏腹水癌细胞及人肝癌细胞(PLC/PRF/5)、肺癌细胞(AGTJ-a)体外增殖的影响,同时采用小鼠骨髓细胞观察了高浓度氨基酸对正常组织细胞可能产生的毒性作用。结果表明,尽管一些氨基酸浓度的增加有显著作用,但是不同肿瘤细胞对不同氨基酸浓度增加的反应不尽一致,而且一些氨基酸的作用受培养介质的明显影响;高浓度色氨酸对小鼠骨髓细胞的体外增殖有显著抑制作用。     

“90增血剂”对特发性血小板减少性紫裥患者的T细胞亚群的作用

作者根据现代免疫学观点,自1989年起采用自制中药“90增血剂”治疗ITP46例。期间,应用间接免疫荧光技术检测了患者外周血T淋巴细胞亚群,结果表明病例组全T细胞(CD_3)、T辅助/诱导细胞(CD_4)降低,T抑制/细胞毒细胞(CD_8)增高,CD_4/CD_8比值明显降低。治疗后,患者T亚群恢复常态,血小板数上升,骨髓产板型巨核细胞数增加,临床总有效率达91.2%,明显优于激素组(71.4%)。提示中药具有显著的疗效和良好的免疫调节作用。同时,动态观察ITP患者T细胞亚群的变化,对帮助临床判断治疗反应和预后有很大意义。     

鼠巨细胞病毒抑制神经干细胞分化及分化基因表达的体外研究

目的 研究鼠巨细胞病毒(MCMV)感染对体外培养神经干细胞(NSCs)分化及分化基因表达的影响,探讨CMV先天感染致神经损伤的机制.方法 体外分离培养和鉴定BALB/c胎鼠NSCs并检测其分化潜能,用感染复数(MOI)为5、1和0.1的MCMV Smith毒株感染NSCs并进行分化培养,倒置显微镜下观察细胞形态学改变,流式细胞术检测分化细胞比率,免疫荧光法观察NSCs及其分化细胞标记物Nestin、胶质纤维酸性蛋白(GFAP)和神经元特异性烯醇化酶(NSE)表达的变化,采用MCMV早期抗原(EA)示踪感染过程(MOI=1),real-time RT-PCR检测分化早期NSCs Wnt信号途径关键分化基因Wnt-3和Wnt-Ta mRNA水平的动态变化.结果 体外培养的NSCs呈球样生长,神经干细胞特异性标记Nestin表达阳性,并可进一步诱导分化为NF-200阳性的神经元和GFAP阳性的星形胶质细胞;分化培养后,感染组NSCs不能贴壁分化生长并逐渐出现肿胀,细胞Nestin表达下调缓慢并显著高于正常对照组,而GFAP和NSE表达显著低于正常对照组(P<0.05),可检测到MCMV EA的阳性表达;分化培养3-9 d,感染组Nestin阳性细胞比率显著高于正常对照组,GFAP和NSE阳性细胞比率显著低于正常对照组(P<0.05);感染组Wnt-3 mRNA水平在分化培养后第1～2天显著低于正常对照组(P<0.05),感染组Wnto-7a mRNA水平在第0.5～2天明显低于正常对照组(P<0.05);感染组和正常对照组的差异随病毒MOI的增加而更加明显.结论 MCMV感染可明显抑制NSCs向神经元和星形胶质细胞方向分化,导致分化细胞比率减少;下调或干扰NSCs wnt信号途径分化基因wnt-3和Wnt-7a的表达;抑制NSCs分化及其分化基因表达的效应与MOI大小存在一定量效依赖关系;MCMV可能通过抑制NSCs分化基因的表达来抑制其分化,这可能是CMV先天感染致脑发育异常的重要机制之一.     

Preparation and characterization of porous beta-tricalcium phosphate/collagen composites with an integrated structure

Porous beta-tricalcium phosphate (TCP)/collagen composites with different beta-TCP/collagen weight ratio were prepared. The influences of the preparation conditions on the microstructure of porous composite and the joint status of beta-TCP particles with collagen fibrils were characterized by X-ray diffractometer, scanning electron microscopy and transmission electron microscopy. The results showed: (1) an acid treatment could effectively disassemble collagen fibrils; (2) in the resulting porous composites, beta-TCP particles homogenously existed on the skeleton of the collagen fibril network and bonded tightly to both the fibrils and themselves. The tight bonding formation could be due to the reaction between Ca ions in the particles and carboxyl groups in collagen polypeptide chains and due to the reprecipitation of partially dissolved beta-TCP during synthesis. The tight bonding between beta-TCP particles and collagen fibrils in the composites demonstrated an integrated structure, which was reproducible when beta-TCP/collagen ratio ranged from 2 to 4. Such integrated structure would make significant contributions in reliably tailoring properties of the porous composites by varying beta-TCP content. In addition, the porous composites had large porosity (approximately 95%) and appropriate pore size (approximately 100 microm), showed no negative impact in cytotoxicity assay and complete bone tissue regeneration after 12 weeks in animal test.     

急慢性MCMV感染对小鼠脾细胞Foxp3/T-bet/GATA-3蛋白表达水平的影响

目的：在整体水平研究鼠巨细胞病毒（MCMV）感染对小鼠辅助性T细胞亚群Th1、Th2和调节性T细胞（Treg）分化特异性转录因子T-bet、GATA-3和Foxp3蛋白表达水平的影响。方法：建立MCMV播散型感染模型,依据主要脏器内病毒滴度,确定感染后28天为本模型急、慢性期界定点。42只模型鼠分别于接种MCMV Smith株后第1、3、7、14、28、45天和60天各处死6只,分离脾细胞;另设42只正常小鼠作为模拟感染对照。Western blot法检测脾细胞中特异转录因子T-bet、GATA-3和Foxp3蛋白表达水平。结果：MCMV感染后第3天T-bet蛋白表达显著增高达峰值,与模拟感染对照组比较有显著差异（P〈0.01）,随后下降,第28天后降至模拟感染对照组相当水平;而GATA-3蛋白表达在感染后第3天开始升高,第7天达峰值（P〈0.01）,第14天开始缓慢下降,但至第60天仍显著高于模拟感染对照组（P〈0.05）;Foxp3蛋白表达在感染后7天明显低于模拟感染对照组,第28天降至最低（P〈0.01）,第45天和60天表达明显上调,并显著高于模拟感染对照组水平（P〈0.05）。结论：感染急性期,MCMV上调Th1/Th2特异性转录因子T-bet和GATA-3的蛋白表达;感染慢性期,MCMV诱导Treg特异性转录因子Foxp3蛋白表达上调,同时显著抑制T-bet和GATA-3蛋白表达,提示CMV诱导Foxp3表达增加可能是其抑制宿主抗病毒免疫,导致慢性持续性感染的重要原因。