大学生神经症环境因素与COMT基因多态性的交互作用研究
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摘要
神经症是影响大学生身心健康的重要精神疾病,严重影响了大学生的学习与生活。探讨大学生神经症的环境危险因素、易感基因以及基因与环境间的交互作用,是目前精神疾病流行病学研究的重要议题。本研究将现场调查与实验室、现况调查与病例对照研究相结合探讨大学生神经症的患病情况及其遗传与环境危险因素,并基于多因素Logistic回归模型探讨COMT基因多态性与环境危险因素交互作用对大学生神经症发病的影响,是基因与环境交互作用研究的有益尝试,为神经症的病因学研究提供了重要线索,研究结果对于大学生神经症的有效防制具有重要意义。
本研究采用WHO-CIDI-3.0对在校本科大学生进行一对一面对面访谈,按ICD-10的神经症性障碍诊断标准筛查大学生中神经症患者,并以现况调查所筛查到的大学生神经症患者为病例组,选择此次调查中排除神经症等精神疾病诊断的健康大学生为对照,采用PCR-LDR的方法检测两组样本COMT基因上8个tag SNPs的基因多态性,经关联分析探讨8个tag SNPs基因多态性与大学生神经症的关联;将筛查到的环境危险因素分别与检测的COMT基因8个tag SNPs多态性进行基于多因素Logistic回归模型的交互作用分析,探讨COMT基因多态性与环境因素交互作用对大学生神经症发病的影响。
研究结果显示目前在校大学生神经症的终生患病率为25.61%,12个月患病率为15.74%,30天患病率为6.84%,大学生神经症的分布存在年级差异,多因素分析发现母亲的心理状况差和童年时期父母对其的照看程度不够为大学生神经症的重要危险因素;关联分析结果显示COMT基因上rs737865、rs174675、rs5993883、rs5992500、rs165656、rs2239393、rs4646316和rs165774共8个tag SNPs位点的多态性与大学生神经症无关联,提示COMT可能不是大学生神经症的主要易感基因;基因与环境交互作用分析发现rs5993883位点的多态性与母亲的心理状况存在超相乘和正相加交互作用。
本研究结果提示神经症是大学生的主要心理健康问题,应积极促进大学生心理健康,有效控制大学生精神疾病的发生。对母亲心理状况不好、童年时期缺少父母照看的大学生应加大防制力度,有效防止神经症的发生或病情的进一步加重。
Neuroses are a group of mental diseases which seriously affect mental and physical health of university students. To explore the environmental risk factors, susceptibility genes and the interactions between genes and environment is an important subject in epidemiological mental disease research. In this study the prevalence of neuroses and its genetics and environment risk factors were conducted in university students based on the combination of field survey with laboratory investigation and case-control study. The interactions between COMT gene polymorphism and environmental risk factors in the development of neuroses in the university students were analyzed based on the multi-factor logistic regression model. The results may provide the important clue for etiology of neuroses and will be very useful for control of neuroses in university students..
Objective
To investigate the prevalence and distribution of neuroses characteristatics and analyze environmental risk factors, and relationship between COMT gene polymorphism and neuroses based on case-control study and interactions between COMT gene and environmental factors on neuroses in undergraduates of a comprehensive university. The present study will provide clue for further etiology study and theoretical basis for control neuroses.
Methods
①We sampled 2,046 undergraduates in a comprehensive university as subjects using a proportional stratified sample method and adopted the WHO-CIDI-3.0 as tool to collect information through face-to-face interview method and meanwhile collected their saliva for laboratory research. Data entry and diagnosis of neuroses according to the ICD-10 were done with CIDI-3.0 attached software. The SPSS12.0 software was used to analyze the prevalence, population distribution characteristics and related risk factors of neuroses in undergraduates.②In case-control study, both cases and controls came from the field survey. Cases were undergraduates who had been diagnosed as neuroses through the survey and controls were those who are healthy and without any mental illness. We extracted the genomic DNA from the saliva samples and detection the polymorphism of eight tag SNPs in COMT gene using PCR-LDR method. We analyzed the relationship of polymorphism of eight tag SNPs in COMT gene and neuroses using the method of correlation analysis based on case-control study, thereby researched the association of COMT gene and neuroses in university students.③Based on②we analyzed the environmental factors obtained from field survey again and got potential environmental influenced factors. Then we studied the interactions between COMT gene polymorphism and the screening environmental influenced factors in causation of neuroses by using multi-factor Logistic regression model method.
Results
①There are 1,848 completed interview questionnaires in 2,046 samples and 1,843 questionnaires are eligible. The response rate is 90.32% (1,848/2,046), the qualification rate is 99.73% (1,843/1,848), and the effective response rate is 90.08% (1,843/2,046). The results show that according to the diagnostic criterion for neuroses of ICD-10 the lifetime prevalence is 25.60%, the 12-month prevalence is 15.74% and 30-day prevalence is 6.84% in 1843 undergraduates who we interviewed. Among the various clinical subtypes of neuroses, the 12-month prevalence of obsessive-compulsive disorder is the highest (9.88%), the second is specific phobia (4.94%) and the third is social phobia (2.39%). The 12-month prevalence with more than two kinds of subtypes of neuroses is 2.71%.②In male college students the lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neurosis is respectively 26.25% (326/1,242), 15.70% (195/1,242) and 7.09% (88/1,242), while in female college students the lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neurosis is respectively 24.29 (146/601), 15.81% (95/601) and 6.32% (38/601). The difference of three kinds of prevalence rate of neuroses in male and female students has no statistical significance (P> 0.05). In different grades the 12-month prevalence rate of neuroses is 16.88% in freshmen, 19.29% in sophomores, 11.76% in juniors and 14.67% in seniors (including the fifth year students majoring in medicine). The difference of 12-month prevalence rate of neuroses in different grades has statistically significance (x~2 = 10.648, P <0.05).③In the field survey, the results of multi-factor non-conditional logistic regression analysis show that juniors have lower risk to neuroses than freshmen (OR = 0.602), the students whose fathers having poor psychological state have 1.545 times risk of neuroses than those whose fathers having good psychological state, the students whose mothers with poor psychological state have 1.565 times risk of neuroses than those whose mothers with good psychological state, the students suffering more quarrel between their parents have 1.546 times risk of neuroses than those suffering less quarrel, and lacking of parents' care in childhood increases risk to neuroses (OR = 1.905).④Genotype distribution of eight tag SNPs in COMT gene(rs737865, rsl74675, rs5993883, rs5992500, rsl65656, rs2239393, rs4646316 and rs165774) do not deviate from the Hardy-Weinberg equilibrium both in case group and control group (P> 0.05), The association analyses found that genotype and allele distribution had no significant difference between case and control group (P>0.05). Both genotype and allele association with clinical subtypes were tested and only tag SNP rs174675 showed association with phobia neuroses (P< 0.05). The haplotype analysis was done using UNPHASED software and showed no haplotypic association between any certain haplotype and neuroses in university students (P> 0.05).⑤The potential environmental factors mining by using multi-factor non-conditional logistic regression analysis finds that family environmental factors including mother's poor psychological state, lacking of parents care in childhood and father's severe restriction are risk factors of neuroses in university students. In interaction study, interaction only exists between rs5993883 polymorphism and the mother's psychological state (P<0.05), which is super multiplicative and positive plus interaction, and there are no interactions between other tag SNPs and the three environmental risk factors of neuroses (P>0.05).
