急性肺血栓栓塞症兔TNF-α、IL-8、IL-10水平及地塞米松的影响

目的:探讨兔急性肺血栓栓塞症(PTE)时血浆及支气管肺泡灌洗液(BALF)中TNF-α,IL-8、IL-10的水平和地塞米松(Dex)的影响。方法:采用自体血栓回输法建立兔急性PTF模型。36只兔随机分为对照组、Dex治疗组和PTE模型组。用ELISA方法检测上述细胞因子(CK)水平,术毕肺组织行病理观察。结果:栓塞后上述CK均有升高,治疗后TNF-α、IL-8均有下降,IL-10变化不明显。组织病理学可见栓塞后肺动脉内血栓形成,肺组织萎缩、出血、炎性反应明显,Dex治疗后肺组织病理改变明显减轻。结论:PTE后促炎性CK在引起肺部炎性反应和肺组织及肺动脉病损中起了重要作用,抗炎治疗可以明显减轻CK引起的这种损伤。抗炎治疗能降低PTE急性期病死率,改善远期预后,CK可能起了很重要的作用。     

Zn~(2+)预处理对离体大鼠缺血再灌注损伤心肌的保护作用

目的 :观察Zn2 + 预处理诱导金属硫蛋白 (MT)在心肌细胞的表达及对离体大鼠缺血再灌注损伤心肌的保护作用。方法 :3 2只Sprague Dawley大鼠随机分为对照组及实验组 ,实验组按腹腔注射ZnSO4 到建立再灌注模型的时间分为E1 2h,E2 4h及E4 8h组 ,每组各 8只。检测LDH ,CK、ATP含量及心功能指标 (LVSP与±dp/dtmax) ,用1 0 9Cd/血红素饱和法测量心肌组织中金属硫蛋白的含量。结果 :E2 4h及E4 8h组MT表达量较对照组高 (P <0 .0 1) ,E1 2h组虽有表达 ,但其与对照组间差异无显著性。E2 4h及E4 8h组LDH与CK较其它二组低 ,而ATP较其它二组高 ,心功能指标较其它二组改善。E1 2h组及对照组之间相应各指标 (LDH ,CK、ATP、LVSP与±dp/dtmax)间差异无显著性 (P >0 .0 5 )。结论 :Zn2 + 预处理可诱导MT在心肌细胞的表达而对离体大鼠缺血再灌注损伤心肌具有保护作用。     

A family-based association study of PLP1 and schizophrenia

Recently, proteolipid protein 1 (PLP1) has been identified as downregulated in schizophrenia by quantitative PCR and other technologies. In this work we attempted to investigate the role of PLP1 in the etiology of schizophrenia using a family based association study in 487 Chinese Han family trios. The TDT for allelic association demonstrated that, in male, a weak association was detected in SNP rs475827 with p=0.0294, suggesting that the genetic polymorphisms within PLP1 in male are likely to confer an increased susceptibility to schizophrenia in the Chinese population.     

Inefficient formation of a complex among CXCR4, CD4 and gp120 in U937 clones resistant to X4 gp120-gp41-mediated fusion

Certain subclones (designated as minus clones) of the promonocytic U937 cell line do not support efficient infection and fusion mediated by T cell line adapted (TCLA) X4 HIV-1 gp120-gp41 (Env) although the CXCR4 and CD4 concentrations at their surfaces are similar to those at the surfaces of clones susceptible to HIV-1 entry (plus clones) (H. Moriuchi et al., J. Virol. 71, 9664-9671, 1997). To test the hypothesis that inefficient formation of gp120-CD4-CXCR4 complexes could contribute to the mechanism of resistance to Env-mediated fusion in the minus clones, we incubated plus and minus cells with HIV-1 LAI gp120 and coimmunoprecipitated CD4 by using anti-CXCR4 antibodies. The gp120 induced inefficient coimmunoprecipitation of CD4 in the minus clones but not in the plus ones. Overexpression of CD4 resulted in significant restoration of the minus clones' susceptibility to fusion in parallel with an increase in the amount of the gp120-CD4-CXCR4 complexes. These results not only suggest that the resistance to TCLA X4 HIV-1 entry in the U937 minus clones is due to the inability of these cells to efficiently form complexes among CD4, gp120, and CXCR4, but also provide a direct evidence for the correlation between fusion and the cell surface concentration of the complexes among CXCR4, CD4, and gp120. These data and similar recent observations in macrophages suggest that inefficient complex formation among CXCR4, CD4, and gp120 could be a general mechanism of cell resistance to gp120-gp41-mediated fusion and a major determinant of HIV-1 evolution in vivo.     

