精神专科医院门诊抑郁症患者就诊影响因素分析

目的 调查精神专科医院门诊抑郁症患者的就诊特点,探讨影响抑郁症患者及时就诊和选择首次就诊(首诊)医疗机构的因素.方法 选择北京市2所精神专科医院的156例抑郁症患者,采用自编调查表对患者的一般情况、患病及就诊情况进行调查.结果 (1)及时就诊组(发病≤3个月到精神科就诊,61例)与非及时就诊组(发病＞3个月到精神科就诊,95例)在对疾病性质的认识、第一主诉、病耻感、首诊医疗机构、就诊途径、花费的医疗费用及抑郁症阳性家族史等的差异有统计学意义(经x<'2>检验,P＜0.05或P＜0.01);(2)精神专科组(首诊医疗机构选择精神专科,52例)与非精神专科组(首诊医疗机构选择非精神专科,104例)在对疾病性质的认识、第一主诉、抑郁症阳性家族史、花费的医疗费用、婚姻状况、受教育程度等的差异有统计学意义(经X<'2>检验,P＜0.05或P＜0.01);(3)以患者首诊医疗机构作为因变量,将以上项目作为自变量进行Logistic回归,第一主诉、疾病性质的认识进入回归方程,各变量比值比分别为6.379和2.714.结论 (1)对疾病性质的认识、第一主诉、病耻感、就诊途径、首诊医疗机构的选择、受教育程度、抑郁症阳性家族史等因素,对抑郁症患者能否及时就诊有较大影响;(2)对疾病性质的认识、第一主诉、抑郁症阳性家族史、受教育程度、婚姻状况等因素可影响抑郁症患者对首诊医疗机构的选择.     

精神卫生机构建设的思考

本文在查阅文献、了解资料、分析资源、总结经验的基础上系统阐述了西方国家精神专科医疗机构"去机构化"运动的时代背景、理由、成果以及存在的问题。探讨西方的去机构化运动是否适合中国国情,为中国精神卫生事业的发展提供参考。     

北京市朝阳区精神卫生医联体模式初步探索

为进一步深化医药卫生体制改革，提高基层精神卫生服务能力，朝阳区充分整合北京市 三级精神专科医院、区域内三级综合医院精神心理科及区域内精神专科医疗机构等市区两级精神卫生 资源，成立区域内精神卫生医联体。凝聚北京市内的优质专家资源，成立朝阳区精神医学联络会诊中心， 提供高水平的专业技术支撑。在辖区内所有社区医疗机构设置精神科，为患者提供方便可及的精神科 专业诊疗服务，同时带动社区精神卫生专业人才队伍培养。     

社区卫生服务中心医务人员精神卫生知识的调查

目的 了解城区一级医疗机构(社区卫生服务中心)中医务人员的精神卫生知识水平,为在一级医疗机构中设置心理咨询专科作可行性的研究。方法 选取三所社区卫生服务中心(其中A院已经设立心理咨询专科6年;B、C院未设,但B院曾协助市精神卫生中心进行专项调研)在岗医务人员进行随机独立问卷调查,内容主要以患者向医务人员提出需了解的精神卫生知识,常见精神疾病的诊断和处理原则。以多选题和是非题的形式解答,解答对象不记名,但记录从医年限、职称、专业科室、精神卫生知识是接受培训还是自学获得。对问卷按掌握、基本掌握、熟悉、了解、基本不了解分成五类。结果A院中医务人员掌握、基本掌握和熟悉精神卫生知识的占81.39％,了解占9.30％,基本不了解仅2.33％。B院中掌握、基本掌握和熟悉精神卫生知识的占32.00％,了解占38.00％,基本不了解30.00％。C院掌握、基本掌握和熟悉精神卫生知识的占8.89％,了解占44.44％,基本不了解46.67％;但已经开设心理咨询专科门诊A院的高、中级人员都达到基本掌握和熟悉程度。工作年限、专业与掌握和了解精神卫生知识无显著关系。结论 在社区卫生服务中心设置心理咨询专科门诊服务是切实可行的,对充实一级医疗机构中医务人员的业务知识结构,完善社区卫生服务中心的功能有明显作用     

