躁狂症与青春型精神分裂症的人格比较

目的：探讨躁狂症与青春型精神分裂症明尼苏达相人格调查表（MMPI）的异同。方法：随机抽取两者各30例的MMPI，比较其原始分和剖析图。结果：Hs,Pd,Ma3个量表有显著差别。躁狂症的Ma较高，Hs,Pd较低，以Pd最明显。结论：MMPI检测可能有助于两者的鉴别诊断。     

酒精依赖与MMPI相关因子分析

目的探讨酒精依赖与明尼苏达多相人格测验(MMPI)临床基本量表各因子的相关性。方法研究组系2008年6月-2010年6月在临沂市精神卫生中心就诊的酒精依赖患者。采用MMPI计算机测试软件,对酒精依赖组(n=162)和正常对照组(n=99)进行测试,对两组MMPI的疑病、抑郁、癔症、人格偏离、男子气、偏执、精神衰弱、精神分裂、躁狂、社会内向10个因子标准分进行统计分析,并进行logistic回归分析。结果除男子气因子外,酒精依赖组MMPI临床基本量表各因子标准分均高于对照组(P0.01);多因素logistic回归分析发现酒精依赖与抑郁、癔症呈正相关,与精神分裂呈负相关(P均0.05)。结论酒精依赖患者可能存在心理及躯体症状,尤其与抑郁、癔症关系密切。     

对海洛因及酒精依赖患者MMPI测试结果的元分析

目的 对11年来海洛因依赖患者及酒精依赖患者的MMPI测验结果进行元分析。方法查阅中国期刊数据网，对选取的17项关于海洛因依赖患者和11项关于酒精依赖患者的MMPI测试数据进行均值比较。结果海洛因依赖患者的MMPI测试结果除L、D、SI三个因子外与常模存在显著差异；酒精依赖患者除L、HY、MF、SI四个因子外都与常模存在显著差异；两类患者除MF外不存在显著差异。结论海洛因依赖患者与酒精依赖患者在人格上具有相似性。     

精神分裂症患者心理防御机制及人格特征

目的 探讨精神分裂症患者的心理防御机制和人格特征以及二者之间的关系.方法 分别运用防御方式问卷(DSQ)和明尼苏达多项个性调查袁(MMPI)对46例精神分裂症患者和45例正常人对照进行防御方式评定和人格特征测定.结果 精神分裂症组同对照组相比,不成熟及中间型防御机制差异有显著性(P＜0.05).精神分裂症患者MMPI中9个量表得分均高于正常对照组;精神分裂症患者的不成熟防御机制同精神病态、偏执、精神分裂、轻躁狂存在显著正相关(P＜0.05);成熟防御机制同社会内向存在负相关;中间型防御机制同癔症呈负相关(P＜0.05),同偏执、轻躁狂呈正相关(P＜0.05).结论 精神分裂症患者更多地使用不成熟防御机制和中间型防御机制,存在病态的人格特征,且二者之间存在明显的相关性.     

法轮功痴迷者人格特征的初步研究

目的：探讨法轮功痴迷者的人格特征。方法：以MMPI人格量表为检测工具，以78名法轮功痴迷者为检测对象，进行人格测试。结果：发现研究组Pd（人格偏离）、D（抑郁）、Pa（偏执）、Si（社会内向）的临床量表分明显高于对照组，T分超过60，达到或超过常模均分的1.5个标准差，两组原始分比较存在显著差异。结论：法轮功痴迷者从练功-痴迷-精神控制到转化-决裂-恢复常人生活的过程，是与人格问题和心理素质密切相关。     

计算机认知矫正治疗联合社交技能训练对精神分裂症患者认知功能的疗效

目的 探讨计算机认知矫正治疗联合社交技能训练改善精神分裂症患者认知功能的效 果。方法 2017 年1—12 月选取168 例慢性精神分裂症患者随机分为干预组（入组82 例，完成79 例）和 对照组（入组86 例，完成84 例），分别接受12 周的计算机认知矫正治疗联合社交技能训练和计算机认知 矫正治疗12周，并随访12个月。采用阳性与阴性症状量表（PANSS）、精神分裂症认知功能成套测验中文 版（MCCB）及个人和社会功能量表（PSP）在基线、12周末及随访12个月末分别进行评估。结果 （1）治疗 12周末，干预组PANSS的认知因子分明显低于对照组（t=-4.22，P＜0.001）；随访12个月末时干预组的阴性 因子分及认知因子分均明显低于对照组（t=-2.36，P=0.020；t=-5.91，P＜0.001）。随访12个月末，干预组的 PANSS总分与基线比较差异有统计学意义（t=3.41，P＜0.001），但与对照组比较差异无统计学意义（t=1.57， P=0.119）。（2）干预组在12个月末的PSP总分、神经认知功能总分和社会认知分均高于对照组，两组比较 差异均有统计学意义（P＜0.05）。结论 计算机认知矫正治疗联合社交技能训练能够显著改善精神分裂 症患者的认知功能，从而有效促进社会功能恢复。     

酒依赖患者人格特征及酒依赖程度的影响因素分析

目的:探索酒依赖患者的人格特征,以及酒依赖程度的影响因素。方法:运用明尼苏达多相人格调查表(MMPI)和酒依赖筛查量表(MAST)测查150例住院酒依赖患者(研究组)进行评估并与正常人(对照组)进行比较。以年龄、受教育年限、病程、发病年龄、饮酒时间、每日饮酒量以及MMPI 10个临床量表分作自变量,依次将酒依赖患者MAST 5个因子分作为因变量,进行多元逐步回归分析。结果:研究组的校正量表分低于对照组,差异具有统计学意义(P0.05),诈病、疑病、抑郁、癔症、精神病态、偏执、神经衰弱、精神分裂、轻躁狂量表分均高于对照组,差异有统计学意义(P0.01)。多元逐步回归分析显示,对饮酒问题的认识分与Pa、Pt、饮酒时间、受教育年限存在相关性(P均0.05);工作社会分与Hy、Pt存在相关性(P均0.05);肝脏疾患分与D、受教育年限存在相关性(P均0.05)。结论:酒依赖患者有明显的人格偏离,某些人格特质、受教育时间和持续饮酒时间影响患者酒依赖程度。     

