美满霉素对MPP+诱导的PC12细胞凋亡的保护作用

目的在离体细胞培养中探讨美满霉素(Minocycline,MC)对1-甲基-4-苯基吡啶离子(MPP )诱导的帕金森病细胞凋亡模型的保护作用.方法将MC或MPP 加入培养的PC12细胞中,建立多巴胺神经元凋亡模型,四甲基偶氮唑盐法(MTT法)检测细胞代谢活性,电泳法检测细胞凋亡,流式细胞术检测细胞凋亡率.结果MPP 浓度为10μmol/L时建立多胺神经元凋亡模型;MC 100 μmol/L预处理可明显升高MPP 处理的PC12细胞活性;MC MPP 组细胞凋亡率显著低于MPP 组(P＜0.01),但仍明显高于阴性对照组(P＜0.05).结论MC对MPP 诱导的细胞凋亡有一定的保护作用.     

MPP~+重新启动多巴胺能神经元细胞周期的作用及机制

目的研究1-甲基-4-苯基吡啶离子(MPP+)重新启动多巴胺能神经元细胞周期的作用及机制。方法使用MPP+处理神经元样分化的PC12细胞,采用四甲基偶氮唑盐(MTT)法检测细胞活力,流式细胞仪检测早期凋亡细胞和细胞周期分布,免疫细胞化学检测ERK/MAPK通路活化水平。结果经MPP+处理后,细胞活力呈浓度依赖性下降,经25、50、75、100、150 mmol/L MPP+处理24 h后细胞存活率分别下降至对照组的(97.32±2.41)%(、67.69±3.03)%、(56.00±3.12)%、(47.23±2.55)%、(40.00±2.46)%,与对照组相比差异均有统计学意义(P<0.01)。经75 mmol/L MPP+处理后出现早期凋亡细胞,随处理时间延长,细胞凋亡率逐渐增加,其处理4、8、16和24 h后细胞凋亡率分别为(7.26±3.43)%、(8.34±3.55)%(、20.04±2.64)%和(28.46±2.35)%(P<0.01)。同时细胞周期中G0/G1期细胞减少,S期和G2/M期细胞增多(P<0.01),细胞内ERK1/2通路活化。结论MPP+可通过活化ERK1/2通路重新启动多巴胺神经元的细胞周期,并诱导多巴胺能神经元凋亡。     

雌激素对MPP+诱导的PC12细胞损伤的防护作用

目的　探讨在离体的细胞培养物中 ,雌激素 (estrogen ,E)对 1 甲基 4 苯基吡啶离子(MPP+ )诱导的帕金森模型是否具有保护作用。方法　以PC12细胞为多巴胺能神经元的细胞模型 ,将MPP+ 或E加入培养的PC12细胞 ,四甲基偶氮唑盐 (MTT)法检测细胞活性及代谢状态 ,SABC法检测酪氨酸羟化酶 (TH)的含量 ,流式细胞术检测细胞凋亡率 ,比较各组的差异。结果　随MPP+ 浓度增加 ,细胞活性下降 ,MPP+ 浓度为 2 5 0 μmol/L时 ,吸光度A570 值为 0 30± 0 0 7,符合帕金森病细胞模型 ;随E浓度增加 ,细胞活性升高 ,呈量效依赖关系 ;当雌激素浓度 >10nmol/L ,细胞活性无明显增加。单纯用E组A570 值为 0 6 1± 0 17,比空白对照组 (0 4 9± 0 11)、MPP+ 组 (0 30± 0 0 7)、E +MPP+ 组 (0 5 6± 0 16 )细胞活性高 (P <0 0 5 ) ;TH阳性细胞平均吸光度E组 (0 4 6± 0 0 6 )比空白对照组 (0 2 2± 0 0 7)、MPP+ 组 (0 10± 0 0 3)、E +MPP+ 组 (0 2 4± 0 0 4 )高 (P <0 0 5 ) ;凋亡率E组(11 5 % )比对照组 (31 3% )、MPP+ 组 (6 3 5 % )、E +MPP+ 组 (33 6 % )低 (P <0 0 5 ) ,每组细胞数为 2× 10 5个 /ml。E +MPP+ 组比MPP+ 组细胞活性高 ,TH含量高 ,凋亡率低 (P <0 0 5 )。结论　雌激素对PC12细胞可     

