BACKGROUND:Glioma is a highly invasive and drug-resistant malignant primary tumor. Increasing research is focusing on the function of neutrophil extracellular traps (NETs) in glioma progress. We aimed to explore the mechanism of NETs-related genes (NETs-RGs) in glioma to find potential biomarkers for glioma. METHODS:The GSE16011 data set was downloaded from the GEO database, and the gene expression matrix and clinical data of glioma patients were downloaded from the TCGA database, the cbioportal website, and the CGGA database, as the training and validation sets. The NETs-RGs were obtained from previous studies. Subsequently, differential expression analysis, WGCNA, GO enrichment, and GSEA analysis. The risk model was established for Cox, LASSO, survival, and independent prognostic analyses. The CIBERSORT algorithm was used for immune infiltration analysis, and pRRophetic was used for drug sensitivity analysis. Finally, the expression levels of genes were validated by data set, glioma patients' tissue samples, and glioma cells, and evaluating cell biological behavior. RESULTS:A total of 57 differential expression genes between Glioma and Normal samples were obtained. Then, two modules with the highest positive correlation with NETs-RGs by WGCNA, the NETs-RGs were obtained from previous studies. Six candidate genes were obtained for subsequent analysis. Then, we conducted functional enrichment of candidate genes and constructed a glioma prognosis model. The prognosis model was indicated as a good predictor of a patient's glioma risk. These genes were related to immune cells significantly. And drug sensitivity analysis predicted 128 differences in chemotherapy drugs and found that MICALL2 had a significant correlation with multiple drugs. Finally, only NFIL3 had the same trend of significantly high expression levels. Moreover, knockdown NFIL3 can inhibit glioma cell malignant growth, and promote apoptosis. CONCLUSION:Three prognosis-related genes have better prognosis values for glioma patients and may be the potential biomarkers for the treatment of glioma.

Traumatic brain injury (TBI) can cause severe neurological damage. Ferroptosis, a recently discovered form of iron-regulated cell death, is closely associated with TBI. Cannabidiol (CBD) has been demonstrated to exhibit neuroprotective effects. However, the antiferroptotic role of CBD in TBI remains unclear. Investigating whether CBD inhibits ferroptosis after brain injury and its underlying mechanisms is of great significance. We find that ferroptosis can be induced in rats after TBI, and CBD significantly inhibits ferroptosis in TBI rats both in vivo and in vitro. MicroRNAs (miRNAs) are highly expressed in the brain. Differentially expressed miRNAs and mRNAs after TBI are detected by RNA sequencing, and miR-320-3p, Negr1, and the ERK/MEK pathway are screened out due to their strong correlations. The results show that CBD inhibits miR-320-3p expression, increases Negr1 expression, and suppresses the ERK/MEK pathway both in vivo and in vitro. Mechanistically, transfection with miR-320-3p mimics or siNegr1 inhibits the intervention effect of CBD on ferroptosis and the ERK/MEK pathway. Additionally, Negr1 gene silencing reverses the effect of the miR-320-3p inhibitor on ferroptosis factors in PC12 cells, which suggests that miR-320-3p can target Negr1. In conclusion, our findings indicate that CBD can inhibit TBI-induced ferroptosis through the miR-320-3p/Negr1/ERK signaling axis.

Traumatic brain injury (TBI), characterized by structural brain damage caused by external physical shocks, is a significant global health challenge. Autophagy plays an important role in the cellular self-protection mechanism during its pathological progression. Traditional Chinese medicine (TCM) has a long history and unique advantages in neuroprotection. This review summarizes the key markers of autophagy and the relevant signaling pathways involved in autophagy in TBI, mainly including the PI3K/Akt/mTOR, AMPK/mTOR, Nrf2, TLR4 signaling pathways, and the endoplasmic reticulum stress autophagy axis. In addition, this paper summarizes the recent advances in TCM approaches in TBI autophagy treatment, such as terpenoids, flavonoids, polyphenols, alkaloids, and carotenoids, which are active components of TCM, as well as acupuncture nonpharmacological therapies.