住院森田疗法治疗33例精神分裂症患者人格特征分析

目的 探讨住院森田疗法对精神分裂症患者人格特征的影响.方法 选择符合入组标准的住院精神分裂症病人66例,随机分为森田组,对照组,共冶疗10周,采用MMPI多相个性测查表（中国版本399题）分别于冶疗前后进行测查.结果 两组中Hs、Pt、Sc、Si量表T分变化组间比较有显著性差异.结论 森田疗法能矫正病人的某些病态人格.     

矛盾性失眠患者个性特征与心理症状分析

目的探讨矛盾性失眠(PI)患者的心理症状和个性特征,为患者的主客观差异原因提供临床依据。方法根据多导睡眠图结果和患者主观感觉差异把患者分为正常组(10例)、PI组(28例)和原发性失眠组(30例),对其分别进行症状自评量表和明尼苏达多项人格测验(MMPI)评估。结果 (1) 3组90项症状自评量表(SCL-90)及各因子分差异均有统计学意义(P0.05)。经过两两比较,PI组和原发性失眠组患者的SCL-90总分、总均分、阴性项目数、阳性项目数、阳性项目平均分、躯体化、强迫状态和其他项目因子分别与正常组比较均明显升高(P0.05)。PI组患者人际关系敏感、抑郁、焦虑、敌对、偏执和精神病性因子明显高于原发性失眠组、正常组(P0.05);(2) 3组MMPI诈分、疑病、抑郁、癔症、心理变态、偏执、精神衰弱、精神分裂和社会内向因子分均有统计学意义(P0.05)。经两两比较,与正常组比较,PI组和原发性失眠组患者的诈分、疑病、抑郁、癔症、心理变态因子分明显升高(P0.05)。与正常组比较,PI组患者偏执、精神衰弱、精神分裂分因子明显升高(P0.05)。与原发性失眠组相比,PI组患者的社会内向因子分明显升高(P0.05)。结论失眠患者具有情绪易波动和神经质人格特点。PI患者在心理症状和个性上有别于原发性失眠,并可能对其主观感觉产生影响。     

改良森田疗法转变康复期精神分裂症患者病态人格初探

目的探讨改良森田疗法对康复期精神分裂症患者人格的影响。方法对康复期精神分裂症患者应用改良森田疗法治疗一个月，前后采用明尼苏达多相个性测查进行测定，并将测定结果进行比较。结果康复期精神分裂症患者在改良森田疗法治疗前后MMPI测定中量表4（Pa）病态人格的标准分值和量表6（Pd）偏执人格的标准分值均下降，两者在治疗前后分别存在统计学上的显著差异（P〈0.01）。结论改良森田疗法有助于转变康复期精神分裂症病态人格和偏执人格。     

精神分裂症暴力行为与人格问题关系的神经影像学研究

精神分裂症患者暴力行为的发生有一定的异质性,阳性精神病症状并不能完全解释其暴力起源。近年的研究开始关注人格障碍在精神分裂症暴力行为中的作用,影像学技术的应用促进了该类研究有了新的进展。现就精神分裂症暴力与人格关系的影像学研究进展进行综述。     

留守儿童人格特征与一般自我效能感的关系

目的 探讨留守儿童人格特征和一般自我效能感的特点及二者之问的关系.方法 使用艾森克人格问卷(EPQ)和一般自我效能感问卷(GSES)对585例留守儿童和320例非留守儿童进行测查.结果 (1)留守儿童与非留守儿童一般自我效能感总分差异上有统计学意义(P＜0.05);(2)留守儿童的EPQP量表男生的T分显著高于女生,差异有统计学意义(P＜0.05);在EPQN量表上女生的T分显著高于男生,差异有统计学意义(P＜0.05)；城镇的留守儿童的得分明显高于农村的留守儿童,差异有统计学意义(P＜0.05);独生子女在EPQP量表得分上明显高于非独生子女,差异上有统计学意义(P＜0.05)；(3)留守儿童一般自我效能感与E人格呈正相关,与N人格呈负相关.结论 留守儿童的人格特征和自我效能感关系密切.     

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.     

青少年强迫症患者父母人格及家庭功能研究

目的 探讨青少年强迫症患者父母的人格特征及家庭功能特点,了解强迫症患者的成长环境,为早期预防及家庭治疗提供依据.方法 采用病例对照研究,对56名青少年强迫症患者及其父母进行艾森克人格问卷及家庭功能问卷的评定,对所得数据进行t检验及Pearson相关分析.结果 研究组的精神质、神经质得分高于对照组(t=4.461,P＜0.01),外向性得分低于对照组(t＝—2.337,P＜0.05);研究组和对照组父亲人格各因子的差异无统计学意义,母亲的神经质得分高于对照组(t＝3.708,P＜0.01);研究组家庭功能在角色、情感反应情感介入、行为控制方面得分高于对照组(t＝3.161,P＜ 0.05).结论 青少年强迫症患者的母亲存在高神经质特点,其家庭功能有较多问题,可能对青少年强迫症患者的人格有较大影响.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

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.     

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.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.     

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。