脑出血患者血清胆红素和脂质变化分析

目的探讨血清胆红素和脂质水平与脑出血（CH）的关系。方法对117例CH患者的血清胆红素、胆固醇等指标进行检测，并与114例健康对照者进行比较。结果CH患者血清甘油三酯（TG）、高密度脂蛋白胆固醇（HDL—C）及DBIL/IBIL比值较对照组显著降低（P〈0.001或P〈0．05），胆固醇（TC）、直接胆红素（DBIL）较对照组低，总胆红素（TBIL）、间接胆红素（IBIL）、低密度脂蛋白胆固醇（LDL—C）较对照组高，但差异无统计学意义（P〉0.05）。结论血清HDL—C降低可作为CH的危险因素，TG和DBIL/TBIL比值与CH关系密切。     

脑出血患者血清胆红素和脂质变化分析

目的探讨血清胆红素和脂质水平与脑出血(CH)的关系。方法对117例CH患者的血清胆红素、胆固醇等指标进行检测,并与114例健康对照者进行比较。结果CH患者血清甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)及DBIL IBIL比值较对照组显著降低(P<0.001或P<0.05),胆固醇(TC)、直接胆红素(DBIL)较对照组低,总胆红素(TBIL)、间接胆红素(IBIL)、低密度脂蛋白胆固醇(LDL-C)较对照组高,但差异无统计学意义(P>0.05)。结论血清HDL-C降低可作为CH的危险因素,TG和DBIL TBIL比值与CH关系密切。     

胆红素和脂质对脑卒中发病影响的差异性探讨

目的探讨血清胆红素和脂质及其综合指数与脑出血(CH)、短暂性脑缺血发作(TIA)及脑梗死(CI)的关系。方法对128例CH、108例TIA及104例CI急性期患者血清胆红素、胆固醇等指标进行检测,并进行对比分析。结果CI组年龄显著高于CH组(P<0.05)。TIA、CI组患者血清总胆红素(TBIL)、间接胆红素(IBIL)、高密度脂蛋白胆固醇(HDL-C)显著低于CH组(P<0.05或P<0.01),血清总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、非高密度脂蛋白胆固醇(n-HDL-C)水平及LDL-C/HDL-C、TC/HDL-CTG/HDL-C比值显著高于CH组(P<0.05或P<0.01);CI组患者血清直接胆红素(DBIL)/IBIL比值显著高于CH组(P<0.01),血清IBIL、HDL-C水平显著低于TIA组(P<0.05),血清LDL-C、n-HDL-C水平及LDL-C/HDL-C、TC/HDL-C比值显著高于TIA组(P<0.05或P<0.01),各组间其它指标间差异无统计学意义(P>0.05)。结论血清胆红素和脂质及其综合指数不同程度的变化与脑卒中关系密切。     

脑血管病患者血脂水平改变的临床意义

目的：探讨脑血管病患者血脂变化规律。方法：脑梗死患者106例、脑出血患者65例和非脑血管病患者83例;脑梗死组又分为初发和复发,＜60和≥60岁、以及合并高血压、糖尿病和冠心病等亚组。用比色法测定甘油三酯（TG）、高密度脂蛋白胆固醇（HDL－C）、总胆固醇（TC）和低密度脂蛋白胆固醇（LDL－C）水平。结果：脑梗死组血清TC、TG和LDL－C水平明显高于对照组,而HDL－C水平与对照组无明显差异。老年脑梗死组TC、TG水平显著高于对照组;复发脑梗死组TC、LDL－C水平显著高于对照组;脑出血患者血脂指标和对照组相比无显著差异;合并高血压和糖尿病组血清TC、TG和LDL－C均高于单纯脑梗死组和对照组。结论：血清TC、LDL－C主要与复发性脑梗死有关,而TC、TG主要与老年脑梗死发生有关;血清TC、TG和LDL－C升高与脑梗死合并高血压和糖尿病有关。     

血清血脂和胆红素水平与脑白质病变的相关性研究

目的探讨血清总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、载脂蛋白A-I (ApoA-I)、载脂蛋白B(ApoB)、脂蛋白(Lp)(a)、ApoB/ApoA-I、总胆红素(TBIL)、直接胆红素(DBIL)、间接胆红素(IBIL)水平与脑白质病变(WML)的关系。方法纳入WML患者106例及对照组80例,根据Fazekas法将WML组分为Ⅰ级组、Ⅱ级组、Ⅲ级组。比较WML组与对照组之间临床资料、血脂及胆红素的水平的差异;采用多变量Logistic回归分析各血脂指标、胆红素与WML的关系;采用单因素方差分析各血脂指标、胆红素与WML严重程度的关系。结果与对照组比较,WML组年龄、高血压病、糖尿病、既往卒中的比例均明显升高(均P0.05),WML组血清TG浓度明显升高,HDL、ApoA-I、TBIL、DBIL、IBIL水平均明显降低(均P0.05)。多变量Logistic回归分析显示,血清HDL(OR=1.49,95%CI:1.02～2.16;P=0.044)、ApoA-I(OR=1.78,95%CI:1.25～2.64;P0.001)、TBIL(OR=0.45,95%CI:0.22～0.63;P=0.007)、DBIL(OR=0.43,95%CI:0.24～0.82;P=0.034)、IBIL(OR=0.51,95%CI:0.31～0.73;P=0.008)是WML的独立危险因素,多因素Logistic回归分析显示,血清HDL、ApoA-I、TBIL、DBIL、IBIL水平与WML严重程度相关(均P0.05)。结论血清HDL、ApoA-I、TBIL、DBIL、IBIL可能是WML的独立危险因素,且与WML严重程度相关。     