上海市精神卫生服务专业机构医生队伍现状分析

目的调查截止2013年底止,上海市24家精神卫生专业机构医生队伍现状及未来需求,以便为更好地实施精神科住院医师规范化培训项目提供科学依据。方法采用问卷调查方法,对上海市24家公立精神卫生专业机构进行问卷调查和个别深入访谈、核实,内容包括床位数量、医生数量、职称情况、需求情况等。结果 24家专科医院实际开放床位13159张,医生数为1046人,床位数与医生数之比为12.58:1;其中具有中、高级职称的医师609人;住院医师323人;各类其他医师114人。最近四年共招录住院医师规范化培训生171人,未来3年在不包括综合性医院的精神(心理)科及其他民营精神专科医疗机构的实际需求下,上海市各级精神卫生医疗机构精神科医师需求则为331人。结论上海市精神科医生供需矛盾突出,职称结构不合理。     

精神卫生医疗机构中社会工作者的职能研究进展

在我国，精神卫生社会工作随着精神疾病的演变而需求量增多，部分精神卫生医疗机构 设置了社工部并配置专业人员，而明确社会工作者在精神卫生医疗机构中的职能十分必要。现对国内 外精神卫生医疗机构社会工作者职能的研究进行综述，总结出主要职能有疾病预防、心理社会评估、心理 支持、危机干预、寻找社会资源等，为我国精神卫生领域社会工作管理人员和临床社会工作者提供参考。     

住院分裂症患者家属的心理健康状况及其干预

精神分裂症患者家属普遍存在各种心理问题,不同程度地影响着他们的生活质量和社会功能。患者家属的心理问题及其干预对策已经引起了一些业内人士,尤其是精神专科医护人员的重视。     

成都市精神卫生专科机构与基层医疗卫生机构建立合作机制的影响因素

目的 分析精神卫生专科机构与基层医疗卫生机构即社区卫生服务中心和乡镇卫生院建立合作机制的影响因素.方法 根据接受精神卫生专科机构技术指导的程度,将成都市基层医疗卫生机构分为良好合作机构组和欠良好合作机构组,并对相关因素进行对照分析.结果 合作良好的基层医疗卫生机构的精神疾病防治人员（简称：精防人员）从事精防工作年限为（2.79±1.88）年,71.43%为专职,85.72%与个案管理小组其他成员有联系,66.67%是由上级精神卫生专业机构提供技术指导,与欠良好合作的基层医疗卫生机构比较,其差异具有统计学意义（P〈0.05）.结论 精神卫生专科机构与基层医疗卫生机构建立良好合作机制,需要保持精防人员队伍稳定,提高人员专职程度,加强与个案小组其他成员的联系,提高精神卫生专业指导机构等级.     

基于Donabedian模型构建精神专科护理质量评价指标的研究进展

本文目的是对近年来国内外关于精神专科护理质量评价指标的研究进行综述。根据Donabedian模型,从结构质量、过程质量和结果质量3个维度对精神专科护理质量评价指标的研究进展进行阐述,总结研究结果现状,指出现有研究不足,为将来精神专科护理质量评价指标的相关研究提供参考。     

精神分裂症患者家属心理健康及其干预的研究进展

精神分裂症患者家属普遍存在各种心理问题,从而不同程度地影响着他们的生活质量和社会功能,同时心理健康状况也影响到患者的康复。精神分裂症患者家属的心理问题及其干预对策己经引起了一些业内人士,尤其是精神专科医护人员的重视。     

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.     

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.     

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。     

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.     

