抑郁症患者自杀时段的调查分析

抑郁症患者受症状影响，半数左右会出现自杀观念，约有110％～15％最终会死于自杀。而分析和研究其自杀好发的时，可以为我们制定合理的干预措施，提高护理质量提供可靠的据。为此，对我院5年来住院期间自杀死亡的抑郁症患者进了回顾性分析。报告如下。     

抑郁症免疫功能变化的研究进展

抑郁症是一种高发病率、高复发率的精神疾病。1994年,美国国家共病调查显示全美人口心境障碍的年患病率为11．3％。抑郁症长期存在会对病人的生理、社会功能产生不良影响,导致死亡率和自杀率上升,带来巨大的经济损失,加重社会疾病负担。Borges通过10年随访美国国家共病调查（NCS）中抑郁症患者发现,     

抗抑郁剂的联合使用

大约50％的抑郁症患者可持续终生.1项对抑郁症首次发病患者历时23年的随访研究显示,15％的患者未能痊愈,35％的患者复发[1].目前的抗抑郁治疗仍有50％的患者不能达到痊愈,为提高抑郁症治疗的痊愈率,改善抑郁症治疗现状,精神科医生一直在探索抑郁症的联合治疗方法.除联合心理治疗、物理治疗、药物增效治疗(如锂盐、激素),甚至抗精神病药之外,抗抑郁治疗中抗抑郁剂之间的联合使用越来越受到关注.     

难治性抑郁症的生化基础

1984年,Keilholz在世界精神病学联合会议上指出,60～70％的抑郁症患者对一线抗抑郁药物有效,而余下的10～15％则可能对紧接一个疗程的电抽搐治疗(ECT)或其他抗抑郁剂有效,还有约15％的患者对单用药物或紧接ECT治疗无效。由于抑郁症在一般人群中的发生率较高,故对一大部分的难治性抑郁症患者     

抗抑郁剂最新研究进展

抑郁症患病率较高,在美国终生患病率约为16％［1］。抑郁症的致残性亦较高,而且可危及生命,10％～15％的抑郁症患者有自杀行为。抑郁症不仅给患者本人造成痛苦,而且给家庭和社会造成严重负担,预测2030年将成为全球第一位威胁人类健康、增加经济负担的疾患。尽管当前可用的抗抑郁剂有很多种,但是疗效远远不够理想。约1／3的患者经数种药物治疗后仍疗效欠佳［2］,而且达到临床症状恢复的服药疗程较长,通常需要连续应用数周或数月。临床上发现,大多数抗抑郁剂主要升高5－羟色胺（5－HT ）和去甲肾上腺素（NE）水平,尽管对很多抑郁症患者有效,但仍需合并应用其他药物。现就抗抑郁剂的新进展进行综述。     

双重抑郁症与抑郁症临床特征的研究

目的 了解双重抑郁症与抑郁症患者的临床特征.方法 采用随机多级抽样方法,以美国精神障碍诊断与统计手册第4版-修订版( DSM-Ⅳ-TR)为诊断标准,以DSM-Ⅳ-TR轴Ⅰ障碍定式临床检查患者版为诊断工具,以河北省流行病学调查的399例抑郁症患者为研究对象,其中符合双重抑郁症诊断标准患者56例(双重抑郁症组),符合抑郁症诊断标准患者343例(单一抑郁症组);采用功能大体评定量表( GAF)评定患者的功能状况.结果 399例抑郁症患者中,双重抑郁症的检出率为14.04％.单一抑郁症组和双重抑郁症组均有较高的其他精神障碍的共病率,分别为39.94％和48.21％,2组比较差异无统计学意义(x2=1.361,P＞0.05);均以共病未特定的焦虑障碍、特殊恐怖症、广泛性焦虑障碍、创伤后应激障碍、惊恐障碍、酒依赖/酒滥用等常见.双重抑郁症组患者精神运动性激越、优柔寡断、自杀未遂症状出现的频率均高于单一抑郁症组(P＜0.05),2组均以忧郁特征为常见临床特征(＞50％).2组GAF评分和疾病的严重程度比较差异无统计学意义(t=0.354,P＞0.05;x2 =0.655,P＞0.05).结论 抑郁症中双重抑郁症的比例不低,共病其他精神障碍均较常见,但双重抑郁症患者自杀的风险更高,做事情总是优柔寡断.     

5-羟色胺转运体基因多态性与青少年抑郁症的关联研究

目的 探讨中国汉族青少年抑郁症与5-羟色胺转运体（5-HTY）基因的启动子区多态（5-HTTLPR）之间的关系。方法 应用聚合酶链式反应（PCR）扩增技术对84例青少年抑郁症患者和85例健康者进行基因型分析。结果 5-HTYLPR基因的3种基因型S／S，L／S和L/L在青少年抑郁症组的分布分别为57．1％，36．9％，6．0％；在对照组分别为57．6％，34．1％，8．2％，两组间差异无显著性（P〉0．05）。抑郁症组中S／S基因型患者HAMD自杀因子评分明显高于L／L和L／S型患者（P〈0.01）。结论 5-HTT基因多态性与青少年抑郁症无明显关联。抑郁症中携带S／S基因型患者的自杀风险相对比L／L型、L／S型患者高。     

抑郁症相关睡眠障碍的研究进展

睡眠障碍在抑郁症中常见,是抑郁症状群的重要组成部分,被列为抑郁症的诊断标准之一。据报道超过90％的重性抑郁症患者存在失眠或白天睡眠,有61．8％的抑郁症患者首发临床症状是睡眠障碍。抑郁症的相关失眠有三种重叠形式,即入睡困难、维持睡眠或睡眠连续性发生障碍以及早醒。而早醒被很多学者认为是抑郁症最具有特异性的睡眠障碍,是抑郁症的生物学标志。     

抑郁症自杀行为患者的神经影像学研究现状与展望北大核心CSCD

抑郁症不仅影响着个体的身心健康、社会功能,而且有很高的自杀风险,约2／3的抑郁症患者曾有自杀观念和行为,其中10％～15％自杀成功,自杀行为是抑郁症最危险的症状。抑郁症自杀行为是一个独立于抑郁症的科学问题,     

百优解治疗98例慢性前列腺炎伴焦虑抑郁症的疗效观察

目的：探讨慢性前列腺炎（CP）患者伴有焦虑抑郁症的解决方法。方法：将98例CP伴有焦虑抑郁症的患者随机分为A、B两组，其中A组53例采用可乐必妥＋哈乐＋百优解；B线45例采用可乐必妥＋哈乐，连续门诊治疗6周。结果：A、B两组CP总有效率分别为87％和56％，焦虑抑郁症的缓解率分别为65％和21％。结论：对伴有焦虑抑郁症的CP患者在对前列腺炎本身治疗的同时也应针对焦虑抑郁症予以足够的重视和治疗，才能达到理想效果。     

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.     

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.     

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。     

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.     

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,     

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.     

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.