Conclusions
①The lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neuroses is respectively 25.61%, 15.74% and 6.84% in undergraduates. Among various clinical subtypes of neuroses, the 12-month prevalence of obsessive-compulsive disorder is the highest. There is no significantly statistical difference in the three kinds of prevalence rate of neuroses between male and female students. The 12-month prevalence rate of neuroses in lower grade students is higher than that in upper grade students. All above results suggest that neuroses may influence the mental health condition of college students. We should act mental health promotion to university students and effectively control the occurrence of mental illness in university students.②The mother's poor psychological condition and lack of parents care in childhood are important risk factors for neuroses in undergraduates, and other factors, such as father's psychological state, quarrel between parents and father's severe restriction, also have a certain impact on neuroses in undergraduates.③The genetic polymorphisms of eight tag SNPs in COMT gene have no association with neuroses in undergraduates and association analysis between tag SNPs and clinical subtypes finds only rs174675 shows association with phobia neuroses. All these results indicate that COMT gene is not the major susceptibility gene for neuroses but can't be excluded micro effect on neuroses.④There is super multiplicative and positive plus interaction between rs5993883 polymorphism and the mother's psychological state, and there are no interactions between other tag SNPs and the three environmental risk factors of neuroses.
本研究采用WHO-CIDI-3.0对在校本科大学生进行一对一面对面访谈,按ICD-10的神经症性障碍诊断标准筛查大学生中神经症患者,并以现况调查所筛查到的大学生神经症患者为病例组,选择此次调查中排除神经症等精神疾病诊断的健康大学生为对照,采用PCR-LDR的方法检测两组样本COMT基因上8个tag SNPs的基因多态性,经关联分析探讨8个tag SNPs基因多态性与大学生神经症的关联;将筛查到的环境危险因素分别与检测的COMT基因8个tag SNPs多态性进行基于多因素Logistic回归模型的交互作用分析,探讨COMT基因多态性与环境因素交互作用对大学生神经症发病的影响。
研究结果显示目前在校大学生神经症的终生患病率为25.61%,12个月患病率为15.74%,30天患病率为6.84%,大学生神经症的分布存在年级差异,多因素分析发现母亲的心理状况差和童年时期父母对其的照看程度不够为大学生神经症的重要危险因素;关联分析结果显示COMT基因上rs737865、rs174675、rs5993883、rs5992500、rs165656、rs2239393、rs4646316和rs165774共8个tag SNPs位点的多态性与大学生神经症无关联,提示COMT可能不是大学生神经症的主要易感基因;基因与环境交互作用分析发现rs5993883位点的多态性与母亲的心理状况存在超相乘和正相加交互作用。
本研究结果提示神经症是大学生的主要心理健康问题,应积极促进大学生心理健康,有效控制大学生精神疾病的发生。对母亲心理状况不好、童年时期缺少父母照看的大学生应加大防制力度,有效防止神经症的发生或病情的进一步加重。
Neuroses are a group of mental diseases which seriously affect mental and physical health of university students. To explore the environmental risk factors, susceptibility genes and the interactions between genes and environment is an important subject in epidemiological mental disease research. In this study the prevalence of neuroses and its genetics and environment risk factors were conducted in university students based on the combination of field survey with laboratory investigation and case-control study. The interactions between COMT gene polymorphism and environmental risk factors in the development of neuroses in the university students were analyzed based on the multi-factor logistic regression model. The results may provide the important clue for etiology of neuroses and will be very useful for control of neuroses in university students..
Objective
To investigate the prevalence and distribution of neuroses characteristatics and analyze environmental risk factors, and relationship between COMT gene polymorphism and neuroses based on case-control study and interactions between COMT gene and environmental factors on neuroses in undergraduates of a comprehensive university. The present study will provide clue for further etiology study and theoretical basis for control neuroses.
Methods
①We sampled 2,046 undergraduates in a comprehensive university as subjects using a proportional stratified sample method and adopted the WHO-CIDI-3.0 as tool to collect information through face-to-face interview method and meanwhile collected their saliva for laboratory research. Data entry and diagnosis of neuroses according to the ICD-10 were done with CIDI-3.0 attached software. The SPSS12.0 software was used to analyze the prevalence, population distribution characteristics and related risk factors of neuroses in undergraduates.②In case-control study, both cases and controls came from the field survey. Cases were undergraduates who had been diagnosed as neuroses through the survey and controls were those who are healthy and without any mental illness. We extracted the genomic DNA from the saliva samples and detection the polymorphism of eight tag SNPs in COMT gene using PCR-LDR method. We analyzed the relationship of polymorphism of eight tag SNPs in COMT gene and neuroses using the method of correlation analysis based on case-control study, thereby researched the association of COMT gene and neuroses in university students.③Based on②we analyzed the environmental factors obtained from field survey again and got potential environmental influenced factors. Then we studied the interactions between COMT gene polymorphism and the screening environmental influenced factors in causation of neuroses by using multi-factor Logistic regression model method.