Traumatic brain injury (TBI) is a prevalent form of cranial trauma that results in neural conduction disruptions and damage to synaptic structures and functions. Cannabidiol (CBD), a primary derivative from plant-based cannabinoids, exhibits a range of beneficial effects, including analgesic, sedative, anti-inflammatory, anticonvulsant, anti-anxiety, anti-apoptotic, and neuroprotective properties. Nevertheless, the effects of synaptic reconstruction and the mechanisms underlying these effects remain poorly understood. TBI is characterized by increased levels of tumor necrosis factor-alpha (TNF-α), a cytokine integral for the modulation of glutamate release by astrocytes. In the present study, the potential of CBD in regulating aberrant glutamate signal transmission in astrocytes following brain injury, as well as the underlying mechanisms involved, were investigated using immunofluorescence double staining, enzyme-linked immunosorbent assay (ELISA), western blot analysis, hematoxylin and eosin (H&E) staining, Nissl staining, transmission electron microscopy, and RT-qPCR. In this study, we examined the impact of CBD on neuronal synapses, focusing on the TNF-α-driven purinergic signaling pathway. Specifically, our research revealed that CBD pretreatment effectively reduced the secretion of TNF-α induced by astrocyte activation following TBI. This reduction inhibited the interaction between TNF-α and P2Y1 receptors, leading to a decrease in the release of neurotransmitters, including Ca2+ and glutamate, thereby initiating synaptic remodeling. Our study showed that CBD exhibits significant therapeutic potential for TBI-related synaptic dysfunction, offering valuable insights for future research and more effective TBI treatments. Further exploration of the potential applications of CBD in neuroprotection is required to develop innovative clinical strategies.

目的:探讨支链氨基酸转氨酶1(BCAT1)基因沉默对大鼠缺血性脑损伤的保护作用.方法:选取40只成年雄性SD大鼠随机分为假手术组(sham)、MCAO模型组(MCAO)、MCAO+空白质粒脑室注射组(NC-shRNA)、MCAO+BCAT1 干扰质粒脑室注射组(BCAT1-shRNA),利用大脑中动脉栓塞法(MCAO)制备脑缺血模型,通过神经功能缺损评分判断大鼠神经功能损伤情况;real time RT-PCR检测大鼠脑缺血部位BCAT1 mRNA的表达水平;利用商品化试剂盒测定缺血脑组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;TUNEL染色检测缺血脑组织细胞凋亡情况.结果:MCAO组大鼠神经功能缺损评分升高(P＜0.05),BCAT1 mRNA 表达水平升高(P＜0.05),脑组织梗死灶增大,SOD活性降低(P＜0.05),MDA水平升高(P＜0.05),TUNEL染色阳性细胞数量增多(P＜0.05).而BCA T1 基因沉默可降低缺血性脑损伤后大鼠神经功能缺损评分(P＜0.05),降低BCAT1 mRNA表达水平(P＜0.05),缩小脑组织梗死灶范围,上调SOD活性(P＜0.05),下调MDA含量(P＜0.05),减少细胞凋亡(P＜0.05).结论:大鼠脑缺血可导致BCAT1 表达上调,BCAT1 基因沉默具有一定神经保护作用.

Cannabidiol is a natural herbal medicine known to protect the brain from traumatic brain injury (TBI). Here, a TBI rat model was established, with cannabidiol administered intraperitoneally at doses of 5, 10, or 20 mg/kg, 30 min before surgery and 6 h after surgery until sacrifice. Brain water content, body weight, and modified neurological severity scores were determined, and enzyme-linked immunosorbent assay, immunofluorescence staining, hematoxylin and eosin staining, Nissl staining, Evans-blue dye extravasation, and western blotting were performed. Results showed that cannabidiol decreased the number of aquaporin-4-positive and glial fibrillary acidic protein-positive cells. Cannabidiol also significantly reduced the protein levels of proinflammatory cytokines (TNF-alpha and IL-1 beta) and significantly increased the expression of tight junction proteins (claudin-5 and occludin). Moreover, cannabidiol administration significantly mitigated water content in the brain after TBI and blood-brain barrier disruption and ameliorated the neurological deficit score after TBI. Cannabidiol administration improved the integrity and permeability of the blood-brain barrier and reduced edema in the brain after TBI.

黄大妈到底怎么了? 黄大妈是位退休人士,今年六十五岁.早些年是单位的一把手,十年前开始退居二线,逐渐把手上的事情交出去.最初是有那么点不甘心,后来自己就想开了,侍弄花草,喝茶看书,还培养了个摄影的爱好,在当地的摄影杂志上获过几个小奖. 六年前孙子出生,儿子连哄带骗让她过来帮忙照顾,就彻底办了退休手续全心照顾家人.儿媳妇肯定不如女儿贴心,也不如女儿会疼人,但磕磕碰碰地日子也就这么过去了.

