阿立哌唑治疗首发精神分裂症的随访对照研究

目的：探讨阿立哌唑与利培酮治疗首发精神分裂症的疗效和安全性。方法：将148例首发精神分裂症患者随机分为阿立哌唑组75例和利培酮组73例。以阳性与阴性症状量表（PANSS）减分率评定疗效同时评定社会功能缺陷筛选表（SDSS）和治疗中出现的症状量表（TESS）,以SDSS评定社会功能,用TESS评定不良反应。结果：阿立哌唑组与利培酮组在痊愈率、显效率、PANSS评分与SDSS评分差异无统计学意义（P均〉0.05）。阿立哌唑组在体质量增加、内分泌失调与锥体外系方面少于利培酮组,而在兴奋激越与恶心呕吐多于利培酮组,差异均具有统计学意义（P均〈0.05）。结论：阿立哌唑与利培酮治疗首发精神分裂症长期疗效均好,阿立哌唑不良反应较少,依从性高。     

阿立哌唑与利培酮治疗精神分裂症研究

目的：评价阿立哌唑治疗精神分裂症的疗效及不良反应。方法：64例精神分裂症患者,随机分为两组,分别给予阿立哌唑与利培酮治疗8周。采用阳性与阴性症状量表（PANSS）、治疗中出现的症状量表（TESS）评定疗效及不良反应。结果：阿立哌唑组显效率为78.1%,利培酮组为75.0%。利培酮组锥体外系反应稍高于阿立哌唑组。结论：阿立哌唑与利培酮疗效相似,锥体外系反应比利培酮少,是一种有效、安全的抗精神病药物。     

阿立哌唑与利培酮治疗精神分裂症对照研究

目的:探讨阿立哌唑与利培酮治疗首发精神分裂症的临床疗效及安全性。方法:将首发精神分裂症患者100例随机分为阿立哌唑组与利培酮组,疗程8周。采用阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效与不良反应。结果:阿立哌唑组与利培酮组的有效率分别为84.1%和88.9%,两组间治疗前后PANSS评分差异均无显著性(P>0.05),而不良反应发生率阿立哌唑组显著低于利培酮组(P<0.05)。结论:阿立哌唑与利培酮对精神分裂症疗效相当,不良反应发生率低,是一种安全有效的抗精神病药物。     

阿立哌唑与利培酮治疗精神分裂症患者对照研究

目的 探讨阿立哌唑治疗精神分裂症的疗效及不良反应。方法 60例精神分裂症患者随机分为两组，分别给予阿立哌唑与利培酮治疗，疗程6周.采用阳性与阴性症状量袁（PANSS），副反应量表（TESS）评定疗效及不良反应。结果 阿立哌唑组显效率70％，利培酮组显效率73.3％。利培酮组锥体外系反应稍高于阿立哌唑组。结论 阿立哌唑疗效与利培酮相似，锥体外系反应比利培酮少，是一种有效、安全的抗精神病药物。     

阿立哌唑与利培酮治疗精神分裂症对照研究

目的:探讨阿立哌唑与利培酮治疗首发精神分裂症的疗效及不良反应。方法:将符合中国精神障碍分类与诊断标准第3版诊断标准的62例首发精神分裂症患者,随机平分为阿立哌唑组与利培酮组。疗程6周。采用阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效和不良反应。结果:阿立哌唑组显效率及有效率分别为64.5%和90.3%,利培酮组分别为61.3%和87.0%,两组疗效相仿(P>0.05)。阿立哌唑组在治疗2周末阴性症状因子分即有明显下降,而利培酮组在治疗4周末才显著下降。阿立哌唑在锥体外系反应,体质量(体重)增加,月经改变等少于利培酮。结论:阿立哌唑对首发精神分裂症的疗效与利培酮相仿,不良反应轻微,阴性症状改善较快。     

阿立哌唑与利培酮治疗儿童精神分裂症对照研究

目的探讨阿立哌唑对首发儿童精神分裂症患者的临床疗效及安全性。方法50例儿童精神分裂症患者随机分为两组,分别给予阿立哌唑与利培酮,治疗8周,用阳性与阴性症状表(PANSS)和副反应量表(TESS)评定疗效和不良反应。结果两组疗效相仿(P>0.05),阿立哌唑不良反应显著少于利培酮(P<0.05)。结论阿立哌唑对儿童精神分裂症是安全有效的。     