Results
①There are 1,848 completed interview questionnaires in 2,046 samples and 1,843 questionnaires are eligible. The response rate is 90.32% (1,848/2,046), the qualification rate is 99.73% (1,843/1,848), and the effective response rate is 90.08% (1,843/2,046). The results show that according to the diagnostic criterion for neuroses of ICD-10 the lifetime prevalence is 25.60%, the 12-month prevalence is 15.74% and 30-day prevalence is 6.84% in 1843 undergraduates who we interviewed. Among the various clinical subtypes of neuroses, the 12-month prevalence of obsessive-compulsive disorder is the highest (9.88%), the second is specific phobia (4.94%) and the third is social phobia (2.39%). The 12-month prevalence with more than two kinds of subtypes of neuroses is 2.71%.②In male college students the lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neurosis is respectively 26.25% (326/1,242), 15.70% (195/1,242) and 7.09% (88/1,242), while in female college students the lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neurosis is respectively 24.29 (146/601), 15.81% (95/601) and 6.32% (38/601). The difference of three kinds of prevalence rate of neuroses in male and female students has no statistical significance (P> 0.05). In different grades the 12-month prevalence rate of neuroses is 16.88% in freshmen, 19.29% in sophomores, 11.76% in juniors and 14.67% in seniors (including the fifth year students majoring in medicine). The difference of 12-month prevalence rate of neuroses in different grades has statistically significance (x~2 = 10.648, P <0.05).③In the field survey, the results of multi-factor non-conditional logistic regression analysis show that juniors have lower risk to neuroses than freshmen (OR = 0.602), the students whose fathers having poor psychological state have 1.545 times risk of neuroses than those whose fathers having good psychological state, the students whose mothers with poor psychological state have 1.565 times risk of neuroses than those whose mothers with good psychological state, the students suffering more quarrel between their parents have 1.546 times risk of neuroses than those suffering less quarrel, and lacking of parents' care in childhood increases risk to neuroses (OR = 1.905).④Genotype distribution of eight tag SNPs in COMT gene(rs737865, rsl74675, rs5993883, rs5992500, rsl65656, rs2239393, rs4646316 and rs165774) do not deviate from the Hardy-Weinberg equilibrium both in case group and control group (P> 0.05), The association analyses found that genotype and allele distribution had no significant difference between case and control group (P>0.05). Both genotype and allele association with clinical subtypes were tested and only tag SNP rs174675 showed association with phobia neuroses (P< 0.05). The haplotype analysis was done using UNPHASED software and showed no haplotypic association between any certain haplotype and neuroses in university students (P> 0.05).⑤The potential environmental factors mining by using multi-factor non-conditional logistic regression analysis finds that family environmental factors including mother's poor psychological state, lacking of parents care in childhood and father's severe restriction are risk factors of neuroses in university students. In interaction study, interaction only exists between rs5993883 polymorphism and the mother's psychological state (P<0.05), which is super multiplicative and positive plus interaction, and there are no interactions between other tag SNPs and the three environmental risk factors of neuroses (P>0.05).
Conclusions
①The lifetime prevalence rate, 12-month prevalence rate and 30-day prevalence rate of neuroses is respectively 25.61%, 15.74% and 6.84% in undergraduates. Among various clinical subtypes of neuroses, the 12-month prevalence of obsessive-compulsive disorder is the highest. There is no significantly statistical difference in the three kinds of prevalence rate of neuroses between male and female students. The 12-month prevalence rate of neuroses in lower grade students is higher than that in upper grade students. All above results suggest that neuroses may influence the mental health condition of college students. We should act mental health promotion to university students and effectively control the occurrence of mental illness in university students.②The mother's poor psychological condition and lack of parents care in childhood are important risk factors for neuroses in undergraduates, and other factors, such as father's psychological state, quarrel between parents and father's severe restriction, also have a certain impact on neuroses in undergraduates.③The genetic polymorphisms of eight tag SNPs in COMT gene have no association with neuroses in undergraduates and association analysis between tag SNPs and clinical subtypes finds only rs174675 shows association with phobia neuroses. All these results indicate that COMT gene is not the major susceptibility gene for neuroses but can't be excluded micro effect on neuroses.④There is super multiplicative and positive plus interaction between rs5993883 polymorphism and the mother's psychological state, and there are no interactions between other tag SNPs and the three environmental risk factors of neuroses.
引文
[1]郝伟.精神病学[M].第四版.北京:人民卫生出版社,2003.
[2]WHO.ICD-10精神与行为障碍:临床描述与诊断要点[M].中文版.北京:人民卫生出版社,1992.
[3]中华医学会精神科分会.中国精神障碍分类与诊断标准(第三版)(CCMD-3).济南:山东科学技术出版社,2001.
[4]Krupp LB.An overview of Chronic fatigue Syndrome[J].J Clin Psychiatry,1991,52:403-410.
[5]沈渔邨.精神病学[M].第四版.北京:人民卫生出版社,2002.
[6]Henderson JG.,Pollard CA.Three types of obsessive compulsive disorder in aconununity sample[J].J Clin Psychol,1988,44(5):747-752.
[7]Akhtar S,Wig NN,Varma VK,et al.A phenomenological analysis of symptoms in obsessive-compulsive neurosis[J].Br J Psychiatry,1975,8:127-342.
[8]Wilne A,Reieh T,Robins I,et al.Obsessive Compulsive neuroses[J].Comprehensive psychiatry,1976,17:527-539.