目的:探讨抑郁症患者血清白介素-6(IL-6)、白介素-18(IL-18)、胶质纤维蛋白(GFAP)、同型半胱氨酸(Hcy)水平与病情严重程度、认知功能的关系.方法:纳入首都医科大学附属北京安定医院、南京医科大学附属无锡精神卫生中心及新乡医学院第二附属医院2019年1月～2019年12月收治的抑郁症患者100例,根据17项汉密尔顿抑郁量表(HAMD-17)评分分成轻度组(n=42,HAMD-17评分为8～16分)、中度组(n=35,HAMD-17评分为17～23分)以及重度组(n=23,HAMD-17评分≥24分).比较三组患者血清IL-6、IL-18、GFAP、Hcy水平.根据蒙特利尔认知评估量表(MoCA)评估结果分成认知障碍组(n=29)、非认知障碍组(n=71),比较两组血清IL-6、IL-18、GFAP、Hcy水平.经Pearson线性相关模型分析抑郁症患者血清IL-6、IL-18、GFAP、Hcy与HAMD-17评分、MoCA评分的相关性.结果:中、重度组的血清IL-6、IL-18、GFAP、Hcy及HAMD-17评分较轻度组明显升高,且重度组高于中度组(P＜0.05).认知障碍组血清IL-6、IL-18、GFAP、Hcy较非认知障碍组明显升高,延迟记忆、抽象思维、注意力、记忆力、视空间执行能力、语言流畅、定向力、命名评分及MoCA总分较非认知障碍组明显降低(P＜0.05).血清IL-6、IL-18、GFAP、Hcy与HAMD-17评分呈正相关(P＜0.05),其与延迟记忆、抽象思维、注意力、记忆力、视空间执行能力、语言流畅、定向力评分及MoCA总分呈负相关(P＜ 0.05).结论:血清IL-6、IL-18、GFAP、Hcy随抑郁症患者的抑郁程度加重而升高,且在有认知障碍的抑郁症患者中明显更高,上述四指标均与HAMD-17、MoCA评分具一定相关性,或可作为评估抑郁症患者病情的辅助指标.

目的 调查抑郁症患者的药物使用情况及抗抑郁药物联合用药的影响因素.方法 采用横断面调查方法,通过电子病历系统调查2019年9月1日至2019年9月30日北京安定医院门诊诊治的抑郁症患者的药物使用情况,分析抗抑郁药物联合用药的影响因素.结果 本研究共纳入5171例抑郁症患者,其中女3575例(69.1％),男1596例(30.9％);年龄10～91(46.5±20.1)岁,<18岁266例,≥18～65岁3788例,≥65岁1117例;自费患者2079例(40.2％),医疗保险付费患者3092例(59.8％).5171例患者中,选择性5-羟色胺再摄取抑制剂(SSRI)类抗抑郁药物使用比例最高[58.7％(3036/5171)],其次是5-羟色胺(5-HT)和去甲肾上腺素再摄取抑制剂(SNRI)类[17.5％(903/5171)],673例(13.0％)使用去甲肾上腺素和特异性5-HT再摄取抑制剂(NaSSA),194例(3.8％)使用5-HT阻滞和再摄取抑制剂(SARI);抗抑郁药物联合用药患者占12.0％(620/5171).在其他抗精神类药物中,苯二氮类药物使用比例最高[36.4％(1881/5171)],其次是二代抗精神病药物[17.5％(904/5171)].<18岁组患者使用多巴胺和去甲肾上腺素再摄取抑制剂(DNRI)、阿扎哌隆类抗焦虑药物、二代抗精神病药物及心境稳定剂的比例高于≥18～65岁组和≥65岁组(P<0.05);≥18～65岁组患者使用DNRI、二代抗精神病药物及心境稳定剂的比例高于>65岁组(P<0.05);>65岁患者使用NaSSA、三环类、四环类、其他抗抑郁药物、苯二氮类药物、非苯二氮类镇静催眠药物及抗抑郁药物联合用药的比例高于<18岁组和≥18～65岁组(P<0.05);≥18～65岁组患者使用NaSSA、SARI、苯二氮类药物、非苯二氮类镇静催眠药及联合用药的比例高于<18岁组(P<0.05).女性患者使用NaSSA的比例高于男性(P<0.05),女性患者抗抑郁药物联合用药比例低于男性(P<0.05).医疗保险付费的患者使用SSRI类药物、非苯二氮类镇静催眠药的比例显著高于自费患者,使用伏硫西汀、二代抗精神病药物及心境稳定剂的比例显著低于自费患者(P<0.05).单因素回归分析显示,性别、年龄是抗抑郁药物联合用药的影响因素(P<0.05),男性、年龄≥18～65岁及≥65岁与抗抑郁药物联合用药显著相关(P<0.05).多因素回归分析结果显示,年龄、付费方式是抗抑郁药物联合用药的影响因素(P<0.05),≥65岁和医疗保险付费是抗抑郁药物联合用药的独立影响因素(P<0.05).结论 抑郁症患者的治疗药物以新型抗抑郁药物为主,其中SSRI类抗抑郁药物所占比重最大;抗抑郁药物联合用药现象并不罕见,≥65岁和医疗保险付费患者更倾向于抗抑郁药物联合用药.

