精神分裂症的自知力与执行功能的关系

目的 :探讨精神分裂症患者的自知力与执行功能的关系。方法 :应用阴性和阳性症状量表 (PANSS) ,韦氏康量卡片分类测验 (WCST)对 6 3例精神分裂症的自知力及执行功能进行了评定。结果 :在WCST测验中自知力有损害组较自知力无损害组持续错误多 ,分类完成数少 ,具有显著差异性 (P <0 .0 5 )。结论 :精神分裂症自知力的恢复受执行功能水平的影响。     

原发性骨质疏松症患者生活质量量表的信度与效度研究

目的:检验原发性骨质疏松症患者生活质量量表(Osteoporosis Quality of Life Scale,OQOLS)测试版的信、效度.方法:应用OQOLS测试版随机抽取240名原发性骨质疏松症患者进行现场测试,计算该量表的重测信度、内部一致性信度和结构效度、效标效度等.结果: OQOLS测试版的重测系数为0.784～0.927,Cronbach's α系数为0.835～0.979,因子分析显示OQOLS的结构效度良好,与SF-36的效标效度为0.301～0.846.结论: OQOLS测试版具有较好的信、效度,可以用于我国原发性骨质疏松症患者生活质量的测评.     

CT三维重建在侧颅底的应用研究

目的 探讨CT三维重建在侧颅底的应用价值。方法 15例健康成人在Picker5000全身CT机上行连续轴位扫描，将扫描获得的原始数据输入Voxel Q图像后处理工作站，采用表面阴影法(surface shaded display，SSD)进行三维重建。结果 侧颅底CT三维重建能清楚显示正常侧颅底孔、裂和重要的骨性标志。重建的结构可整体显示或切割后单独显示，两均可在三维空间绕任意轴旋转任意角度。结论 三维CT能立体而直观的显示侧颅底骨性结构，有利于侧颅底外科手术方案的设计。     

apoH基因多态性与脑卒中的相关性研究及其对血脂的影响

目的：探讨载脂蛋白H（apolipoprotein H,apoH）基因第8外显子G1025C（Try316Ser）多态性与长沙地区汉族人脑卒中的关系及其对血 脂的影响。方法：采用PCR－单链构象多态技术和DNA直接测序法检测长沙地区汉族260例脑卒中患者、20个脑卒中家系成员和100名健康对照者的apoH基因第8外显子G1025C（Try316Ser）多态性；酶联免疫吸附法检测抗磷脂抗体水平；酶法测定总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL－C）、低密度脂蛋白胆固醇（LDL－C），免疫比浊法测定apoA-I及apo B100，酶联免疫吸附法测定脂蛋白a血清水平。结果：长沙地区汉族人apoH基因G1025C（Try316Ser）多态存在GG、GC两种基因型，脑卒中组及其各亚组G1025C（Try316Ser）多态基因频率分布与对照组比较差异无显著性（P＞0．05）；分析不同基因型对血脂、脂蛋白水平的影响，发现脑梗塞组和对照组GC基因型血清TG水平均明显高于GG基因型（P＜0．05）。结论：长沙地区汉族人apoH基因G1025C（Try316Ser）多态性可能与脑卒中的易患性无关，但与血脂代谢有一定关联。     

siRNA抑制外源绿色荧光蛋白在neuro-2a细胞株中的表达

目的：用RNAi技术抑制哺乳动物神经元中外源报告基因的表达，并探讨该过程中RNAi的时间及剂量效应，为利用RNAi技术研究神经元基因功能提供参考。方法：采用神经细胞来源的细胞系neuro-2a小鼠神经瘤细胞为模型，将外源绿色荧光蛋白（GFP）基因转染到neuro-2a细胞内，利用体外转录法合成siRNA，分为3个剂量组对其进行干扰。结果：Neuro-2a细胞可以被有效地转染，而且siRNA在neuro-2a细胞内可以有效发挥干扰作用。这种干扰作用呈现出一定的剂量效应。结论：RNAi技术可以成功用于neuro-2a细胞抑制基因的表达，这种对GFP表达规律及RNAi剂量效应的研究为利用RNAi技术研究神经元基因功能提供了一定的理论参考和依据。     

Folic acid reduces chemokine MCP-1 release and expression in rats with hyperhomocystinemia.

OBJECTIVE: This study aimed to investigate the effects of folate on the monocyte chemoattractant protein-1 (MCP-1) expression and release in rats with hyperhomocystinemia induced by ingestion of excess methionine. METHODS AND RESULTS: Thirty male Sprague-Dawley rats (200+/-20 g) were randomly divided into three groups (n=10 for each group): control group (Control), high-homocystinemia (Hhcy) group, and folate treatment (FA) group. They were fed with a normal regular diet, enriched by 1.7% methionine plus 1.7% methionine and 0.006% folate for 45 days. Our study showed the following: (a) A high methionine diet for 45 days is sufficient to induce hyperhomocystinemia; folate supplementation to the rats fed the high-methionine diet prevented an elevation homocysteine (Hcy) levels in the blood (P<.01). (b) Compared with the Control group, the Hhcy group had elevated plasma levels of MCP-1, and Hcy was significantly correlated with MCP-1 (P<.05). (c) The protein and mRNA expression of MCP-1 in the aorta was higher in rats from the Hhcy group than in rats from the Control group. (d) Most important, after folic acid supplementation, the lowering of Hcy levels was accompanied by a marked reduction of MCP-1 expressed in aortae and released from plasma and peripheral blood mononuclear cells (PBMCs) stimulated by oxidized low-density lipoprotein (P<.05, P<.01). CONCLUSION: Folic acid supplementation not only can blunt the rise in Hcy and reduce MCP-1 released from both plasma and PBMCs of rats with hyperhomocystinemia but also can downgrade MCP-1 expression in the aorta of rats with hyperhomocystinemia.     