[9]胡宜,王静舒.现代医学200词:分离性障碍(Dissociative disorders)[J].日本医学介绍,2004,25(4):191-192.
[10]郝伟.精神病学[M].第六版.北京:人民卫生出版社,2008.
[11]张春美.大学生神经衰弱的身心疗法治疗150例报告[J].中国临床康复,2004,8(3):556.
[12]Kessler,Ronald C,Ustun T,et al.The World Mental Health(WMH) Survey Initiative Version of the World Health Organization(WHO) Composite International Diagnostic Interview(CIDI)[J].Int J Methods Psychiatr Res,2004,13(2):93-121.
[13]First,Spitzer著,张波译,刘协和审校.DSM-Ⅳ轴Ⅰ障碍用临床定式检查使用指南(研究版)[M].四川大学华西医学中心附属第一医院心理卫生研究所,2001.
[14]Michael BF,Robert LS,Miriam G,et al.User's Guide for Structured Clinical Interview for DSM-Ⅳ Axis Ⅰ Disorders-Research Version[M].New York:Biometrics Research,1996.
[15]张岿.一所高校学生神经症患病状况分析[J].中国心理卫生杂志,2003,17(5):340-341.
[16]田旭.大学生神经症患者个性与应付方式探讨[J].中国校医,2002,16(6):554.
[17]Marks I,刘志中译.神经症的流行病学与病因学[J].国外医学精神病学分册,1983,10(1):1-6.
[18]王娴贤,林启瑞,江小平.大学生神经症患者的心理状况调查[J].保健医学与实践,2008,5(4):27-28.
[19]Noyes R Jr,Clarkson C,Crowe RR,et al.A family study of generalized anxiety disorder[J].Am J Psychiatry,1987,144(8):1019-1024.
[20]刘协和.神经症:夏镇夷等主编,精神医学丛书(第二卷),临床精神医学[M].长沙:湖南科学技术出版社,1994:451-455.
[21]许明定.神经症家系中几种疾病流行病学初步调查[J].遗传与疾病,1985,2(4):233-235.
[22]12地区精神疾病流行学调查协作组.向孟泽执笔.12地区神经症流行学调查[J].中华神经精神科杂志,1986,19(2):87-91.
[23]李心天.医学心理学[M].北京:中国医科大学中国协和医科大学联合出版社,1997.
[24]汪向东.心理卫生评定量表手册[J].中国心理卫生杂志,1993(增刊):202-209.
[25]林雄标,黄明生.惊恐障碍与广泛性焦虑的临床对比及血乳酸、胆碱酯酶测定[J].中华神经精神科杂志,1993,26(6):348-351.
[26]马震祥,刘玉局.广泛性焦虑遗传效应和遗传方式研究[J].临床精神医学杂志,2006,16(6):336-337.
[27]马震祥,王蕾,卞正发,等.惊恐障碍的遗传方式探讨[J].临床精神医学杂志.2004,14(3):137-138.
[28]Pauls DL,Alsobrook JP,Goodman W,et al.A family study of obsessive-compulsive disorder[J].Am J Psychiatry,1995,152(1):76-84.
[29]Samuels JF,Riddle MA,Greenberg BD,et al.The OCD Collaborative Genetic Study:methods and sample description[J].Am J Med Genet B Neuropsychiatr Genet.2006,141B(3):201-207.
[30]杨彦春,刘协和.强迫症的家系遗传研究[J].中华医学遗传学杂志,1998,15(5):303-306.
[31]Jonnal AH,Gardner CO,Prescott CA,et al.Obsessive and compulsive symptoms in a general population sample of female twins[J].Am J Med Genet,2000,96(6):791-796.
[32]Liebowitz MR:Social phobia.Modern Problems of Pharmacopsychiatry[J].1987, 22:141-173.
[33]Williams RB,Marchuk DA,Gadde KM,et al.Serotonin-related gene polymorphisms and central nervous system serotonin function[J].Neuropsychopharmacology,2003,28(3):533-541.
[34]Denys D,Zohar J,Westenberg HG.The Role of Dopamine in Obsessive Compulsive Disorder:Preclinical and Clinical Evidence[J].J.Clin Psychiatry,2004,65(14):11-17.
[35]Fineberg NA,Roberts A,Montgomery SA.Brain 5-HT function in obsessive compulsive disorder[J].Br J Psychiatry,1997,171:280-282.
[36]Catalano M,Sciuto G,Di Bella D,et al.Lack of association between obsessive-compulsive disorder and the dopamine D3 receptor gene:some preliminary considerations[J].Am J Med Genet,1994,54(3):253-255.
[37]陈邵建.大学生心理卫生状况及其原因分析[J].应用心理学,1988,4:46-54.
[38]刘美娟,余华.大学生SCL-90测试研究的结果[J].心理科学,1995,18(5):289-290.
[39]郑延平,林克明.洛杉矶地区美国华人的神经衰弱流行病学研究[J].上海精神医学,1997,9(3):129-134.
[40]长虹,丛中.临床心理治疗[M].北京:人民军医出版社,2004.
[41]邹文华,张宏根.神经症与正常人的社会心理因素个性和躯体症状的对照研究[J].中国神经精神疾病杂志,1998,2(4):211-214.
[42]冯丽云,李克均.通径分析在大学生神经症危险因素研究中的应用[J].郑州大学学报·医学版,2003,38(2):239-242.
[43]陈复平.神经症的流行学调查[J].中华神经精神科杂志,1986,5:301-305.
[44]邱德胜,罗小年,金卫东.大学生精神障碍与生活事件[J].中原精神医学杂志,1997,3(1):8-10.
[45]李书平,郑烈,李映原,等.宁夏回族自治区城市居民神经症流行病学调查[J].中国心理卫生杂志,1999,13(3):160.
[46]章秀娟,胡岳松,俞承烈.余姚市神经症流行病学调查[J].临床精神医学杂志,1999,9(4):251-252.
[47]周天骍,张少平,江渝琦.社区老年神经症流行病学调查[J].上海精神医学,2000,12(3):125-128.