目的:分析住院精神病患者并发躯体疾病的危险因素.方法:住院治疗的精神疾病并发躯体疾病患者846例纳入研究.统计患者并发躯体疾病的类型,分析年龄、性别、病程、学历、住院时间对并发躯体疾病的影响.结果:住院精神病患者合并的躯体疾病以高血压、脑血管病、高脂血症、糖尿病的发生率较高.住院精神病并发躯体疾病与患者的年龄、病程和住院时间有关,其中40～60岁、病程>10年、住院时间>11月的住院精神病并发躯体疾病患者人数较高(P<0.05).年龄、病程和住院时间是影响住院精神病并发躯体疾病的独立危险因素(P<0.05).结论:住院精神分裂症患者发生躯体疾病的概率较高,年龄、病程和住院时间是住院精神病患者并发躯体疾病的主要危险因素.

目的 探讨人血免疫球蛋白在自身免疫性脑炎患者中的应用及对患者免疫水平、死亡率的影响.方法 选取2015年5月～2017年5月北京南苑医院、解放军总医院附属第一医院收治的42例自身免疫性脑炎患者作为研究对象,采用随机数字公式将其分为对照组(21例)和观察组(21例).对照组患者采用甲泼尼龙(甲强龙)治疗3周,观察组患者在对照组的基础上联合人血免疫球蛋白治疗3周.治疗完毕后,采用简易智能精神状态检查量表(MMSE)评估患者的认知水平;采用流式细胞仪测定两组患者治疗前、治疗后3周的CD3+、CD4+、CD8+及CD4+/CD8+细胞水平;采用酶联免疫吸附试验测定两组患者治疗前、治疗后3周的降钙素原(PCT)、干扰素-γ(INF-γ)、白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)水平;随访12个月并统计两组患者治疗后的死亡率.结果 两组患者治疗后1、2、3周的MMSE评分均显著高于治疗前,差异有统计学意义(P＜0.05);观察组患者治疗后1、2、3周的MMSE评分均显著高于对照组,差异有统计学意义(P＜0.05).两组患者治疗后3周的CD3+、CD4+、CD4+/CD8+细胞水平均显著高于治疗前,CD8+细胞水平显著低于治疗前,差异有统计学意义(P＜0.05);观察组患者治疗后3周的CD3+、CD4+、CD4+/CD8+细胞水平均显著高于对照组,CD8+细胞水平显著低于对照组,差异有统计学意义(P＜0.05).两组患者治疗后3周的PCT、INF-γ、IL-6及TNF-α水平均明显低于治疗前,差异有统计学意义(P＜0.05);观察组患者治疗后3周的PCT、INF-γ、IL-6及TNF-α水平均明显低于对照组,差异有统计学意义(P＜0.05).观察组患者治疗后4、8及12个月的死亡率均低于对照组,差异有统计学意义(P＜0.05).结论 人血免疫球蛋白治疗自身免疫性脑炎,有助于提高机体免疫功能,改善患者的认知功能,降低炎症因子水平及死亡率.

