双相障碍与脑源性神经营养因子外周血mRNA和蛋白表达相关性的研究

目的 探讨脑源性神经营养因子(BDNF)外周血mRNA表达和血清蛋白水平与双相障碍、双相躁狂和双相抑郁的关系.方法 应用TaqMan探针及荧光实时定量逆转录-聚合酶链反应方法,检测并比较双相障碍组(61例)、双相躁狂组(29例)、双相抑郁组(32例)和对照组(61名)外周血白细胞BDNF基因的mRNA表达水平的差异;采用酶联免疫吸附方法测定血清BDNF浓度;应用17项汉密尔顿抑郁量表(HAMD17)和Young氏躁狂量表(YMRS)评定患者抑郁症状严重程度和躁狂症状的严重程度,采用Pearson相关分析分析BDNF基因mRNA表达水平和血清蛋白浓度与HAMD17和YMRS评分的关系.结果 (1)双相障碍组BDNF基因mRNA相对表达水平(0.0077±0.0019)较对照组(0.0096±0.0028)下降(t=-3.74,P＜0.01);双相躁狂组(0.0081±0.0023)、双相抑郁组(0.0073±0.0024)与对照组3组间BDNF基因mRNA相对表达水平的差异有统计学意义(F=7.55,P＜0.01),且双相躁狂组和双相抑郁组均低于对照组(P＜0.05或P＜0.01).(2)双相障碍组BDNF血清蛋白浓度低于对照组(t=-2.90,P＜0.01);双相躁狂组、双相抑郁组与对照组3组间BDNF血清蛋白浓度的差异有统计学意义(F=4.21,P＜0.05);双相躁狂组和双相抑郁组BDNF血清蛋白浓度均低于对照组(P均＜0.05),但双相躁狂组与双相抑郁组比较差异无统计学意义(P＞0.05).(3)双相躁狂组BDNF基因mRNA表达水平及血清蛋白浓度与YMRS评分未见相关(P＞0.05),双相抑郁组BDNF基因mRNA表达水平及血清蛋白浓度与HAMD17评分未见相关(P＞0.05).结论 双相障碍与BDNF水平下调可能相关,这种下降贯穿于躁狂相和抑郁相,而且BDNF的变化不会因双相障碍患者极性的变化而处于两极状态.     

亚综合征抑郁B细胞淋巴瘤白血病-2基因表达研究

目的 探讨B细胞淋巴瘤白血病-2(Bcl-2)基因与亚综合征抑郁的关系.方法 应用TaqMan探针及荧光实时定量逆转录-聚合酶链反应方法,检测亚综合征抑郁组(64例)与正常对照组(64例)外周血白细胞Bcl-2基因的mRNA表达水平的差异;应用汉密尔顿抑郁量表17项(Hamilton Depression Rating Scale 17,HAMD17)评定患者的抑郁症状.结果 亚综合征抑郁组Bcl-2基因mRNA相对表达水平低于正常对照组[(0.34±0.11)vs (0.41±0.13),P<0.01],亚综合征抑郁组Bcl-2表达水平与HAMD17评分的相关不具有统计学意义(r＝-0.22,P>0.05).结论 Bcl-2基因低表达可能与亚综合征抑郁的病理生理机制有关.     

环氧化酶-2抑制剂对裸鼠胶质瘤移植瘤Ang基因表达的影响

目的 探讨环氧化酶-2(COX-2)抑制剂尼米舒利(NIM)对裸鼠胶质瘤移植瘤血管生成素(Ang)基因表达的影响及意义.方法 人胶质瘤SHG44细胞接种于裸鼠皮下,建立裸鼠胶质瘤移植瘤模型,并按随机数字表法分为对照组(灌注等量生理盐水)和NIM治疗组[6 mg/(kg·d)],逆转录PCR技术检测移植瘤组织Ang-1、Ang-2mRNA表达,免疫组织化学染色测定肿瘤组织微血管密度(MVD),并绘制肿瘤生长曲线和计算肿瘤抑制率.结果 NIM可有效抑制移植瘤的生长,其抑瘤率为42.03%.NIM治疗组肿瘤组织Ang-2 mRNA表达水平(0.2032±0.0185)较对照组(0.6024±0.0289)明显降低,差异有统计学意义(P＜0.05);Ang-1 mRNA表达水平无明显改变,差异无统计学意义(P＞0.05);Ang-2/Ang-1 mRNA比值下降(0.5825±0.0621vs 1.5847±0.1948),差异有统计学意义(P＜0.05).NIM治疗组肿瘤组织MVD较对照组明显下降,差异有统计学意义(P＜0.05).结论 COX-2抑制剂NIM可下调Ang-2基因表达,改变Ang-2/Ang-1 mRNA比值,抑制肿瘤生长.