血浆谷胱甘肽过氧化物酶研究进展

谷胱甘肽过氧化物酶（glutathione peroxidases,GPX）是在哺乳动物中发现的,可通过还原性谷胱甘肽催化还原过氧化物和有机过氧化氢物,从而保护细胞和其他如DNA、蛋白及脂质体等敏感生物分子免受氧自由基的损伤。血浆谷胱甘肽过氧化物酶（GPx-3）是1987年Takahashi等从人的血浆中纯化得到的,是目前已知的GPX家族8个成员中唯一的细胞外亚型。研究发现有多种因素影响GPx-3的表达,并参与了多种疾病的发生、发展,本文就GPx-3的结构、功能、基因表达及其与疾病的关系作一综述。     

癫痫持续状态危险因素及神经化学的改变

癫痫持续状态是内科常见的急症,了解其常见的危险因素有利于病因的明确.其发生过程中的神经化学改变如γ氨基丁酸活性的变化,谷氨酸、离子通道及相关炎性因子的改变正逐渐被认识.明确神经化学的变化将有助有癫痫持续状态发病机制的研究和干预手段的改进.     

神经生长因子促再生坐骨神经血管生成的作用

BACKGROUND： It remains to be determined whether nerve growth factor （NGF） can promote angiogenesis in regenerating peripheral nerves during repairing peripheral nerve injury.
OBJECTIVE： To evaluate the effects of NGF on angiogenesis, and to analyze the influencing mechanisms of NGF, according to the expression patterns of CD34, von Willebrand factor （vWF）, vascular endothelial cell growth factor （VEGF）, and the NGF receptor TrkA in proliferating vascular endothelial cells from a rat model of sciatic nerve injury.
DESIGN, TIME AND SETTING： Randomized, controlled study performed at the Research Institute of Field Surgery, Daping Hospital affiliated to the Third Military Medical University of Chinese PLA, between October 2003 and July 2005.
MATERIALS： Forty-five healthy, adult, Wistar rats underwent sciatic nerve injury. The rats were randomly divided into four groups： NGF ＋ chitosan （n = 15）, NGF ＋ chitosan ＋ anti-VEGF （n = 10）, chitosan （n = 10）, and physiological saline （n = 10）. METHODS： A 1 -cm defected sciatic nerve was bridged with a silica gel conduit. NGF ＋ chitosan group： 100 μ L chitosan and 5 μ L NGF （20 mg/L） were injected into the silica gel conduit; NGF ＋ chitosan ＋ anti-VEGF group： an additional 5μ L anti-VEGF monoclonal antibody （1 g/L） was injected into the silica gel conduit; chitosan group： 100μL chitosan and 5 μL physiological saline were injected into the silica gel conduit; physiological saline group： only 5μL physiological saline was injected into the silica gel conduit.
MAIN OUTCOME MEASURES： CD34 and vWf were used to label blood capillaries and large-diameter blood vessels in the regenerating peripheral nerves, respectively. At day 14 following surgery, immunohistochemistry was used to detect and semi-quantitatively analyze expressions of CD34, vWf, VEGF, and TrkA in proliferating vascular endothelial cells in the regenerating sciatic nerve. A confocal laser microscope was used to determine co-expression. RESULTS： Expressions of TrkA, CD34, vWf, and VEGF in the NGF ＋ chitosan group were significantly greater than the physiological saline and chitosan groups （P 〈 0.05-0.01）. Expressions of CD34 and VEGF in the NGF ＋ chitosan ＋ anti-VEGF group were completely inhibited, while expressions of vWf and TrkA gradually decreased, compared with the NGF ＋ chitosan group （P 〈 0.01）. Confocal microscopy revealed strong co-expression of VEGF and CD34 in the regenerating sciatic nerve, and CD34 expression positively correlated with VEGF expression. In addition, VEGF expression was greater than CD34 expression, and coexpression of VEGF and vWf was also strong.
CONCLUSION： VEGF was expressed in blood capillaries and large-diameter blood vessels, while exogenous NGF promoted VEGF expression in regenerating sciatic nerves, thereby increasing angiogenesis.     

