Wallerian degeneration in a patient with Schilder disease: MR imaging demonstration

Wallerian degeneration in the corticospinal tract was demonstrated by magnetic resonance (MR) imaging in a patient with Schilder disease. The histochemical stages of myelin breakdown that allow its demonstration by MR imaging are reviewed.     

用细口径反相柱HPLC分离多种前列腺素

HPLC与放射性同位素联用,可同时分离鉴定多种花生四烯酸代谢产物。目前国外一般是使用普通口径(4.6 mm)的反相柱,以30%左右乙腈为流动相,流速为1～3 ml/min。这种HPLC方法乙腈用量较大,费用太贵,不适合国内实验室常规操作。据报道,细口径     

Childhood scoliosis: MR imaging

The spinal cords of 28 scoliosis patients between the ages of 1 month and 17 years were examined with magnetic resonance (MR) imaging. Complete visualization was obtained in all cases. In 15 patients (53%) neuropathologic abnormalities demonstrated by MR imaging significantly affected their clinical course, including tethered cords (n = 7), syringomyelia (n = 5), Arnold-Chiari I malformation (n = 4), spinal cord tumors (n = 2), Arnold-Chiari II malformation (n = 3), and diastematomyelia (n = 1). The advantages of MR imaging in the evaluation of the scoliotic spine in children include a high sensitivity for the occult conditions associated with scoliosis, good anatomic demonstration of the cord, and absence of bone artifacts. MR imaging is recommended as a primary imaging modality in scoliosis, following conventional radiography.     

Monoclonal antibody to human high-molecular-weight kininogen recognizes its prekallikrein binding site and inhibits its coagulant activity

We developed a mouse monoclonal antibody (MoAb 115-21) to human high- molecular-weight kininogen (HK) that recognizes its prekallikrein binding site (residues 565 through 595 of HK). The corresponding synthesized 31-amino acid peptide (peptide IV) was recently shown to retain native HK's prekallikrein binding property. The same peptide bound factor XI also, although less avidly. Our MoAb recognizes purified HK, peptide IV, and the light chain moiety of HK (where the peptide IV resides), as shown by enzyme-linked immunosorbent assay (ELISA) and Western blotting experiments. The apparent dissociation constant for the HK and MoAb 115-21 interaction was 2.2 nmol/L. It does not recognize low-molecular-weight kininogen (LK) with which HK shares its heavy chain moiety or any antigens in human plasma congenitally deficient in kininogens. The binding of MoAb 115-21 to purified light chain of HK was competitively inhibited by peptide IV. In addition, the antibody inhibits HK-dependent clotting activity of normal human plasma and dextran sulfate-mediated activation of prekallikrein in plasma and retards cleavage of HK in normal plasma after contact activation with dextran sulfate. Also, purified Fab fragments of MoAb 115-21 inhibited the HK-dependent coagulant activity and dextran sulfate-mediated prekallikrein activation in normal plasma. Since the kd for HK-MoAb 115- 21 interaction is ten times lower than that of HK-prekallikrein, our data suggest that binding of MoAb 115-21 to HK's peptide IV site increases the free prekallikrein concentration in plasma and thus results in the decreased efficiency of factor XIIa-mediated activation of prekallikrein. Decreased levels of kallikrein thus formed may be responsible for the inhibition of HK-dependent clotting activity and the decrease in rate and extent of HK cleavage in normal plasma on contact activation with dextran sulfate. MoAb 115-21 may thus prove very useful, especially with its high affinity for HK, in further delineation of the role of HK and prekallikrein in contact activation and kinin-related human pathology.     

力竭运动大鼠心室肌蛋白质组表达特征

目的:采用蛋白质组学技术,建立安静和递增运动负荷训练后力竭大鼠心室肌蛋白质组的差异性表达谱,初步筛选出心室肌对力竭运动产生反应的目标蛋白质。方法:实验于2007-03在湖南师范大学生命科学学院蛋白质化学与蛋白质组学国家教育部重点实验室和省级运动人体科学实验室完成。①实验分组:10只SD雄性大鼠随机分为对照组和运动组,每组5只。②实验方法:运动组经过7周的大强度递增运动负荷训练后(最后一次力竭),对两组心室肌组织的全蛋白进行双向凝胶电泳分离。结果:经图像分析,在运动组的电泳图谱上共展现蛋白质点(338±17)个,对照组展现蛋白质点(352±17)个。运动后差异表达的蛋白质点共有99个。对其中差异表达的9个蛋白质点进行质谱鉴定,共鉴定出7个蛋白质,Stress-70protein,NADH-ubiquinone oxidoreductase Mr75000subnunit,Long-chain specific acyl-CoA dehydrogenase,Tropomyosin-1alphachain在运动后"缺失",Nitrilase family,member2在运动后表达上调在5倍以上,一个相对分子质量为21000的未知蛋白在运动后表达下调在5倍以上,另外有两个点经鉴定均为Myosin-6,在运动后表达量相反。这些蛋白质属于收缩蛋白、能量代谢酶、分子伴侣等。结论:递增运动负荷训练后力竭时,大鼠心室肌蛋白质组明显地发生了反应。运动后"缺失"和下调的蛋白质点与心肌收缩的调控和能量代谢的方式转变以及细胞的应激反应有关,其中,成功筛选出6种在运动医学领域尚未涉足的、具有运动应激特点的目标蛋白质。     

急性心肌梗死后外周血单个核细胞表面CD147与基质金属蛋白酶-9 mRNA表达的相关性

目的：基质金属蛋白酶在急性心肌梗死后的心室重构中起着重要作用，但其调节机制目前尚未明确。实验拟通过动物模型的建立及体外细胞培养，观察急性心肌梗死后单个核细胞表面CD147与心肌成纤维细胞基质金属蛋白酶-9 mRNA表达的关系。 方法：实验于2006—08／2007-06在河北省人民医院临床实验中心完成。实验材料：SD大鼠及SD仔鼠（出生1～3d）购自河北医科大学试验动物中心。实验过程中对动物处置符合动物伦理学标准。实验方法：①将30只大鼠随机分为急性心肌梗死组（n=15）和假手术组（n=15），假手术组只过线不结扎。流式细胞分析法检测大鼠术后24h外周血单个核细胞表面CD147表达。②选择SD仔鼠制备心肌成纤维细胞。将单个核细胞与心肌成纤维细胞以细胞数0．5：1，1：1，2：1混合培养24h后，半定量反转录一聚合酶联反应法检测基质金属蛋白酶-9 mRNA表达。当单核细胞与心肌成纤维细胞2：1混合时，加入CD147单克隆抗体1，2，4μL/L，培养24h后检测基质金属蛋白酶-9 mRNA表达。 结果：①急性心肌梗死后外周血单个核细胞表面CD147表达明显增加。②单个核细胞与心肌成纤维细胞混合培养，随着单个核细胞比例的增加，心肌成纤维细胞基质金属蛋白酶-9 mRNA表达增加。③在单个核细胞与心肌成纤维细胞2：1混合培养体系中，随着加入CD147单克隆抗体浓度的增加，基质金属蛋白酶-9 mRNA生成减少。 结论：急性心肌梗死后单个核细胞表面CD147表达明显增加，对心肌成纤维细胞基质金属蛋白酶-9生成起上游调节作用。