人工晶体植入前后视觉诱发电位的临床分析

目的:(1)探讨白内障囊外摘除术前术后及人工晶体植入术后视觉诱发电位幅值及潜时变化特征;(2)探讨白内障囊外摘除术术前P—VEP,F—VEP,F—ERG联合预测的必要性。方法:采用重庆泰克医电仪器公司产TEC—100C视觉电生理仪。对白内障患者实行分组测量。术前均测F—ERG,P—VEP,部分病例增测F—VEP。结果:114例术前F—ERG正常,P—VEP测量其P_(100)波幅值潜时均异常:P_(100)波幅值降低,潜时延长,术后及人工晶体植入后幅值,潜时都有所改善,而并发性白内障,代谢性白内障变化不明显。结论:据视觉诱发电位的变化,老年性白内障组,外伤性白内障组术后应及时装入人工晶体,并发性白内障组,代谢性白内障组装入人工晶体临床意义不大。术前联合测试(VEP ERG)对视力预后、以及眼底病变的定量诊断意义重大。     

女贞子、刺五加对T细胞促进作用的实验研究

女贞子和刺五加都是扶正中药.女贞子在体内体外对 T 细胞均有促进作用,但对其作用机理报导很少。刺五加是典型的“适应原样”药物,对机体免疫功能亦有促进作用,但其对 T 细胞的作用尚未见报导.     

The Hermansky-Pudlak syndrome (HPS) protein is part of a high molecular weight complex involved in biogenesis of early melanosomes

Hermansky-Pudlak syndrome (HPS) is a rare autosomal recessive disorder in which oculocutaneous albinism, bleeding tendency and a ceroid-lipofuscin lysosomal storage disease result from defects of multiple cytoplasmic organelles: melanosomes, platelet dense granules and lysosomes. The HPS polypeptide, a 700 amino acid protein which is unrelated to any known proteins, is likely to be involved in the biogenesis of these different organelles. Here, we show that HPS is a non-glycosylated, non-membrane protein which is a component of two distinct high molecular weight complexes. In non-melanotic cells the HPS protein is contained almost entirely in an approximately 200 kDa complex that is widely distributed throughout the cytosol. In melanotic cells the HPS protein is partitioned between this cytosolic complex and a >500 kDa complex that appears to consist of the approximately 200 kDa complex in association with membranous components. Subcellular fractionation, immunofluorescence and immunoelectron microscopy studies indicate that the membrane-associated HPS complex of melanotic cells is associated with tubulovesicular structures, small non-coated vesicles, and nascent and early-stage melanosomes. These findings suggest that the HPS complex is involved in the biogenesis of early melanosomes.     

Quantitation of human total IgG, kappa IgG and lambda IgG in serum using monoclonal antibodies

Monoclonal antibodies to human IgG have been applied, in parallel with polyclonal antisera, to the routine quantitation of human IgG. Two monoclonal antibodies directed against spatially distinct epitopes have been used in combination to form insoluble complexes exhibiting turbidity. Quantitation was performed using a centrifugal fast analyser and a correlation coefficient of 0.979 was obtained for the two estimations. The technique has been further developed to allow the separate quantitation of kappa IgG and lambda IgG in whole serum.     

大脑中动脉供血区脑缺血后同侧丘脑继发性损害的MR实验研究

本文应用磁共振(magnetic resonance,MR)成像在体观察大脑中动脉(middle cerebral artery,MCA)供血区脑缺血后同侧丘脑的信号变化。结果显示:(1)通过MRA(magnetic resonance angiography)可以观测到单侧MCA的闭塞与血流再通,而供应丘脑的大脑后动脉信号无变化;(2)脑缺血后1d MR T2WI(T2weighted imaging)显示单侧MCA供血区原发病灶呈高信号,3d、7d时此原发病灶信号增高程度有所降低,至14d信号强度再次明显增高;(3)脑缺血后1d和3d时双侧丘脑T2信号无差别,7d和14d时脑缺血同侧丘脑T2信号减低,T2值降低;(4)MCA供血区脑缺血后原发病灶和同侧丘脑T2值的变化不同步。上述结果证实MR能够在活体显示MCA供血区脑缺血后同侧丘脑的继发性损害。