MPP+对培养中脑多巴胺能神经元的影响

目的通过观察MPP+对体外培养的中脑多巴胺能神经元多巴胺及胆碱摄取能力、多巴胺含量变化及细胞形态的改变等,研究MPP+对中脑多巴胺能神经元功能的影响,探讨利用MPP+建立体外PD细胞模型的可能性及实际意义.方法用孕14天Wistar大鼠,氯胺酮麻醉后取胚胎,按本室常规方法分离培养中脑多巴胺能神经元,培养至第7天后将不同浓度的MPP+加入培养有神经元的培养基中,使其终浓度分别为0.1μM,1μM,10μM.分别测定不同时相点[3H]多巴胺和[3H]胆碱摄取能力及细胞内多巴胺含量变化,并进行TH免疫细胞化学染色.结果MPP+浓度为0.1μM、1μM和10μM时,其[3H]多巴胺摄取力分别是为6.2±0.7、5.9±0.5、5.4±04,较之对照组100±1.7的结果看,MPP+对中脑多巴胺能神经元多巴胺摄取力有明显抑制作用(P＜0.05);而[3H]胆碱摄取力其值为98±3.1,较之对照组100±2.4,差异不显著,说明MPP+对多巴胺能神经元胆碱摄取力无抑制作用(P＞0.05).另一个有趣的结果是胶质细胞的存在对MPP+的作用有明显影响,未抑制胶质细胞组其作用明显强于抑制胶质细胞组(P＜0.05);同时MPP+使中脑多巴胺能神经元细胞内多巴胺含量明显减少(P＜0.05);TH阳性细胞明显减少(P＜0.05).结论MPP+对体外培养的中脑多巴胺能神经元多巴胺摄取力有明显的抑制作用,不仅使多巴胺的摄取降低,而且细胞内的多巴胺含量也显著减少,TH免疫组化染色结果也支持这一结果.MPP+对多巴胺能神经元胆碱摄取能力无明显抑制作用.     

美满霉素对脂多糖诱导的BV-2小胶质细胞肿瘤坏死因子-α表达的影响

目的探讨美满霉素(MC)对脂多糖(LPS)诱导的BV-2小胶质细胞肿瘤坏死因子-α(TNF-α)表达的影响。方法采用相应浓度的MC或LPS(100 ng/ml)对MC组及0.1、1、10、100μmol/L MC+LPS组、LPS组、空白对照组BV-2小胶质细胞进行预处理。ELISA法检测BV-2小胶质细胞TNF-α蛋白的表达,逆转录-PCR检测细胞TNF-αmRNA表达。结果与空白对照组比较,0.1、1μmol/L MC+LPS组及LPS组的TNF-α水平显著升高(均P0.01)。10、100μmol/L MC+LPS组TNF-α水平显著低于LPS组(均P0.01)。与空白对照组比较,LPS组及10μmol/L MC+LPS组TNF-αmRNA的表达水平显著增高(均P0.01)。10μmol/L MC+LPS组TNF-αmRNA表达水平显著低于LPS组(P0.01)。结论 MC预处理(≥10μmol/L)可显著抑制LPS诱导的小胶质细胞TNF-α的表达。     