[48]韩岭,杨德森.机械工业人群神经症流行病学调查[J].中国心理卫生杂志,1989,3(2):55-58.61.
[49]吴传东,官尚工,朱国钦,等.三亚市牛兰镇回、黎、汉神经症流行病学调查[J].中国民政医学杂志,1994,增(1):19-20.
[50]赵虎,赵丹青,朱少毅,等.汕头市神经症流行病学调查[J].中国民政医学杂志,2000,12(2):80-81.
[51]王天根.流行病学研究方法[M].北京:人民卫生出版社,1991:83.
[52]向孟泽.神经症的流行病学调查[J].中华神经精神科杂志,1996,19(5):301.
[53]李真,胡季明,陈贻华,等.中山市神经症流行病学调查报告[J].临床精神医学杂志,2004,14(3):145-146.
[54]张毅宏,胡纪泽,胡赤怡,等.深圳市神经症流行病学调查[J].中国公共卫生,2006,22(7):866-867.
[55]唐宏.用MMPI、SCL-90调查大学生神经症结果分析[J].赣南医学院学报,2003,23(4):449-451.
[56]高作咏,陈晓姣,雷平冲.1542在校大学生神经症流行病学调查分析[J].咸宁医学院学报,1995,9(1):27-28,30.
[57]王志铭,王宇中,冯丽云,等.河南某医学院校学生神经症流行病学调查及其成因分析[J].河南医科大学学报,2000,35(5):438-441.
[58]梁执群,王建本,岳月仙,等.医科大学生神经症患病倾向调查[J].山西医学院学报,1993,24(3):274-275.
[59]黄周忠,陈小维,吴小南,等.福州市大学生神经症的患病状况的调查研究[J].四川精神卫生,1998,11(4):230-232.
[60]陈继军,武雪冰,刘清波.用SCL-90、EPQ调查某部队神经症结果分析[J].健康心理学杂志,2000,8(1):112-114.
[61]高平青,周宁,严昌安,等.武警部队神经症流行病学调查[J].武警医学,1999,10(2):100-101.
[62]林慰慈.南京市738名中小学生神经症患病情况的调查[J].中国校医,2000,14(4):283.
[63]吴传东,余慧菲,叶廷蔚,等.社区14-18岁中学生神经症流行病学调查[J].海南医学,1991,2(4):61-62.
[64]沈蕴华,张希良.大学生因病辍学情况调查[J].中国心理卫生杂志,1989,3(3):117.
[65]Hettema JM,Neale MC,Kendler KS.A review and meta-analysis of the genetic epidemiology of anxiety disorders[J].Am J Psychiatry,2001,158(10):1568-1578.
[66]陈婷婷.复杂疾病基因定位的统计学方法[J].黑龙江医药,2008,21(2):48-50.
[67]张学军.复杂疾病的遗传学研究策略[J].安徽医科大学学报,2007,42(3):237-240.
[68]Rutter M.Biological implications of gene-environment interaction[J].J Abnorm Child Psychol,2008,36(7):969-975.
[69]Caspi A,Moffitt TE,Cannon M,et al.Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene:longitudinal evidence of a gene X environment interaction[J].Biol Psychiatry,2005,57(10):1117-1127.
[70]Gatt JM,Nemeroff CB,Dobson-Stone C,et al.Interactions between BDNF Va166Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety[J].Biol Psychiatry,2009,doi:10.1038/mp.2008.143.
[71]Wagner S,Baskaya O,Lieb K,et al.The 5-HTTLPR Polymorphism modulates the association of serious life events(SLE) and impulsivity in patients with Borderline Personality Disorder[J].J Psychiatr Res,2009,doi:10.1016/j.jpsychires.2009.03.004
[72]Chattopadhyay A,Rukmini R,Mukherjee S.Photophysics of a neurotransmitter:ionization and spectroscopic properties of serotonin[J].Biophys J,1996,71(4):1952-1960.
[73]Artigas F,Romero L,de Montigny C,et al.Acceleration of the effect of selected antidepressant drugs in major depression by 5-HT1A antagonists[J].Trends Neurosci,1996,19(9):378-383.
[74]Ramboz S,Oosting R,Amara DA,et al.Serotonin receptor 1A knockout:an animal model of anxiety-related disorder[J].Proc Natl Acad Sci U S A,1998,95(24):14476-14481.
[75]Chavarria-Siles I,Walss-Bass C,Quezada P,et al.TGFB-induced factor(TGIF):a candidate gene for psychosis on chromosome 18p[J].Mol Psychiatry,2007,12(11):1033-1041.
[76]Choudhury K,McQuillin A,Purl V,et al.A genetic association study of chromosome 11q22-24 in two different samples implicates the FXYD6 gene,encoding phosphohippolin,in susceptibility to schizophrenia[J].Am J Hum Genet,2007,80(4):664-672.
[77]Albert PR,Lemonde S.5-HT1A receptors,gene repression,and depression:guilt by association[J].Neuroscientist,2004,10(6):575-593.
[78]Drago A,Ronchi DD,Serretti A.5-HT1A gene variants and psychiatric disorders:a review of current literature and selection of SNPs for future studies[J].Int J Neuropsychopharmacol,2008,11(5):701-721.
[79]Lin PY.Links Meta-analysis of the association of serotonin transporter gene polymorphism with obsessive-compulsive disorder[J].Prog Neuropsychopharmacol,2007,31(3):683-689.
[80]Lopez-Figueroa AL,Norton CS,Lopez-Figueroa MO,et al.Serotonin 5-HT1A,5-HT1B,and 5-HT2A receptor mRNA expression in subjects with major depression,bipolar disorder,and schizophrenia[J].Biol Psychiatry,2004,55(3):225-233.
[81]郭慧荣,肖泽萍.强迫症候选基因研究进展[J].国外医学遗传学分册,2003,26(5):303-306.