Abstract：

Objective To investigate the effect of nimesulide (NIM), a selective cyclooxygenase-2 (COX-2) inhibitor, on angiopoietins (Ang) gene expression of human glioma xenografts in nude mice and its significance. Methods Human SHG44 glioma cells were inoculated subcutaneously in 16 nude mice to establish xenograft models, and then these mouse models were randomly divided into NIM treatment group and control group. NIM (6 mg/kg) and saline were poured into the stomachs of the mice in each group, respectively, once daily for 35 d. The mRNA expressions of Ang-1 gene and Ang-2 gene in the xenografts were determined by RT-PCR. Microvessel density (MVD) in the xenografts was assessed by immunohistochemical technique. The tumor growth curve was drawn and the inhibition ratio of tumor growth was calculated. Results NIM could significantly inhibit the glioma xenografts growth with its inhibition rate reaching 42.03%. The mRNA expression of Ang-2 gene in NIM treatment group (0.2032±0.0185) was significantly lower than that in control group (0.6024±0.0289, P＜0.05), but that of Ang-1 gene showed no significant changes; therefore, the mRNA ratio of Ang-2/Ang-1 genes was decreased (0.5825±0.0621 vs. 1.5847±0.1948, P＜0.05). MVD in the xenografts of the NIM treatment group was significantly lower than that in the control group (P＜0.05). Conclusion NIM, by down-regulating the mRNA expression ofA ng-2 gene and changing the mRNA ratio of Ang-2/Ang-1 genes, can inhibit the tumor growth     

母爱剥夺对大鼠行为及纹状体前列腺凋亡反应蛋白基因表达的影响

目的 研究早期母爱剥夺对大鼠成年后的抑郁水平及纹状体前列腺凋亡反应蛋白(par-4)表达的影响,以及甲基化是否参与par-4基因表达的调控.方法 按照随机数字表法,将新生幼鼠按窝分为母爱剥夺组和对照组,每组17只;母爱剥夺组仔鼠在出生后的第1～14天,每天接受6 h母子分离,对照组不接受任何实验处理;13周龄时,采用强迫游泳实验和糖水偏爱实验测定大鼠的抑郁水平,采用实时定量聚合酶链反应检测纹状体par-4及多巴胺受体2(DRD2)信使RNA(mRNA)表达水平,采用亚硫酸盐测序法检测par-4基因启动子区DNA甲基化水平.结果 母爱剥夺组大鼠漂浮时间[(152.80±74.21)s]较对照组[(63.80±80.55)s]延长,糖水偏爱率(0.45±0.23)较对照组(0.69±0.25)降低,差异均有统计学意义(t=2.79,P<0.05;t=-2.57,P<0.05);母爱剥夺组大鼠纹状体内par-4(0.02±0.02)及DRD2 mRNA表达量(0.11±0.09)分别为对照组[(0.04±0.02)、(0.32±0.21)]的0.53倍和0.31倍;母爱剥夺组大鼠par-4基因启动子区DNA甲基化水平与对照组相比差异无统计学意义(t=-0.748,P>0.05).结论 母爱剥夺能引发大鼠抑郁样行为表现,并能抑制纹状体par-4的表达,基因甲基化可能不是其调控机制.