黄连碱上调miR-146a-5p后通过PI3K/AKT通路减轻由MPP+诱导的帕金森病细胞模型损伤

目的探讨黄连碱对1-甲基-4-苯基吡啶离子(MPP+)诱导的帕金森病(PD)细胞损伤的影响及其机制。方法用0.3 mmol/L的MPP+处理SK-N-SH细胞作为PD细胞模型,记为MPP+组,以正常培养的细胞作为空白对照组。用浓度分别为10μmol/L、20μmol/L、40μmol/L的黄连碱预处理4h后再用0.3 mmol/L的MPP+处理作为不同浓度黄连碱处理组。将miR-con、miR-146a-5p转染至SK-N-SH细胞后再用0.3 mmol/L的MPP+处理记为MPP++miR-con组、MPP++miR-146a-5p组;将anti-miR-con、anti-miR-146a-5p转染至SK-N-SH细胞后用20μmol/L的黄连碱预处理4h及0.3 mmol/L的MPP+处理记为MPP++Cop+anti-miR-con组、MPP++Cop+anti-miR-146a-5p组。四甲基偶氮唑盐比色法(MTT)检测细胞存活率;Western blotting实验检测活化的半胱氨酸天冬氨酸蛋白酶-3(caspase-3)、细胞周期蛋白D1(Cyclin D1)、磷酸化蛋白激酶B(p-AKT)、磷酸化磷脂酰肌醇3激酶(p-PI3K)蛋白表达水平;流式细胞术检测细胞凋亡;实时荧光定量PCR(RT-qPCR)检测miR-146a-5p表达水平。结果与空白对照组比较,MPP+处理后SK-N-SH细胞存活率显著降低,活化caspase-3表达水平显著升高,细胞凋亡率显著升高,CyclinD1、miR-146a-5p表达水平显著降低,差异均有统计学意义(P<0.05)。黄连碱处理及miR-146a-5p过表达后MPP+诱导的SK-N-SH细胞中细胞存活率显著升高,活化caspase-3表达水平显著降低,细胞凋亡率显著降低,CyclinD1、miR-146a-5p表达水平显著升高,差异均有统计学意义(P<0.05)。低表达miR-146a-5p逆转了黄连碱对SK-N-SH细胞增殖促进和凋亡抑制的作用。黄连碱处理后MPP+诱导的SK-N-SH细胞中p-AKT、p-PI3K表达水平显著升高,低表达miR-146a-5p逆转了黄连碱对p-AKT、p-PI3K表达水平的促进作用。结论黄连碱可促进细胞存活,抑制MPP+诱导的细胞凋亡,其机制可能与miR-146a-5p及PI3K/AKT信号通路有关。     

反义IGF-ⅠR基因片段诱导胶质瘤细胞凋亡的流式细胞仪分析和电镜观察

目的探讨反义胰岛素样生长因子-Ⅰ受体(IGF-ⅠR)基因片段诱导胶质瘤细胞凋亡的作用及其形态学的变化。方法根据IGF-ⅠRcDNA序列设计其正义、反义基因片段,并对部分碱基进行硫代磷酸修饰。实验分为空白对照组、正义寡核苷酸组和反义寡核苷酸组,应用流式细胞仪检测DNA含量,根据DNA直方图分析凋亡细胞发生率。应用透射电镜观察凋亡细胞的形态学变化。结果经反义寡核苷酸5μmol/L、10μmol/L、15μmol/L、20μmol/L等4种浓度处理的胶质瘤细胞的凋亡率分别为(16.06±3.86)%、(24.52±4.84)%、(36.69±5.53)%和(43.85±5.72)%;而经同样浓度正义寡核苷酸处理的胶质瘤细胞的凋亡率分别为(3.76±1.22)%、(3.14±1.15)%、(2.51±0.93)%和(3.26±1.15)%;空白对照组(野生型)的自然凋亡率为(1.01±0.89)%。反义寡核苷酸组与空白对照组相比差异有显著性意义(P<0.05),而正义寡核苷酸组与空白对照组之间差异则无显著性意义(P>0.05)。透射电镜观察显示,凋亡细胞表现为细胞体积缩小,染色质凝聚,并聚集于核膜下呈新月状或块状,胞膜内陷形成膜包裹的核碎片或细胞器,最后出泡形成凋亡小体。结论反义IGF-ⅠR基因片段可诱导胶质瘤细胞发生凋亡。     

99mTc-Annexin V检测早期凋亡多巴胺能神经元的实验研究

目的 研究放射性核素标记的膜联蛋白V(Annexin V)与凋亡的多巴胺能神经元的结合特性,探讨使用凋亡显像剂99mTc-Annexin V早期活体显像诊断帕金森病的可行性.方法 采用不同浓度的1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium, MPP+)处理大鼠肾上腺嗜铬细胞瘤细胞(PC12)和人神经母细胞瘤细胞(SH-SY5Y)以诱导其凋亡(PC12 0～200 μm/L, SH-SY5Y 0～500 μm/L),FITC -Annexin V及碘化吡啶(propidiumiodide, PI)双染进行流式细胞仪凋亡检测.以99mTc-Annexin V与凋亡的细胞进行饱和结合实验及细胞摄取实验,研究凋亡细胞与Annexin V的亲和力及其摄取99mTc-Annexin V的动力学.结果 MPP+可诱导PC12细胞及SH-SY5Y细胞发生凋亡,并有明显的量效关系.凋亡细胞可特异性与99mTc-Annexin V结合,亲和力可达(7.16±1.78)nmol/L,每个凋亡的多巴胺能神经元表面的结合位点可达到(179±33)fmol/106cells (PC12)及(220±26)fmol/106cells (SH-SY5Y),且神经元的凋亡水平与其膜结合的99mTc-Annexin V放射性强度有相关性(P＜0.001).结论 凋亡的多巴胺能神经元与99mTc-Annexin V有高度亲和力,其所结合的99mTc-Annexin V放射性强度与细胞的凋亡水平相关,99mTc-Annexin V可用于检测多巴胺能神经元的早期凋亡.     