[82]Bloch MH,Landeros-Weisenberger A,Sen S,et al.Association of the serotonin transporter polymorphism and obsessive-compulsive disorder:systematic review[J].Am J Med Genet B Neuropsychiatr Genet,2008,147B(6):850-858.
[83]张岚,刘协和,李涛,等.不同发病年龄强迫症患者6种功能基因的分子遗传学研究[J].中华精神科杂志,2004,37(4):198-201.
[84]Murphy DL,Brodie HK,Goodwin FK,et al.Regular induction of hypomania by L-DOPA in 'bipolar' manic-depressive patients[J].Nature,1971,229(5280):135-136.
[85]Frederickson A.The dopamine hypothesis of schizophrenia[M].Second Web Rep,1998.
[86]Bonhomme N,Esposito E.Involvement of serotonin and dopamine in the mechanism of action of novel antidepressant drugs:a review[J].J Clin Psychopharmacol,1998,18(6):447-454.
[87]Georgieva L,Dimitrova A,Nikolov I,et al.Dopamine transporter gene(DAT1) VNTR polymorphism in major psychiatric disorders:family-based association study in the Bulgarian population[J].Acta Psychiatr Scand,2002,105(5):396-399.
[88]周云飞,张亚林,胡纪泽,等.多巴胺转运体基因多态性与强迫症的关联[J].中国行为医学科学,2006,15(7):586-587.
[89]徐勇,王振,肖泽萍,等.多巴胺D4受体基因与强迫症的关联[J].上海交通大学学报(医学版),2006,26(4):362-364.
[90]Olsson CA,Byrnes GB,Anney RJ,et al.COMT Val(158)Met and 5HTTLPR functional loci interact to predict persistence of anxiety across adolescence:results from the Victorian Adolescent Health Cohort Study[J].Genes Brain Behav,2007, 6(7):647-652.
[91]张野,江三多,钱伊萍,等.情感性精神障碍与儿茶酚邻位甲基转移酶基因的关联性研究[J].中华精神科杂志,2002,5(4):206-208.
[92]Stein DJ,Daniels WM,Savitz J,et al.Brain-derived neurotrophic factor:the neurotrophin hypothesis of psychopathology[J].CNS Spectr,2008,13(11):945-949.
[93]谭树凯,袁琼兰.脑源性神经营养因子(BDNF)与脑缺血性损伤[J].四川解剖学杂志,2008,16(4):39-41.
[94]Krebs MO,Guillin O,Bourdell MC,et al.Brain derived neurotrophic factor(BDNF)gene variants association with age at onset and therapeutic response in schizophrenia [J].Mol Psychiatry,2000,5(5):558-562.
[95]T L Petryshen,P C Sabeti,K A Aldinger,et al.Population genetic study of the brain-derived neurotrophic factor(BDNF) gene[J].Mol Psychiatry,2009,doi:10.1038/mp.2009.24
[96]Katerberg H,Lochner C,Cath DC,et al.he role of the brain-derived neurotrophic factor(BDNF) va166met variant in the phenotypic expression of obsessive-compulsive disorder(OCD)[J].Am J Hum Genet,2003,73(2)370-376.
[97]李军,罗忠金,张吉翔.脑源性神经营养因子突变与焦虑[J].生命的化学,2008,28(2):217-219.
[98]Eser D,Leicht G,Lutz J,et al.Functional neuroanatomy of CCK-4-induced panic attacks in healthy volunteers[J].Hum Brain Mapp,2009,30(2):511-522.
[99]Karayiorgou M,Sobin C,Blundell ML,et al.Family-based association studies support a sexually dimorphic effect of COMT and MAOA on genetic susceptibility to obsessive-compulsive disorder[J].Biol Psychiatry.1999,45(9):1178-1189.
[100]Grossman MH,Littrell JB,Weinatein R.Identification of the possible molecular basis for inherited differences in human catechol-O-methyltransferase[J].Soc Neurosci,1992,18:70
[101]Lundstrom K,Tenhunen J,Tilgmann C,et al.Cloning,expression and structure of catechol-O-methyltransferase[J].Biochem Biophys Acta,1995,1251(1):1-10
[102]吴怀安.儿茶酚氧位甲基转移酶与精神障碍相关性研究[J].现代康复,2001,5(3):107-108.
[103]Kaakkola S,Ctordin A,Mannisito PT.General properties and clinical possibilities of new selective inhibitors of catechol-O-methyltransferase[J].Gen Pharmac,1994,25(5):813-824.
[104]贺斌.COMT抑制剂治疗帕金森病展望[J].国外医药·合成药生化药制剂分册,2001,22(1):29-31.
[105]Spielman RS,Weinshilboum RM.Genetics of red cell COMT activity:Analysis of thermal stability and family data[J].Am J Med Genet,1981,10(3):279-290.
[106]Lotta T,Vidgren J,Tilgmann C,et al.Kinnetic of human soluble and membrane-bound catechol-O-methyltransferase:A revised mechanism and description of the thermolabile variant of the enzyme[J].Biochemistry,1995,34(13):4202-4210.
[107]高清玲,邵明,李勇杰,等.儿茶酚胺氧位甲基转移酶基因多态性研究[J].首都医科大学学报,2002,22(2):113-115.
[108]Hoda F,Nicholl D,Bennett P,et al.No association between Parkinson's disease and low-activity alleles of catechol-O-methyltransferase[J].Biochem Biophys Res Commun,1996,228(3):780-784.
[109]王振,肖泽萍,陈珏.儿茶酚-邻-甲基转移酶基因多态性与强迫症[J].临床精神医学杂志,2004,14(6):321-323.
[110]Karayiorgou M,Altemus M,Galke BL,et al.Genotype determining low catechol-O-methyltransferase activity as a risk factor for obsessive-compulsiv disorder[J].Proc Natl Acad Sci USA,1997,94(9):4572-4575.
[111]Karayiorgou M,Sobin C,Blundell ML,et al.Family-based association studies support a sexually dimorphic effect of COMT and MAOA on genetic susceptibility to obsessive-compulsive disorder[J].Biol Psychiatry,1999,45(9):1178-1189.