Abstract：

Objective To study the effect of maternal deprivation on the depressive behaviors and the expression of prostate apoptosis response-4(par-4)in adult rats'striatum,and to explore whether DNA methylaion be involved in the regulatory mechanism of par-4 expression.Methods Newborn rats were randomly divided into two groups,the maternal deprivation group rats(n=17)were deprived from their mother 6 hours per day from postnatal day 1 to 14,while the control group rats(n=17)received no experimental handle.When they grew up to thirteen weeks,their depressive level was assessed with forced swimming test and sucrose consumption test,the mRNA expression of par-4 and DRD2 in rats'striatum was detected by real-time Polymerase Chain Reaction(real-time PCR),and the DNA methylation level of par-4 was determined by bisulfated DNA sequencing.Results The float time of maternal deprivation rats [(152.80±74.21)s]was longer than the control rats[(63.80±80.55)s](t=2.79,P<0.05),and the sucrose preference rate of maternal deprivation rats (0.45±0.23)was reduced compared with the control rats(0.69 ±0.25)(t=-2.57,P<0.05).The fold changes of par-4(0.02±0.02)and DRD2(0.11±0.09)mRNA expression in maternal deprivation rats compared to control rats[(0.04±0.02),(0.32±0.21)]were 0.53 and 0.31 respectively.However,there was no significant difference between two groups in methylation level of par-4 promoter region(t=-0.748,P>0.05).Conclusion Maternal deprivation could induce the depressive behavior of rats and influence the expression of par-4,but DNA methylation may not be involved in the regulatory mechanism.     

乌司他丁对实验性自身免疫性脑脊髓炎小鼠神经的保护作用

目的 研究乌司他丁(UTI)对实验性自身免疫性脑脊髓炎(EAE)髓鞘再生及脑源性神经营养因子(BDNF)表达的影响.方法 24只C57BIZ6雌性小鼠随机分成UTI组(U组)、对照组(S组)和正常组(N组),每组8只,以髓鞘染色观察腰髓髓鞘脱失情况,采用Western blot技术检测并比较各组脑组织BDNF、髓鞘碱性蛋白(MBP)、2',3'-环核甘酸-3'-磷酸水解酶(CNPase)表达浓度.结果 U组小鼠神经功能评分(第12、13、14、22、23、31、33、34、35天时分别为0、0.25、0.38、0.63、0.63、0.40、0.40、0.40和0.40分)明显低于S组(相同时点分别为0.55、0.88、1.00、1.75、2.25、1.00、1.00、1.00和1.00,U=16.00、15.00、14.50、7.50、0.00、14.0、14.50、12.00和14.50,均P＜0.05).U组小鼠髓鞘脱失程度较S组轻.Western blot结果显示U组脑组织BDNF、MBP、CNP(1.96±0.29、2.67±0.48和1.75±0.20)较S组(0.80±0.15、1.36±0.38和1.06±0.18)表达增高,差异具有统计学意义(LSD法,P＜0.05).结论 UTI对EAE具有神经保护作用,其机制可能是通过促进脑组织BDNF表达,保护少突胶质细胞、神经元及促进髓鞘再生.

Abstract：

Objective To investigate the effect of ulinastatin (UTI) on the expression of brainderived neurotrophic factor ( BDNF ) and remyelination in mice with experimental autoimmune encephalomyelitis ( EAE).Methods Twenty-four C57BL/6 mice were randomly divided into UTI group (U),normal saline treated group (S) and normal control group (N,n = 8,respectively).Demyelinations in the spinal cord were observed by solochrome cyanin staining.The expression of BDNF,myelin basic protein (MBP),and 2',3 '-cyclic nucleotide 3'-phosphodiesterase (CNP) in brain tissue of each group were evaluated by Western blot.Results Average clinical scores in group U at the 12,13,14,22,23,31,33,34 and 35 days were 0,0.25,0.38,0.63,0.63,0.40,0.40,0.40 and 0.40 respectively.They were significantly lower than group S at the same time ( U= 16.00,15.00,14.50,7.50,0.00,14.50,14.50,12.00 and 14.50,all P ＜0.05).Solochrome cyanin staining showed that demyelination of spinal cord in group U was also significantly improved than group S.Expressions of BDNF ( 1.96 ± 0.29),MBP (2.67 ± 0.48 ) and CNP ( 1.75 ± 0.20) in group U were all significantly higher than group S ( There were 0.80 ± 0.15,1.36 ± 0.38 and 1.06 ± 0.18 respectively,all P ＜ 0.05).Conclusions UTI has protective effect on EAE.The possible mechanism is that it could promote remyelination,and protect oligodendrocytes and neurons in EAE model by increasing BDNF expression in brain.     