2型糖尿病伴发腔隙性脑梗死相关因素分析

目的 探讨2型糖尿病伴发腔隙性脑梗死的相关危险因素.方法 选择驻马店市中心医院综合内科收治的210例2型糖尿病患者为研究对象,将其分为A组:2型糖尿病未伴发腔隙性脑梗死组(1 19例),B组:2型糖尿病伴发单发性腔隙性脑梗死组(67例),C组:2型糖尿病伴发多发性腔隙性脑梗死组(24例).收集各组患者性别、年龄,既往史、实验室检查指标等各项临床资料,通过单因素分析及多因素分析行统计学比较.结果 B组、C组患有高血压病史比例明显高于A组,差异有统计学意义(P＜0.05).C组患者重度颈动脉狭窄率明显高于A组、B组,而B组患者重度颈动脉狭窄率明显高于A组,差异均有统计学意义(P＜0.05).C组患者三酰甘油(TG)、血清总胆固醇(TC)、高密度脂蛋白阻固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)与A组、B组比较差异有统计学意义(P＜0.05);B组患者TG与A组比较差异有统计学意义(P＜0.05).B组、C组患者糖化血红蛋白(HbArc)、C-反应蛋白(CRP)、尿微量白蛋白(MA)、颈动脉内膜中层厚度(CIMT)与A组比较差异有统计学意义(P＜0.05).高血压史、重度颈动脉狭窄率、TG 、HbArc 、CRP 、MA 、CIMT为2型糖尿病伴发单发性腔隙性腩梗死的独立危险因素,而高血压史、重度颈动脉狭窄率、TC、HDL-C、TG、LDL-C、HbArc、CRP、MA,CIMT为2型糖尿病伴发多发性腔隙性脑梗死的独立危险因素.结论 影响2型糖尿病伴发单发性腔隙性脑梗死和伴发多发性腔隙性脑梗死的危险因素各有不同,临床上应加以区分对待.     

瑞舒伐他汀钙对急性期脑梗死患者血脂和C反应蛋白水平的影响

目的观察瑞舒伐他汀钙对脑梗死患者的血脂和C反应蛋白（CRP）水平的影响。方法选取96例脑梗死合并高脂血症的患者,随机分为治疗组和对照组。治疗组应用瑞舒伐他汀钙治疗（10rag／d）,对照组使用阿托伐他汀钙或其他他汀类药物治疗,用药2周后检测患者血清总胆固醇（Tc）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL—C）和CRP水平。结果与治疗前相比,2组患者血清TC、TG、LDL—C和CRP均有明显下降;与对照组比较,治疗组患者上述指标下降程度更大。结论瑞舒伐他汀钙能更有效降低脑梗死急性期患者的血脂及CRP水平。     

颈动脉粥样硬化斑块及血脂与脑梗死的相关研究

目的探讨颈动脉粥样硬化斑块、血脂与脑梗死（CI）之间的关系。方法对117例脑梗死患者、98例体检健康人群进行血脂测定和颈动脉粥样硬化斑块检测,并行对照分析。结果脑梗死组中伴颈动脉粥样硬化斑块患者明显多于对照组,且以不稳定斑块患者为主,颈动脉分叉处（BIF）常见。不稳定斑块组的总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）水平明显高于对照组。脑梗死组的TC、TG、LDL-C载脂蛋白B（ApoB）水平均明显高于对照组,高密度脂蛋白胆固醇（HDL-C）水平明显低于对照组。不同年龄脑梗死患者的血脂水平无明显差异。结论血清TC、TG、LDL水平与颈动脉粥样硬化斑块稳定性有关。血脂异常是独立于年龄之外的脑梗死和颈动脉粥样硬化的重要危险因素。     

中青年人脑卒中与血脂关系的研究

目的 探讨血脂与中青年人脑卒中的关系。方法 检测了206例中青年脑卒中患者及80例对照者的甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL－C）、低密度脂蛋白胆固醇（LDL－C）、载脂蛋白A－I（ApoA-I)、载脂蛋白B100（ApoB100)和脂蛋白（a)[Lp(a)]血清含量。结果 脑梗死组TG、TC、LD-L－C、ApoB100及Lp(a)水平显著高于对照组,Lp(a)水平亦高于脑出血组,异常的血脂成分随年龄变化而发生改变;皮层动脉区脑梗死组Lp(a)水平显著高于穿通动脉区脑梗死组;脑出血组血脂指标与对照组比较差异无显著。结论 血脂代谢紊乱是中青年人脑梗死的危险因素。     