利培酮和氟哌啶醇对无血清诱导PC12细胞凋亡的作用

目的探讨利培酮对神经的保护作用。方法以100 mg/L神经生长因子诱导大鼠PC12细胞7 d后,将细胞随机分为无血清组、氟哌啶醇组、利培酮组(氟哌啶醇组和利培酮组的浓度均分为10,20,40,60,80μmol/L)和血清组,每组5孔。采用四甲基偶氮唑盐(MTT)法测定细胞活性,流式细胞仪检测细胞凋亡率、细胞周期,用Hoechst33342染色法观察细胞形态学变化。结果(1)给予利培酮(20,40μmol/L)72 h后,细胞活性[(64.2±4.4)%,(60.8±3.9)%]高于无血清组[(48.0±2.8)%;P<0.01],而10μmol/L、20μmol/L、40μmol/L、60μmol/L、80μmol/L各浓度氟哌啶醇组的细胞活性[分别为(31.8±3.9)、和(24.4±1.3)%、(14.3±2.6)%、(10.5±2.1)%和(4.1±1.4)%]均低于无血清组(P<0.01)。(2)流式细胞仪检测,利培酮组的凋亡率[(34.6±2.8)%]低于无血清组[(50.7±3.1)%;LSDt-=-16.0,P<0.01],而氟哌啶醇组的凋亡率[(59.3±5.2)%]高于无血清组(LSD-t=8.6,P<0.01);血清组和利培酮组细胞滞留于G1期的比例[分别为(53.5±5.4)%和(71.1±3.7)%]低于无血清组[(81.2±3.0)%]和氟哌啶醇组[(82.1±5.7)%;P<0.01]。(3)无血清组和氟哌啶醇组多见凋亡细胞,其中氟哌啶醇组更明显;而利培酮组偶见凋亡细胞,以核浓缩为主。结论利培酮对PC12细胞有抗凋亡作用,可能是其参与神经保护作用的机制之一。     

人参皂甙Rb1对模拟缺血环境中的大鼠神经元胞内游离钙的影响

目的探讨人参皂甙Rb1(GSRb1)对模拟缺血环境中的大鼠神经元胞内游离钙的影响。方法对大鼠胚胎脑海马神经元进行体外培养,将其置于正常细胞外液(正常对照组)、模拟缺血的细胞外液(缺血组)、无钙的模拟缺血液(缺血+无钙组)、以及模拟缺血液+不同浓度的GSRb1溶液[缺血+GSRb1(20、40、60、80μmol/L组)],采用激光共聚焦技术测定各组细胞内钙荧光强度,并计算与正常对照组相比荧光强度变化百分比。结果与正常对照组相比,荧光增强度缺血组为(73.5±10.31)%,缺血+无钙组为(4.5±2.58)%,缺血+不同浓度GSRb1组(20、40、60、80μmol/L组)分别为(20.2±3.41)%、(13.6±2.98)%、(10.5±3.62)%和(12.7±4.51)%;缺血+各浓度GSRb1组的荧光增强度明显小于缺血组(均P<0.01)。结论缺血缺氧时神经细胞内游离钙的上升主要是来自细胞外钙离子内流;GSRb1可通过抑制细胞外钙离子内流,减轻细胞内的钙超载,保护缺血神经元;保护作用呈浓度依赖性,在60μmol/L时达到最大。     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