Effects of ginsenoside on brain-derived neurotrophic factor and tyrosine kinase B mRNA expression in the hippocampal formation of aged rats*☆

BACKGROUND： There are a limited number of studies involving the effects of ginsenosides, the active component of ginseng, on expression of hippocampal TrkB mRNA in aged rats.
OBJECTIVE： To observe expression of brain-derived neurotrophic factor （BDNF） and tyrosine kinase B （TrkB） mRNA in the hippocampal formation of aged rats, as well as changes after ginsenoside administrated.
DESIGN, TIME AND SETTING： A randomized, controlled experiment was performed at the Department of Anatomy, College of Basic Medical Sciences, China Medical University in March 2005.
MATERIALS： A total of 39 female, Wistar rats were randomly divided into 3 groups （n = 13 each）： young （3-5 months old）, aged （27 months old）, and ginsenoside group （received 25mg/kg/d ginsenoside in the drinking water between 17 and 27 months of age）.
METHODS： Following anesthesia, the rats were exsanguinated and perfused transcardially with chilled, heparinized, 0.9% saline. The brains were removed and post-fixed in 40 g/L paraformaldehyde/phosphate buffer for 20 minutes, and further incubated in 30% sucrose/phosphate buffer overnight.
MAIN OUTCOME MEASURES： In situ hybridization, immunohistochemistry, and image analysis were used to investigate expression of BDNF and TrkB mRNA in the hippocampal formation. RESULTS： The expression levels of BDNF in the hippocampal CA3 and CA1 of aged rats was significantly less than the young group （t = 2.879, 1.814, 1.984, P 〈 0.05）. BDNF expression was significantly greater in the dentate gyrus of the ginsenoside group, compared with the aging group （t = 1.943, P 〈 0.01）. The expression of TrkB mRNA in the hippocampal CA3, CA1, and dentate gyrus of aged rats was less than the young group （t = 3.540, 3.629, 17.905, P 〈 0.01）. TrkB mRNA expression in the CA3 region and dentate gyrus of the ginsenoside group was significantly greater compared with the aging group （t = 1.293, 3.386, P 〈 0.05, 0.01 ）.
CONCLUSION： BDNF and TrkB mRNA expression in the hipp     

晚发性抑郁症患者血浆脑源性神经营养因子水平与认知功能

目的 探讨晚发性抑郁症患者血浆脑源性神经营养因子(BDNF)水平与抑郁症发病及认知功能之间的关系.方法 采用酶联免疫吸附法测定34例未经治疗的晚发性抑郁症患者(患者组)和32名正常对照(对照组)血浆BDNF水平;对患者组及对照组进行17项汉密尔顿抑郁量表( HAMD17)评估及神经心理学测试;对患者组的血浆BDNF水平及HAMD17总分与认知功能进行Pearson相关分析.结果 患者组治疗前的神经认知测试成绩显著差于对照组(P＜0.01);患者组的血浆BDNF水平[(3.24±2.67) μg/L]低于对照组[(6.71±3.16)μg/L,P＜0.01].血浆BDNF水平与各项认知成绩、HAMD17总分值均无显著相关性(P＞0.05).结论 部分晚发性抑郁症患者存在认知功能广泛受损;血浆BDNF水平低下与晚发性抑郁症发病密切相关,与认知功能可能无直接相关性.     