[112]Alsobrook JP,Zohar AH,Leboyer M,et al.Association between the COMT locus and obsessive-compulsive disorder in females but not males[J].Am J Med Genet,2002,114(1):116-120.
[113]Schindler KM,Richter MA,Kennedy JL,et al.Association between homozygosity at the COMT gene locus and obsessive compulsive disorder[J]Am J Med Genet,2002.96(6):721-724.
[114]Niehaus DJ,Kinnear CJ,Corfield VA,et al.Association between a catechol-O-methyltransferase polymorphism and obsessive-compulsive disorder in the Afrikaner population[J].J Affect Disord,2001,65(1):61-65.
[115]Zinkstok J,van Nimwegen L,van Amelsvoort T,et al.Catechol-O-methyltransferase gene and obsessive-compulsive symptoms in patients with recent-onset schizophrenia:Preliminary results[J].Psychiatry Res,2008,157(1-3):1-8.
[116]Barr CL,Wigg KG,Sandor P.Catechol-O-methyltransferase and Gilles de la Tourette syndrome[J].Mol Psychiatry,1999,4(5):492-495.
[117]Ohara K,Nagai M,Suzuki Y,.et al.No association between anxiety disorders and catechol-o-methyltransferase polymorphism[J].Psychiatry Res,1998,80(2):145-148
[118]Azzam A,Mathews CA.Meta-Analysis of the Association Between the Catecholamine-O-Methyl-Transferase Gene and Obsessive-Compulsive Disorder[J].Am J Med Genet B Neuropsychiatr Genet,2003,123B(1):64-69
[119]邹政,李春波,方芳,等.儿茶酚邻甲基转移酶基因多态性与焦虑症的关联研究[J].上海精神医学,2005,17(3):139-141.
[120]Woo JM,Yoon KS,Yu BH.Catechol-O-Methyltransferase Genetic Polymorphism in Panic Disorder[J].Am J Psychiatry.2002,159(10):1785-1787.
[121]Hamilton SP,SlagerSL,HeimanGA,eta.l Evidence fora susceptibility locus for panic disorder near the catecol-O-methyltransferase gene on chromosome 22[J].BiolPsychiatry,2002,51(7):591-601.
[122]Rothe C,Koszycki D,Bradwejn J,et al.Association of the Val158 Met Catechol-O-Methyltransferase Genetic Polymorphism with Panic Disorder[J].Neuropsychopharmacology,2006,31(10):2237-2242.
[123]Woo JM,Yoon KS,ChoiYH,et a.l The association between panic disorder and the L/L genotype of catechol-O-methyltransferase[J].J PsychiatrRes,2004,38(4):365-370.
[124]Stein MB,Fallin MD,Schork NJ,et al.COMT polymorphisms and anxiety-related personality traits[J].Neuropsychopharmacology,2005,30(11):2092-2102.
[125]Olsson CA,Anney RJ,Lotfi-Miri M,et al.Association between the COMT Val158Met polymorphism and propensity to anxiety in an Australian population-based longitudinal study of adolescent health.[J].Psychiatric Genetics,2005,15(2):109-115.
[126]Ohara K,Nagai M,Suzuki Y,et al.No association between anxiety disorders and cateehol-O-methyltransferase polymorphism[J].Psychiatry Res,1998,80(2):145-148.
[127]Wray NR,James MR,Dumenil T,et al.Association Study of Candidate Variants of COMT With Neuroticism,Anxiety and Depression[J].Am J Med Genet B Neuropsychiatr Genet,2008,147B(7):1314-1318.
[128]Kolassa IT,Buchmann A,Lauche R,et al.Spider phobics more easily see a spider in morphed schematic pictures [J]. Behav Brain Funct, 2007,3:59.
[129] Samochowiec J, Hajduk A, Samochowiec A, et al. Association studies of MAO-A,COMT, and 5-HTT genes polymorphisms in patients with anxiety disorders of the phobic spectrum[J]. Psychiatry Res, 2004, 128(1):21-26.
[130] McGrath M, Kawachi I, Ascherio A, et al. Association Between Catechol-O-Methyltransferase and Phobic Anxiety[J]. Psychiatry, 2004, 161(9):1703-1705.
[131] Gershon ES, Badner JA, Goldin LR, et al. Closing in on genes for manic-depressive illness and schizophrenia [J]. Neuropsychopharmacology, 1998,18(4): 233-242.
[132] Holmans P. Detecting gene-gene interactions using affected sib pair analysis with covariates [J]. Hum Hered, 2002,53(2):92-102.
[133] Weeks DE, Lange K. The affected-pedigree-member method of linkage analysis [J].Am J Hum Genet, 1988,42(2):315-326.
[134] Schaid DJ, Rowland C. Use of parents, sibs, and related controls for detection of associations between genetic markers and disease [J]. Am J Hum Genet, 1998, 63(5):1492-1506.
[135] Bellodi L, Bussoleni C, Scorza-Smeraldi R, et al. Family study of schizophrenia:exploratory analysis for relevant factors [J]. Schizopr Bull, 1986,12(1): 120-128.
[136] Thomson G Mapping disease genes: family-based association studies [J]. Am J Hum Genet, 1995, 57(2):487-498.
[137] Falk CT, Rubinstein P. Haplotype relative risks: an easy reliable way to construct a proper control sample for risk calculations [J]. Ann Hum Genet, 1987,51(Pt3):227-233.
[138] Spielman RS, McGinnis RE, Ewens WJ. Transmission test for linkage disequilibrium:the insulin gene region and insulin-dependent diabetes mellitus (IDDM) [J]. Am J Hum Genet, 1993, 52(3):506-516.
[139] Spielman RS, Ewens WJ. The TDT and other family-based for linkage disequilibrium and association [J]. Am J Hum Genet, 1996, 59(5): 983-989.