腺垂体功能减退症临床特征变化分析

目的探讨腺垂体功能减退症患者的病因结构变化及临床表现。方法回顾性分析我院2013-01—2016-12住院及门诊78例腺垂体功能减退症患者的临床资料。结果男32例(41.03%),女46例(58.97%);诊断时年龄11~89岁,平均62.5岁;鞍区占位(包括术前及术后)52例(66.67%),席汉综合征8例(10.26%),空泡蝶鞍9例(11.65%),病因不明8例(10.26%),垂体-下丘脑发育不良1例(1.28%)。首次就诊科室:纳差厌食、恶心呕吐就诊于消化内科36例(46.15%)最常见。ACTH+TSH+Gn+G激素缺乏为19例最多,占24.36%,ACTH+TSH+Gn缺乏15例,占19.23%。结论腺垂体功能减退症病因结构发生变化,发病人群、首发症状及受累激素也不同,患者女性多于男性,发病年龄偏高,症状不典型,分布于临床多个科室,其中以低钠血症为首发临床表现就诊消化内科最多。     

Standards of instrumentation of EMG

Standardization of Electromyography (EMG) instrumentation is of particular importance to ensure high quality recordings. This consensus report on “Standards of Instrumentation of EMG” is an update and extension of the earlier IFCN Guidelines published in 1999. First, a panel of experts in different fields from different geographical distributions was invited to submit a section on their particular interest and expertise. Then, the merged document was circulated for comments and edits until a consensus emerged.The first sections in this document cover technical aspects such as instrumentation, EMG hardware and software including amplifiers and filters, digital signal analysis and instrumentation settings. Other sections cover the topics such as temporary storage, trigger and delay line, averaging, electrode types, stimulation techniques for optimal and standardised EMG examinations, and the artefacts electromyographers may face and safety rules they should follow. Finally, storage of data and databases, report generators and external communication are summarized.     

Release of endogenous catecholamines from slices of hypothalamus of rats

The release of endogenous catecholamines from superfused slices of rat hypothalamus was studied under basal conditions and during release evoked by 40 mM K⁺. Catecholamines in superfusates, and in extracts of the tissue after stimulation, were isolated by column chromatography and quantitated by liquid chromatography with electrochemical detection. Norepinephrine (NE) was not consistently demonstrable in superfusate collected under basal conditions, but 40 mM K⁺ caused the release of from 2 to 4 ng/g of tissue per min. The addition of cocaine to the superfusate caused increases in basal and evoked release of NE. Epinephrine (E) could be measured in superfusates of slices from male but not female rats and then only when cocaine was added to the superfusate. Accordingly, the concentration of E in hypothalamus was greater in male rats than in female rats. Dopamine (DA) was not consistently measurable in the spontaneous overflow from slices either in the presence or absence of cocaine. K⁺-evoked release of DA could be demonstrated in slices from female rats. The addition of cocaine increased the evoked release of DA from slices from both sexes. Corticosterone, added to cocaine, had no effects on the efflux of any of the catecholamines. The experiments suggest that neuronal reuptake of all catecholamines is very efficient in the hypothalamus both under basal conditions and during evoked release.     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

《绵阳市社会心理服务工作管理办法》解读

2018年,国家卫生健康委员会等10部委联合发布《关于印发全国社会心理服务体系建设试点工作方案的通知》,四川省绵阳市被列为全国第一批试点地区。绵阳市人民政府依据《中华人民共和国精神卫生法》等相关法律法规和文件精神,结合前期调查研究和社会心理服务工作的试点实际,编制出台了《绵阳市社会心理服务工作管理办法》,并于2021年12月25日起施行。本文围绕社会心理服务的相关概念、办法总则、重点内容、保障措施等方面进行解读,以期为社会心理服务工作的规范、持续和有效开展提供参考。     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

阿立哌唑对精神分裂症患者生活质量的影响

目的:比较阿立哌唑与利培酮对精神分裂症患者生活质量的影响。方法:60例精神分裂患者随机平分为两组各30例,分别给予阿立哌唑和利培酮治疗。疗程8周。用生活质量综合评定问卷-74(GQOLI-74)、阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效及不良反应。结果:阿立哌唑与利培酮均能显著提高精神分裂症患者生活质量,但阿立哌唑在改善GQOLI-74总分、躯体健康及社会功能维度优于利培酮。结论:阿立哌唑治疗有利于提高精神分裂症患者生活质量。