抑郁症首次发病患者情绪加工特征及抗抑郁剂治疗前后的变化

目的 探讨首次发病(以下简称首发)抑郁症情绪加工特征及抗抑郁剂治疗前后变化与症状改善的关联作用.方法 17例抑郁症首发患者治疗前后及22名对照者完成情绪词识别任务.患者组抗抑郁剂治疗9周,以汉密尔顿抑郁量表(17项,HAMD)评估疗效.结果 (1)患者组治疗有效率为88%,HAMD总分减分率75%.(2)情绪词识别任务:抑郁症组治疗前后正性词遗漏数[分别为(7.4±6.9)个和(4.1±5.3)个]均大于负性词遗漏数[分别为(3.2±3.3)个和(1.8±2.7)个;P＜0.05),治疗后正性词遗漏数小于治疗前(P=0.002),与对照组[(3.0±2.6)个]差异无统计学意义(P=0.44);治疗前后负性词遗漏数[分别为(3.2±3.3)个和(1.8±2.7)个]与对照组[(2.1±2.4)个],以及正负性词错判数与对照组差异均无统计学意义(P＞0.05);正性词平均反应时治疗后[(514±68)ms]短于治疗前[(550±75)ms;P=0.036],负性词平均反应时治疗前后[分别为(540±80)ms和(521±61)ms]差异无统计学意义(P=0.16).(3)治疗前正性词遗漏数与抑郁症状和负性思维评分正相关(r=0.36～0.50,P＜0.05).(4)治疗前后正、负性词遗漏数变化对HAMD分数变化有不同预测作用(r_( chang) ~2=0.45,P=0.002).结论首发抑郁症患者可能存在正性情绪加工缺陷,治疗后可恢复至正常水平;以负性情绪加工占优势的认知结构不因抑郁症状缓解而改变;正负性情绪加工变化与症状改善可能有不同的关联作用.     

老年卒中后抑郁患者血清细胞因子的研究

目的 探讨老年卒中后抑郁患者(PSD)血清细胞因子白细胞介素-1β(II-1β)、白细胞介素-6(IL-6)以及肿瘤坏死因子(TNF-α)的水平.方法 采用酶联免疫吸附法检测PSD组(36例)及卒中后无抑郁患者(对照组;32例)的血清IL-1β、IL-6及TNF-α水平,并以汉密尔顿抑郁量表(HAMD)评分将PSD组分为轻度组(8～16分;9例)、中度组(17～23分;17例)及重度组(≥24分;10例),比较各组血清IL-1β、IL-6及TNF-α水平的差异.结果 (1)PSD组血清IL-1β[(35.2±4.2)ng/L]、IL-6[(11.3±4.3)ng/L]及TNF-α[(32.4±6.9)ng/L]水平,均高于对照组[分别为(18.1±3.3)ng/L、(6.1±1.9)ng/L及(21.6±4.8)ng/L;P＜0.01];(2)卒中后重度抑郁组血清IL-1β[(41.8±3.2)ng/L]、IL-6[(17.5±5.7)ng/L]及,TNF-α[(38.8±5.8)ng/L]水平,均高于轻度抑郁组[分别为(29.1±2.3)ng/L、(6.6 ±1.7)ng/L及(25.9 ±3.3)ng/L;P＜0.05]、中度抑郁组[分别为(34.6±2.6)ng/L、(10.2 ±3.5)ng/L及(32.1±3.6)ng/L;P＜0.05],中度抑郁组亦高于轻度抑郁组(P＜0.05);(3)血清IL-1β(r=0.637)、IL-6(r=0.698)、TNF-α(r=0.722)水平均与抑郁的严重程度显著相关(P＜0.01).结论 IL-1β、IL-6及TNF-α可能在卒中后抑郁的发生发展中起重要作用.     

单相与双相抑郁症患者沉思反应及拖延行为的比较

目的:探讨单相与双相抑郁患者沉思反应及拖延行为的差异。方法:对32例单相抑郁(单相组)及31例双相抑郁(双相组)患者分别评定沉思量表(RRS)、一般拖延行为问卷(GPS)和汉密尔顿抑郁量表(HAMD-17)评定;对26名正常对照者(健康组)给予RRS和GPS评定,然后进行组间比较。结果:抑郁组的RRS总分(55.8±9.5)显著高于健康组[(45.8±8.1),P0.01)],抑郁组的GPS总分(57.2±8.9)也显著高于健康组[(49.3±8.4),P0.05];单相组和双相组的RRS总分及GPS总分与HAMD总分及阻滞、绝望感因子分均呈显著正相关(r=0.368~0.491,P0.05或P0.01);单相组与双相组的RRS总分及各因子分和GPS总分差异无统计学意义(P0.05)。结论:抑郁症患者比健康人更易陷入沉思,且也较易采取拖延方式;单相与双相抑郁症患者的沉思反应及拖延行为未见实质性差别,但在临床上需加以关注。     

