青少年抑郁症患者的社会功能研究进展

抑郁症是青少年时期最常见的情感障碍之一，综合国内外研究可见抑郁症对青少年社会功能的影响很大，主要表现在人际关系、生活质量和学习能力3个方面。本文从这3个方面深入探讨了抑郁症对青少年社会功能的影响，并对青少年抑郁症患者社会功能评估及其治疗现状进行了综述，结果发现，目前国内外对青少年抑郁症患者的研究重点在其核心症状的改善，对其社会功能的评估及干预关注甚少。鉴于国内外指南均对抑郁症提出了“功能全面恢复”的治疗目标，在未来的研究中应考虑结合社会情境开发适用于我国国情的青少年抑郁症社会功能评估及干预测量工具，从而为改善青少年抑郁症患者的治疗结局提供依据。     

青少年非自杀性自伤行为动机的研究进展

青少年是发生非自杀性自伤行为的高发群体。相关研究显示，青少年发生非自杀性自伤 行为的动机对自伤行为有很大影响。现从调节情绪、影响人际和自我强化三方面对青少年发生自伤行 为的动机进行综述，希望能对青少年自伤行为的干预和治疗提供参考。     

不同民族青少年自杀特点对照研究

不同民族青少年自杀特点对照研究金泰安，万学东，刘红霞，曾国珩青少年自杀享有上升趋势，故研究其特点，为预防青少年自杀提供科学依据很有必要。我们于１９９１年１２月～１９９３年３月在贵州农村进行少数民族自杀流行学调查，对年龄在１５～２５岁的苗族和布依族自杀...     

80名青少年违法者的个性探讨

作者使用艾森克个性问卷对某劳教所８０名青少年违法者进行了测试研究。结果表明，青少年违法者个性特点为外倾，并且情绪不稳定，尤以２０岁年龄组明显。     

儿童青少年严重心境障碍研究进展

儿童青少年严重心境障碍（severe mood dysfunction，SMD），或称儿童青少年宽表型双相障碍（broad bipolar disorder phenotype），有别于典型双相障碍（窄表型双相障碍），是儿童青少年双相障碍表型之一。上述概念是由Leibenluft等于2003年提出的。此后，已经有一些研究者对其特征进行了研究。本文将从SMD的临床表现、诊断评估、神经心理特征、脑影像学特征、治疗以及随访等方面对相关研究做一综述。     

青少年非自杀性自伤心理干预的研究进展

青少年非自杀性自伤（NSSI）是全球重大公共卫生事件之一，对其进行有效干预具有重要意义。本文对青少年常见NSSI特定和非特定性的心理干预进行综述，以期提高医护人员对NSSI的重视，为后续研究选择合适的干预方式提供借鉴。     

人格特质和社会支持对青少年抑郁特质和抑郁状态的影响

目的 探讨人格特质和社会支持对青少年抑郁特质和抑郁状态的独立作用，以及在压力性生活事件对抑郁特质和状态影响中的调节作用。方法 采用方便抽样法，于2022年7—8月选取四川省某所中学的303名中学生为研究对象。采用青少年生活事件量表、中国大五人格问卷简版、青少年社会支持量表、特质抑郁量表、流调用抑郁量表在线调查青少年的压力性生活事件、人格特质、社会支持、抑郁特质、抑郁状态。采用多重线性回归分析人格特质和社会支持对青少年抑郁特质和抑郁状态的影响，并分析人格特质和社会支持在青少年压力性生活事件对抑郁特质和抑郁状态影响中的交互作用。结果 多重线性回归分析结果显示，开放性人格特质与青少年抑郁特质呈负相关（β=-0.17,95%CI:-0.27～-0.08,P<0.05），社会支持与青少年抑郁特质（β=-0.16,95%CI:-0.21～-0.10,P<0.05）和抑郁状态呈负相关（β=-0.13,95%CI:-0.19～-0.07,P<0.05）。交互作用结果显示，开放性人格在生活事件对青少年抑郁特质的影响中表现出调节作用（P<0.05），社会支持在生活事件对青少年抑郁状...     

氯氮平血浓度与疗效,剂量及副反应的关系

青少年犯罪的影响因素研究韦志岩韦学斌王天祥王世纪于１９９５年２～４月对两个劳教单位在押青少年罪犯中，随机整群抽样２６０名进行有关因素研究，以２４９名正常在校学生为对照。研究组男２５６名，女４名；年龄１５～２０岁，平均１６．５±１．３岁。对照组男２４６...     

青少年游戏成瘾共病抑郁症状的心理危险因素研究进展

目前，游戏成瘾和抑郁症状在青少年群体中的共同患病率不断上升，但关于两种心理问题的关联及两者共病的危险因素却并不清晰。因此，本文对近年来青少年游戏成瘾共病抑郁症状的研究进展进行综述。患有游戏成瘾的青少年产生抑郁症状的风险更高，还会影响情绪调节与社会功能。青少年游戏成瘾共病抑郁症状的影响因素主要包括自我逃避、父母教养方式和朋辈关系，三者分别与孤独感、自我控制和同伴依恋有关。家庭干预是目前最可行有效的应对策略，建议根据实际情况灵活结合互动型和限制型的干预方式。针对游戏成瘾及抑郁症状青少年的家长课堂建设需侧重于构建亲子关系、积极关注孩子情绪及校园生活等方面，未来研究可进一步明确网络课堂背景下青少年游戏成瘾和抑郁发作的关系，并通过长期随访探索家庭干预的治疗效果。     

青少年非自杀性自伤的神经生物学机制

本文目的是对近年来青少年非自杀性自伤(NSSI)的神经生物学机制的相关研究进行归纳汇总,并探讨青少年NSSI相关研究现状。NSSI在青少年中多发,是自杀的独立危险因素,严重影响青少年的身心健康,已成为普遍关注的公共卫生问题。本文总结青少年的NSSI研究现状及其神经生物学机制,以期为青少年NSSI的临床干预提供参考。     

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.     

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.     

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。     

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。     

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.