良性阵发性位置性眩晕的治疗进展及心理评估

良性阵发性位置性眩晕（BPPV）是在头位改变时出现的以短暂眩晕发作为主要特征的外周前庭性疾患,耳石复位治疗具有独特的疗效。体位限制对耳石复位后的治疗及预后是否有效尚未明确。前庭康复对反复发作的BBPV及其预后有一定疗效。BPPV引起的眩晕／头晕、姿势不稳等不适症状明显影响患者心理状态,更多表现为焦虑状态,因此心理评估及心理干预在BPPV的康复治疗中愈显重要。现对良性阵发性位置性眩晕的复位手法、体位限常】、前庭康复及心理评估作一综述。     

p75 neurotrophin receptor signal pathway influence on apoptosis in anterior horn neurons of the spinal cord in a rat model of cauda equina compression injury

BACKGROUND： Studies have demonstrated that cauda equina compression results in apoptosis of motor neurons in the spinal cord. The combination of p75 neurotrophin receptor （p75NTR） and precursor of nerve growth factor （pro-NGF） expression initiates the apoptotic pathway and induces neuronal apoptosis. However, few reports have focused on the p75-mediated mechanism of neuronal apoptosis following cauda equine compression injury OBJECTIVE： To determine apoptosis of spinal cord neurons and activation of the pro-NGF-p75NTR-JNK（c-Jun N-terminal kinase） signal pathway in rats following cauda equina compression, and to verify experimental outcomes. DESIGN, TIME AND SETTING： A randomized, controlled, in vivo experiment was performed at the Medical Experimental Center of Xi＇an Jiaotong University between April and November in 2008. MATERIALS： Streptavidin-perosidase kit was purchased from Wuhan Boster, China; in situ end labeling detection kit was provided by Promega, USA; type AEG-220G electron microscope was purchased from Hitachi, Japan. METHODS： A total of 48 healthy, adult, female, Sprague Dawley rats were randomly assigned to three groups： normal （n = 6）, sham-surgery （n = 6）, and compression （n = 36）. The compression group was randomly assigned to six subsets at 1,3, 5, 7, 14, and 28 days, respectively, with 6 rats in each subset. A cylindrical silica gel stick was implanted into the rats to compress 75% of the vertebral canal in the compression group; in the sham-surgery group, only vertebral resection was performed; and no procedures were performed in the normal group. MAIN OUTCOME MEASURES： At 1,3, 5, 7, 14, and 28 days following compression, L2-3 spinal cord segments were processed for immunohistochemistry, in situ cell apoptosis detection, and transmission electron microscopy observation. Nissl staining was used to observe neuronal survival in the L2 spinal cord segment. Immunohistochemistry was applied to detect expressions of pro-NGF, p75NTR, and JNK in the L2 segment. TUNEL fluorometric method was used to observe apoptosis of neurons in the L2 segment. RESULTS： In the normal and sham-surgery groups, little neuronal apoptosis was observed in the L2-3 spinal cord segment. At 3 days after compression injury, pro-NGF, p75NTR and JNK expression was observed in the spinal cord. Expression levels reached a peak at 7 days, and then gradually decreased. In the compression and sham-surgery groups, neurons primarily expressed pro-NGF and p75NTR. The number of JNK-positive neurons in the compression group was dramatically increased compared with the sham-surgery group （P〈 0.05）. A few neurons were apoptotic in the spinal cord 1 day after compression injury. The number of apoptotic neurons gradually increased and reached a peak at 7 days, and subsequently decreased. Apoptosis was still detectable at 28 days. There was a positive correlation between p75NTR expression and neuronal apoptosis （r= 0.75, P〈 0.05）. CONCLUSION： Following cauda equina compression injury, apoptosis of spinal cord neurons was observed. The compression-induced neuronal apoptosis was associated with p75NTR expression in the L2-3 spinal cord segment.     

Neuronal failure in Alzheimer＇s disease： a view through the oxidative stress looking-glass

Considerable debate and controversy surround the cause（s） of AIzheimer＇s disease （AD）. To date, several theories have gained notoriety, however none is universally accepted. In this review, we provide evidence for the oxidative stress-induced AD cascade that posits aged mitochondria as the critical origin of neurodegeneration in AD.