抑郁发作自杀未遂患者脑源性神经营养因子水平及其相关因素研究

目的 探讨脑源性神经营养因子(BDNF)在抑郁发作自杀未遂者中的可能作用.方法 对抑郁发作自杀未遂患者(自杀未遂组,23例)和抑郁发作无自杀行为患者(无自杀组,24例)采用汉密尔顿抑郁量表(24项,HAMD24)、Beck绝望量表(BHS)和自杀意念自评量表(SIOSS)评定抑郁严重程度、绝望程度及自杀意图的强烈程度;采用酶联免疫吸附法测定其血清BDNF浓度,并与正常对照者(对照组,30名)比较;对自杀未遂组的血清BDNF浓度与各相关因素进行Pearson相关分析.结果 (1)自杀未遂组的HAMD24[(37.8±8.7)分]、BHS[(13.0±3.8)分]及SIOSS评分[(18.1±3.9)分]均高于无自杀组[分别为(26.0±6.0)分、(7.5±4.3)分、(12.0±4.0)分;P<0.01].(2)自杀未遂组的BDNF平均浓度[(57 ±16)ng/L]低于无自杀组[(75 ±28)ng/L;P<0.05],无自杀组的BDNF平均浓度亦低于正常对照组[(111±39)ng/L;P<0.01].(3)自杀未遂组的血清BDNF浓度与抑郁发作的病程(r=-0.541)、BHS总分(r=-0.494)、SIOSS总分(r=-0.754)呈负相关(P<0.01-0.05).结论 低水平的BDNF可能是抑郁发作自杀未遂的一个危险因素.     

γ-氨基丁酸对亚综合征性抑郁认知功能的作用

目的:探讨舍曲林联合γ-氨基丁酸(GABA)对亚综合征性抑郁(SSD)认知功能的影响。方法:83例SSD患者分为单用药组(单用舍曲林治疗)45例和合用药组(舍曲林联合GABA治疗)38例。疗程12个月。于治疗前和治疗12个月采用抑郁自评量表(SDS)、韦氏成人智力量表(WAIS)、临床记忆量表、威斯康星卡片分类测验(WCST)评定认知功能和抑郁症状严重度。结果:治疗后两组SDS、WAIS、WCST和临床记忆量表的指向记忆、联想学习、记忆商数以及合用药组的图像自由回忆均较治疗前有显著改善(P<0.05或P<0.01);以合用药组的联想学习、记忆商数、WCST正确百分数和随机错误数成绩较单用药组明显为好(P<0.05)。结论:GABA联合舍曲林对亚综合征性抑郁认知功能的改善较单用舍曲林更为显著。     

舍曲林与帕罗西汀治疗抑郁症首次发病患者认知功能的相关研究

目的 比较舍曲林与帕罗西汀对抑郁症首次发病患者认知功能的影响及其相关因素.方法 将符合国际疾病分类第10版关于抑郁发作诊断标准、17项汉密尔顿抑郁量表(HAMD17)评分≥17分、年龄18～65岁的100例首次发病的门诊患者,按照随机数字表法分为舍曲林组(51例,剂量范围25～150 mg/d)和帕罗西汀组(49例,剂...     