目的 分析抗N-甲基-D-天冬氨酸受体(N-methyl-D-aspartate receptor,NMDAR)脑炎精神症状特点,以帮助早期识别该疾病.方法 回顾11例抗NMDAR脑炎患者临床资料,采用神经精神症状问卷(neuropsychiatric inventory,NPI)及精神检查评估患者精神症状出现时间及特点.结果 11例抗NMDAR脑炎患者精神症状NPI评分症状呈现多样性,得分中位数(下四分位数,上四分位数)为63(41,66)分.精神症状主要表现为激越冲动、情感异常、幻觉妄想、紧张症及感觉异常、现实解体、失眠等.在发病后的第1周,感觉异常、失眠等最常见(10例),其次是情感异常(8例),以及幻觉妄想(4例),激越冲动在第2～3周最多见(8例),紧张症第2周出现最多(3例),所有精神症状均可在第1～3周出现.所有患者在发病第1周即伴随言语异常、谵妄、抽搐、自主神经功能异常等多种神经症状.结论 抗NMDA受体脑炎的精神症状出现时间早、症状表现丰富,早期即伴随神经症状.

Glioblastoma multiforme (GBM) is the most common and aggressive brain tumor and patients with this disease tend to have poor clinical outcome. MicroRNAs (miRs) are important regulators of a number of key pathways implicated in tumor pathogenesis. Recently, the expression of miR‑378 was shown to be dysregulated in several different types of cancer, including gastric cancer, colorectal cancer and oral carcinoma. Additional studies have demonstrated that miR‑378 may serve as a potential therapeutic target against human breast cancer. However, the underlying mechanisms and potential targets of miR‑378a‑3p involved in GBM remain unknown. The aim of the present of was to determine the effects of miR‑378a‑3p and its potential targets. Tetraspanin 17 (TSPAN17) is involved in the neoplastic events in GBM and is a member of the tetraspanin family of proteins. The tetraspanins are involved in the regulation of cell growth, migration and invasion of several different types of cancer cell lines, and may potentially act as an oncogene associated with GBM pathology. The results of the present study showed that high miR‑378a‑3p and low TSPAN17 expression levels were associated with improved survival in patients with GBM. Additionally, high levels of TSPAN17 were linked to the poor prognosis of patients with GBM aged 50‑60, larger tumor sizes (≥5 cm) and an advanced World Health Organization stage. TSPAN17 was identified and confirmed as a direct target of miR‑378a‑3p using a luciferase reporter assay in human glioma cell lines. Overexpression of miR‑378a‑3p in either of U87MG or MT‑330 cells decreased the expression of TSPAN17, promoted apoptosis and decreased proliferation, migration and invasion. Overexpression of TSPAN17 attenuated the aforementioned effects induced by miR‑378a‑3p overexpression. The present study indicated that miR‑378a‑3p suppresses the progression of GBM by reducing TSPAN17 expression, and may thus serve as a potential therapeutic target for treating patients with GBM.

Alzheimer disease (AD), is a typical progressive and destructive neurodegenerative disease. It is the leading cause of senile dementia that is mainly represented as neurocognitive symptoms, including progressive memory impairment, cognitive disorder, personality change and language barrier, etc. The pathogeny and nosogenesis of AD have not been clearly explained. AD is characterized by extracellular senile plaques (SP) formed by beta amyloid (Aβ) deposition and neurofibrillary tangles in neuronal cells formed by hyperphosphorylation of tau, as well as the deficiency of neuronal with gliosis. However, the complete spectrum of regulating factors in molecular level that affect the pathogenesis of AD is unclear. Long non-coding RNAs (lncRNAs) are involved in numerous neurodegenerative diseases, such as Parkinson’s disease (PD) and AD. It is increasingly recognized that lncRNAs is tightly related to the pathogenesis and prevention and cure of AD. In the review, we highlighted the roles of lncRNAs in AD pathways and discussed increasing interest in targeting and regulating lncRNAs for the therapeutics of AD.

药理学是药学院相关专业的主干课程,主要分为基础药理学和临床药理学,基础药理学主要向学生阐明药物作用及作用机制,临床药理学是近年来逐渐发展和设立的学科,旨在通过基础和临床试验改善药物质量、提高药物疗效、研究开发新药、发现药物新用途等.药理学是医学与药学之间的桥梁学科,在药理学科学的指导下进行临床实践,在实验研究的基础上丰富药理学理论,两者相结合以满足教学及实践的需求,从而真正做到理论源于临床实践,最终服务于临床工作.笔者从事药理学教学工作多年,总结了在教学中的一些心得体会,希望能进一步提高药理学教学质量,培养高素质应用型药理学人才.