阿立哌唑与利培酮治疗精神分裂症的疗效对照分析

目的分析阿立哌唑治疗精神分裂症的疗效和安全性。方法将80例精神分裂症患者分为阿立哌唑和利培酮治疗组，每组40例，分别治疗6周。以阴性、阳性症状量表（PANSS）、临床病情严重程度量表（CGI-SI）和不良反应量表（TESS）分别评定疗效、病情严重程度和不良反应。结果阿立哌唑组与利培酮组的疗效相当，前者的不良反应较后者少而轻。结论阿立哌唑有显著改善精神分裂症症状的效果。     

阿立哌唑与利培酮治疗首发精神分裂症的对照研究

目的比较阿立哌唑与利培酮治疗首发精神分裂症的疗效和安全性。方法将70例首发精神分裂症患者随机分为阿立哌唑组(n=35)和利培酮组(n=35)进行治疗,疗程8周。在治疗前及治疗后第1、2、4及8周末采用阳性阴性症状量表(PANSS)及不良反应量表(TESS)评定其疗效及药物不良反应。结果阿立哌唑的治疗有效率为64.7%,利培酮的治疗有效率为63.6%,两组疗效差异无显著性。两药均无严重不良反应,但阿立哌唑的肌强直、静坐不能以及泌乳、月经紊乱的发生率明显低于利培酮。结论阿立哌唑与利培酮治疗首发精神分裂症均有效,前者不良反应更少、更安全。     

阿立哌唑治疗晚发精神分裂症对照研究

目的：比较阿立哌唑与利培酮对晚发精神分裂症的疗效和不良反应.方法：选取60例符合中国精神障碍分类与诊断标准第3版中精神分裂症诊断标准的晚发患者,随机平分为阿立哌唑组30例和利培酮组30例.治疗8周.采用阳性与阴性症状量表（PANSS）评定疗效,用治疗中出现的症状量表（TESS）评定不良反应.结果：治疗8周后,2种药物对晚发精神分裂症患者的疗效相当（P＞0.05）.阿立哌唑组和利培酮组的显效率差异无显著性（P＞0.05）.结论：阿立哌唑治疗晚发精神分裂症的疗效好,不良反应少.     

阿立哌唑与利培酮治疗女性精神分裂症的对照分析

目的探讨阿立哌唑治疗女性精神分裂症患者的疗效及安全性。方法将符合入组标准的60例患者随机分为两组，分别给予阿立哌唑和利培酮治疗，疗程8周，采用阳性与阴性症状量表（PANSS），不良反应量表（TESS）评定临床疗效及不良反应。结果治疗8周末，阿立哌唑与利培酮两药疗效相当，但阿立哌唑不良反应少而轻微。结论阿立哌唑治疗女性精神分裂症疗效确切。不良反应少，服药依从性好。     

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.     

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.     

雷公藤内酯对癫痫大鼠神经元P13K／Akt／mTOR蛋白的影响

目的通过检测癫痫大鼠海马神经元P13K、Akt和mTOR蛋白表达,探讨雷公藤内酯抑制癫痫大鼠神经元凋亡的分子机制。方法30只大鼠随机分为对照组、海人酸组、雷公藤内酯干预组,免疫组化法检测各组大鼠海马神经元P13K、Akt和mTOR蛋白的表达情况。结果海人酸组神经元胞体皱缩,形态不规则,数量减少,而雷公藤内酯干预组神经元的数量和形态与对照组相似,海人酸组海马神经元P13K、Akt、ITITOR蛋白表达与对照组比较均减少,而雷公藤内酯干预组海马神经元的P13K、Akt、mTOR蛋白表达均较海人酸组增加,差异均有统计学意义（P〈0．05）。结论雷公藤内酯可能通过上调P13K／Akt／mTOR信号通路蛋白表达对癫痫大鼠海马神经元发挥保护作用。     

Dysfunctional autophagy in Alzheimer＇s disease： pathogenic roles and therapeutic implications

Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer＇s disease （AD）. The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.     

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。     

Oxidative stress in Alzheimer＇s disease

Oxidative stress plays a significant role in the pathogenesis of Alzheimer＇s disease （AD）, a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons （lipids, proteins, and nucleic acids） can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, inflammation, and β-amyloid （Aβ） peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment.     

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.     

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.