抑郁症患者治疗前后血清脑源性神经营养因子水平变化及相关因素分析

目的 探讨抑郁症患者血清脑源性神经营养因子(BDNF)水平及其变化与负性生活事件、抑郁症发病及治疗效应的关系.方法 采用横断面的病例-对照及前瞻性自身对照设计.对所有抑郁症患者给予抗抑郁治疗(包括抗抑郁药和改良电抽搐治疗),并随访治疗8周;采用酶联免疫吸附法测定63例抑郁症患者(抑郁症组)治疗前和治疗第2,4,8周末及80名正常对照(以下简称对照组)血清BDNF水平,并评定汉密尔顿抑郁量表(HAMD)和生活事件量表.结果 抑郁症组治疗前血清BDNF水平[(24±14)μg/L]显著低于对照组[(36±15)μg/L](t=-4.863,P=0.000),并与病前1年负性生活事件刺激值、治疗前HAMD总分均显著负相关(r=-0.331,P=0.008;r=-0.343,P=0.006),而后两者有相互正相关(r=0.292,P=0.020);治疗第2周末血清BDNF水平仍显著低于对照绢(t=-5.990,P=0.000),并与其抑郁症状严重度平行负相关(r=-0.269,P=0.033),且其血清BDNF增加率与HAMD减分率平行正相关(r=0.252,P=0.047);治疗第4,8周末血清BDNF水平均显著高于治疗前(经ISD检验,P=0.000;P=0.005),与对照组的差异均无统计学意义(P均＞0.05).治疗第2,4,8周末HAMD总分渐减并均低于治疗前(P均=0.001),且其HAMD平均减分率渐升(分别为40%,66%和74%).结论血清BDNF低下与负性生活事件、抑郁症发病密切相关,血清BDNF升高可能为抗抑郁治疗临床疗效的重要指标之一.     

舍曲林联合归因训练对脑卒中后抑郁及神经功能康复的影响

目的探讨舍曲林联合归因训练对脑卒中后抑郁及神经功能康复的影响。方法共78例脑卒中后抑郁患者,随机分为研究组和对照组,研究组给予舍曲林联合归因训练,对照组单用舍曲林治疗,疗程8周。在治疗前及治疗的第2、4、6、8周末用汉密尔顿抑郁量表(Hamilton depression rating scale,HAMD)和美国国立卫生研究院卒中量表(National Institute of Health stroke scale,NIHSS)分别评定抑郁症状和神经功能康复情况。结果经重复测量方差分析显示,患者HAMD总分的时间主效应、分组主效应以及时间与分组交互效应均有统计学意义(P0.05)。其中研究组在2、4、6、8周末HAMD总分均明显低于对照组[(18.25±4.27)vs.(20.81±4.63),(15.94±3.47)vs.(18.12±4.51),(12.85±3.12)vs.(16.54±3.70),(10.42±3.66)vs.(13.09±3.59)],差异有统计学意义(P0.05);研究组与对照组HAMD总分在各个时点均较治疗前降低(P0.01)。治疗8周后研究组有效率(以HAMD减分率评价)高于对照组(77.5%vs.52.6%),差异有统计学意义(P0.05)。两组NIHSS总分的时间主效应有统计学意义(P0.01),分组主效应、时间与分组交互效应无统计学意义(P0.05)。研究组与对照组NIHSS总分在各个时点均较治疗前降低(P0.01)。结论舍曲林联合归因训练可明显缓解脑卒中后抑郁患者的抑郁症状,但归因训练对患者神经功能改善不明显。     

Subsyndromal symptomatic depression: a new concept

Although DSM-IV acknowledged the clinical significance of some subthreshold forms of unipolar depression, such as minor depression (MinD) and recurrent brief depression (RBD), clinicians continued to struggle with the concept of "subthreshold" depression. A substantial number of patients continued to present with depressive symptoms that still did not satisfy any DSM-IV diagnosis. Generally, these patients failed to complain of anhedonia and depressed mood, a criterion that DSM-IV mandates for any diagnosis of depression. Therefore, researchers reexamined the question of whether this cluster of depressive symptoms, in the absence of anhedonia and depressed mood, was clinically significant. Some researchers labeled this cluster of symptoms, "subsyndromal symptomatic depression" (SSD). Specifically, SSD is defined as a depressive state having two or more symptoms of depression of the same quality as in major depression (MD), excluding depressed mood and anhedonia. The symptoms must be present for more than 2 weeks and be associated with social dysfunction. Using Medline Search, the authors reviewed the literature on the epidemiology, demographics, clinical characteristics, and psychosocial impairment of SSD. SSD is found to be comparable in demographics and clinical characteristics to MD, MinD, and dysthymia. SSD is also associated with significant psychosocial dysfunction as compared with healthy subjects. Further; it has significant risk for suicide and future MD. Few studies have been conducted on the treatment of SSD. The high prevalence of SSD, the significant psychosocial impairment associated with it, and the chronicity of its course make subsyndromal symptomatic depression a matter for serious consideration by clinicians and researchers.