目的 分析丁螺环酮与帕罗西汀联合治疗广泛性焦虑障碍的效果.方法 选择广泛性焦虑症障碍患者100例,随机分成对照组和观察组,各50例.对照组单纯应用帕罗西汀治疗.观察组给予帕罗西汀联合丁螺环酮治疗.比较治疗前后两组HAMA评分变化、不良反应发生情况.结果 治疗后,观察组HAMA评分低于对照组(P＜0.05).观察组不良反应发生率低于对照组(P＜0.05).结论 丁螺环酮与帕罗西汀联合治疗广泛性焦虑障碍的临床效果显著,可显著缓解患者焦虑症状、降低并发症发生率.

药理学实验教学在药学专业整个教学过程中占有主导地位,因此药学实验教学的改革推动药学专业教学的不断向前发展,使其得到不断完善.针对药理学的学科特点,在教学过程中,通过改变实验教学方法、实验教学考核方式、增强师资队伍建设等方面进行药理学实验教学改革,将理论与实践有效地统一起来,提高学生对药理学实验的兴趣,以期培养学生主动分析解决问题的能力及勇于自主创新性的精神,这也是新时代下对培养创新、实用型人才的要求.药学实验教学的实践性很强,改革教学本身是个漫长的探索过程,希望本文一些阐述能起推进作用,也希望大家一起为之努力.

目的:研究灯盏乙素对大鼠实验性动脉粥样硬化的防治作用.方法:复制免疫损伤加高脂喂养大鼠AS模型,观测灯盏乙素对大鼠血清SOD、NO、MDA、血脂、tPA和PAI-1水平及主动脉病变的影响.结果:10、20 mg/kg的灯盏乙素明显升高血清SOD和NO水平,降低血清MDA水平;明显降低TG、TC和LDL-C水平,同时升高HDL-C水平;能明显降低血清PAI-1水平,同时升高血清tPA水平;并可减轻主动脉病变.结论:灯盏乙素体内具有抗氧化、改善血脂异常、维持纤溶系统平衡和减轻主动脉病变的作用.

目的 利用功能核磁共振成像(functional magnetic resonance imaging,fMRI)技术探讨抗抑郁治疗对抑郁症患者识别动态面部表情神经基础改变的影响.方法 选取自愿参加试验的35例重性抑郁症患者,在治疗前后进行fMRI扫描同时进行悲伤、喜悦及中性的面部表情视频分辨测试.fMRI原始图像数据转化格式后经SPM2软件处理.采用治疗前后自身对照研究,行配对t检验统计分析.结果 识别喜悦表情时治疗后较治疗前激活增加的脑区包括右颞中回(BA37)、左颞下回(BA37)、左颞上回(BA39)、左梭状回(BA20)、右海马、左海马、右额中回(BA10)、右后扣带回(BA30)、右海马回(BA36)及左海马回(BA30);而治疗前较治疗后激活增加的脑区包括右梭状回(BA19)、左颞中回(BA21)及左楔前叶(BA19).识别悲伤表情时治疗后较治疗前激活增加的脑区包括左梭状回(BA19)和右颞中回(BA21),而治疗前较治疗后激活增加的脑区包括右梭状回(BA19)及右海马回(BA35),差异有显著性(P<0.05).结论 有效的抗抑郁治疗后抑郁症患者情绪相关脑区有所改变,主要表现在喜悦表情的识别中,患者情绪相关皮质区域激活较治疗前增加,但短期的抗抑郁治疗对悲伤表情的识别改善甚微.

目的 通过动态面部表情识别任务,探讨抑郁症患者治疗前后识别具有正、负性情绪信息的面部表情的特征,为认识抑郁症的病理心理学机制提供新的证据.方法 选择2008年于南京医科大学附属脑科医院住院的抑郁症患者42例(观察组),并招募与抑郁症患者性别、年龄、教育程度、居住地相匹配的30例健康志愿者作为对照组.对两组研究对象进行悲伤、喜悦及中性的动态面部表情识别测试,记录反应时间,并于观察组患者治疗后再次测试.结果 与对照组相比,观察组动态面部表情的识别反应时延长,在有效的抗抑郁治疗后反应时间明显缩短,但仍然长于对照组,差异具有显著性(P<0.05).结论 有效的治疗可能改善抑郁症患者在情绪识别中的部分反应,而注意偏向仍然存在,不随临床症状的改善而改善.