Binswanger病患者血脂水平分析

目的探讨Binswanger病（BD）患者血脂的变化情况。方法分别测定73例BD患者和64例健康志愿者甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、载脂蛋白A1（ApoA1）及载脂蛋白B（ApoB）的浓度,用T检验分析血脂水平与BD的关系。结果 BD组TG、TC水平均显著高于对照组,而ApoA1水平显著低于对照组（P〈0.01）。2组间LDL-C、HDL-C、ApoB水平差异无统计学意义。BD组患者TG、TC及ApoB水平异常检出率均高于对照组。对照组HDL-C、ApoA1异常检出率高于BD组。结论 BD患者血浆TG、TC、ApoA1水平差异显著,可能为BD发病的危险因素。     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

在SK-N-SH细胞中抑制干预β-淀粉样前体蛋白裂解酶基因和淀粉样β前体蛋白基因

BACKGROUND： Previous studies have demonstrated that Piper futokadsura stem selectively inhibits expression of amyloid precursor protein （APP） at the mRNA level. In addition, the piperlonguminine （A） and dihydropiperlonguminine （B） components （1 ： 0.8）, which can be separated from Futokadsura stem, selectively inhibit expression of the APP at mRNA and protein levels. OBJECTIVE： Based on previous findings, the present study investigated the effects of β-site amyloid precursor protein cleaving enzyme （BACE1） and APP genes on the production of β-amyloid peptide 42 （Aβ42） in human neuroblastoma cells （SK-N-SH cells） using small interfering RNAs （siRNAs） and A/B components separated from Futokadsura stem, respectively. DESIGN, TIME AND SETTING： A gene interference-based randomized, controlled, in vitro experiment was performed at the Key Laboratory of Cardiovascular Remodeling and Function Research, Ministries of Education and Public Health, and Institute of Pharmacologic Research, School of Pharmaceutical Science ＆ Department of Biochemistry, School of Medicine, Shandong University between July 2006 and December 2007. MATERIALS： SK-N-SH cells were provided by Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai, China; mouse anti-human BACE1 monoclonal antibody was purchased from R＆D Systems, USA; mouse anti-human APP monoclonal antibody was purchased from Cell Signaling Technology, USA; and horseradish peroxidase （HRP）-conjugated goat anti-mouse IgG was provided by Sigma, USA. METHODS： The human BACE1 cDNA sequence was obtained from NCBI website （www.ncbi.nlm.nih.gov/sites/entrez）. Three pairs of siRNAs, specific to human BACE1 gene, were synthesized through the use of Silencer pre-designed siRNA specification, and were transfected into SK-N-SH cells with siPORT NeoFX transfection agent to compare the effects of different concentrations of siRNAs （10-50 nmol/L） on SK-N-SH cells. Futokadsura stem was separated and purified with chemical methods, and the crystal was composed of A/B components, with an A to B ratio of 1：0.8. The A/B （1 ： 0.8） components were added to the SK-N-SH cells at different concentrations （13.13, 6.56, and 3.28 mg/mL）. MAIN OUTCOME MEASURES： Using RT-PCR and Western blot methods, BACE1 and APP expression at mRNA and protein levels was detected in SK-N-SH cells following treatment with different siRNAs and concentrations of Futokadsura stem-separated A/B components, respectively. Altered Aβ42 secretion by SK-N-SH cells was determined by ELISA. RESULTS： BACE1 mRNA and protein levels were significantly suppressed by 40 and 50 nmol/L siRNAs at 48 hours post-transfection. A/B components （1 ： 0.8）, which were separated from Futokadsura stem, selectively inhibited mRNA and protein expression of APP in SK-N-SH cells. Aβ42 secretion by SK-N-SH cells was significantly decreased following treatment with siRNAs or A/B components. CONCLUSION： Inhibition of BACE1 and APP genes by various materials and methods efficiently decreased production of Aβ42.     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

癫痫与自杀

自杀而导致死亡被为是增加癫痫患者死亡率的最重要原因之一。国外许多研究报道都表明癫痫患者的自杀率比普通人群的自杀率高几倍到二十几倍。可能导致癫痫患者自杀的危险性因素是有多方面的,本文将从5-HT、抗癫痫药及癫痫手术治疗、精神病理等方面对癫痫患者可能存在自杀危险因素进行综述,并希望在癫痫的综合治疗中对这些危险因素能加以考虑。     

Wnt信号通路与骨髓间充质干细胞增殖及分化的关系

骨髓间充质干细胞（bonemarrow—derived mesenchymal stem cells,BMSCs）是骨髓中不同于造血干细胞的一类细胞,其来源丰富,取材简便,易分离、纯化、培养,在一定的条件下可以迅速体外扩增,具有多向分化潜能,可以通过不同的方法被诱导分化成骨细胞、软骨细胞、肌细胞、神经胶质细胞、神经元细胞等,而且它具有低免疫源性,向病变部位迁移的能力,     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.