Defective Treg response in acute kidney injury was caused by a reduction in TIM-3+ Treg cells

Background: Despite years of research, the treatment of acute kidney injury (AKI) remains a significant challenge. Animal studies presented causal links between elevated regulatory T cell (Treg) response and better prognosis in AKI. Previous studies in mice and humans showed that TIM-3+ Treg cells were more potent than TIM-3- Treg cells. In this study, we investigated the role of TIM-3 in Treg in AKI patients.

Methods: Peripheral blood from AKI patients and healthy controls were gathered, and TIM-3+ Treg subset was examined.

Results: Compared to healthy controls, the AKI patients presented a significant upregulation in the frequency of circulating CD4+CD25+ T cells; however, the majority of this increase was from the CD4+CD25+TIM-3- subset, and the frequency of CD4+CD25+TIM-3+ T cells was downregulated in AKI patients. In both healthy controls and AKI patients, the CD4+CD25+TIM-3+ T cells expressed higher levels of Foxp3, and were more potent at expressing LFA-1, LAG-3, CTLA-4, IL-10 and TGF-β. In addition, the CD4+CD25+TIM-3+ T cells from both healthy controls and AKI patients presented higher capacity to suppress CD4+CD25- T cell proliferation than the CD4+CD25+TIM-3- T cells. Interestingly, the total CD4+CD25+ T cells from AKI patients presented significantly lower inhibitory capacity than those from healthy controls, indicating that the low frequency of CD4+CD25+TIM-3+ T cells was restricting the efficacy of the Treg responses in AKI patients.

Conclusions: We demonstrated that TIM-3 downregulation impaired the function of Treg cells in AKI. The therapeutic potential of CD4+CD25+TIM-3+ T cells in AKI should be investigated in future studies.     

教育心理学和教学效益相关性的研究

本研究在罗马尼亚Oradea大学医药学院进行，始于1998年，结束于2003年。研究的出发点为该学院的学生们提出不少的教师，包括一些国内外知名的学者和医生，因缺乏教育心理学知识，不能很好地理解学生，组织教学和传授知识。因此，本研究设置了问卷调查，学院向教员开设了教育心理学课程(1998年10月～1999年7月)，与学生和教师座谈，统计并比较学生的考试成绩，特别地跟踪研究全国年度(1999年～2003年)医学证书汇考结果。研究结果客观地证实了教育心理学能够提高学习(工作)效益和成果，因为教育心理学知识使得教师(和医师)更好地与学生(或病人)沟通、理解和组织、合作。     

Gemins modulate the expression and activity of the SMN complex

Reduction in the expression of the survival of motor neurons (SMN) protein results in spinal muscular atrophy (SMA), a common motor neuron degenerative disease. SMN is part of a large macromolecular complex (the SMN complex) that includes at least six additional proteins called Gemins (Gemin2-7). The SMN complex is expressed in all cells and is present throughout the cytoplasm and in the nucleus where it is concentrated in Gems. The SMN complex plays an essential role in the production of spliceosomal small nuclear ribonucleoproteins (snRNPs) and likely other RNPs. To study the roles of the individual proteins, we systematically reduced the expression of SMN and each of the Gemins (2-6) by RNA interference. We show that the reduction of SMN leads to a decrease in snRNP assembly, the disappearance of Gems, and to a drastic reduction in the amounts of several Gemins. Moreover, reduction of Gemin2 or Gemin6 strongly decreases the activity of the SMN complex. These findings demonstrate that other components of the SMN complex, in addition to SMN, are critical for the activity of the complex and suggest that Gemin2 and Gemin6 are potentially important modifiers of SMA as well as potential disease genes for non-SMN motor neuron diseases.     

突变MyD88重组质粒的构建及其抑制绿脓杆菌诱导的A549细胞IL-8表达

构建突变MyD88真核表达质粒(MyD88 DN),转染人呼吸道上皮细胞株A549,探讨其对绿脓杆菌及其分泌产物刺激IL-8表达的影响.结果显示突变MyD88成功构建入pcDNA3.1/zeo真核表达质粒,转染A549细胞后,可降低绿脓杆菌培养上清或活菌刺激诱导的IL-8分泌.提示突变MyD88可阻断绿脓杆菌感染引起的呼吸道上皮细胞IL-8释放,为呼吸道炎症的基因治疗提供了新的靶基因.