[140] Botstein D, White RI, Skolnick M, et al. Construction of genetic linkage map in man using restriction fregment length polymorphisms [J]. Am J Hum Genet, 1980,32(3):314-331.
[141] Donis-Keller H, Green P, Helms C, et al. A genetic linkage map of the human genome [J]. Cell, 1987, 51(2):319-337.
[142] Lander ES. The new genomics: global views of biology [J]. Science, 1996, 274(5287):536-539.
[143]Heid CA,Stevens J,Livak KJ,et al.Real time quantitative PCR[J].Genome Res,1996,6(10):986-994.
[144]Alderborn A,Kristofferson A,Hammerling U.Determination of single nucleotide polymorphisms by real-time pyrophosphate DNA sequencing[J].Genome Res,2000,10(8):1249-1258.
[145]Zhenxian Xiao,Junxua Xiao,Yuexing Jiang,et al.A novel method based on ligase detection reaction for low abundant YIDD mutants detection in hepatitis B virus[J].Hepatology Research,2006,34(3):150-155.
[146]肇旭,秦胜营,冯国鄞,等.基于连接酶检测反应的基因芯片分型技术的建立[J].国际遗传学杂志,2006,29(3):178-182.
[147]Makino R,Yazyu H,Kishimoto Y,et al.F-SSCP:fluorescence-based polymerase chain reaction-single-strand conformation polymorphism(PCR-SSCP) analysis[J].PCR Methods Appl,1992,2(1):10-13.
[148]彭翠英,廖端芳,张佳,等.单核苷酸多态性及其检测方法[J].中华检验医学杂志,2004,27(10):703-705.
[149]Myers RM,Maniatis T,Leman LS.Detection and localization of single base changs by denaturing gradient gel electrophoresis[J].Methods Enzymol,1987,155:501-527.
[150]O'Donovan MC,Oefner PJ,Roberts SC,et al.Blind analysis of denaturing hing-performance liquid chromatography as a tool for mutation detection[J].Genomics,1998,52(1):44-49.
[151]赵春霞,石先哲,吕申,等.人类基因组的单核苷酸多态性及其研究进展[J].色谱,2003,21(2):110-114.
[152]赵广荣,扬帆,元英进,等.单核苷酸多态性的检测方法的新进展[J].遗传,2005,27(1):123-129.
[153]Pease AC,Solas D,Sullivan EJ,et al.Light-generated oligonucleotide arrays for rapid DNA sequence analysis[J].Proc Natl Acad Sci USA,1994,91(11):5022-5026.
[154]Lipshutz RJ,Morris D,Chee M,et al.Using oligonucleotide probe arrays to access genetic diversity[J].Biotechniques,1995,19(3):442-447.
[155]Griffin TJ,Tang W,Smith LM.Genetic analysis by peptide nucleic acid affinity MALDI-TOF mass spectrometry[J].Nat Biotechnol,1997,15(13):1368-1372.
[156]Monforte JA,Becker CH.High-throughout DNA analysis by Time-of-Flight mass spectrometry[J].Nature Medicine,1997,3(3):360-362.
[157]Kofiadi IA,Rebrikov DV.Methods for detecting single nucleotide polymorphisms: Allele-specific PCR and hybridization with oligonucleotide probe[J].Genetika,2006,42(1):16-26.
[158]Lucarelli F,Marrazza G,Mascini M.Design of an optimal allele-specific oligonucleotide probe for the efficient discrimination of a thermadynamically stable (G-T) mismatch[J].Anal Chim Acta,2007,603(1):82-86.
[159]高秀丽,景奉香,杨建波,等.单核苷酸多态性检测分析技术[J].遗传,2005,27(1):110-122.
[160]Prince JA,Brookes AJ.Towards high-throughput genotyping of SNPs by dynamic allele-specific hybridization[J].Expert Rev Mol Diagn,2001,1(3):352-358.
[161]Ottman R.Gene-environment interaction;definitions and study designs[J].Preventive Medicine,1996,25(6):764-770.
[162]Murtaugh MA,Sweeney C,Ma KN,et al.The CYP1A1 genotype may alter the association of Meat consumption patterns and preparation with the risk of colorectal cancer in men and women[J].J Nutr,2005,135(2):179-186.
[163]黄悦勤.临床流行病学[M].北京:人民卫生出版社,2002:143-146.
[164]王培桦,沈洪兵,陈峰,等.叉生分析在基因-环境交互研究中的应用与意义[J].中华流行病学杂志,2005,26(1):54-57.
[165]Rubinstein P,Ginsberg-Fellner F,Falk C.Genetic of Type Ⅰ diabetes mellitus:a single.recessive predisposition gene mapping between HLA-B and GLO.with an appendix on the estimation of selection bias[J].Am J Hum Genet,1981,33(6):865-882.
[166]Schaid DJ.Case-parents design for gene-environment interaction[J].Genet Epidemiol,1999,16(3):261-273.
[167]杨仕贵.病例父母对照研究在遗传性疾病中的应用[J].疾病控制杂志,2002,6(2):143-145.
[168]Yang Q,Khoury MJ.Evolving methods in genetic epidemiology Ⅲ Gene-environment interaction in epidemiologic research[J].Epidemiol Rev,1997,19(1):33-43.
[169]Piegorsch WW,Weinbegr CR,Taylor JA.Non-hierarchical logistic models and case-only designs for assessing susceptibility in population-based case-control studies[J].Stat Med,1994,13(2):153-162.
[170]Hmaajima N,Yuasa H,Matsuo K,et al.Detection of gene-environment inieraction by case-only studies[J].JPn J Clin Oneol,1999,29(10):490-493.
[171]李大林,李立明.基因-环境交互作用研究方法:无对照病例研究[J].中华流行病学杂志,2002,23(4):304-307.
[172]柏建岭,荀鹏程,赵扬,等.不完全病例对照研究基因环境交互作用研究的应用与意义[J].中华流行病学杂志,2006,27(1):72-75.
[173]Gerry NP,Witowski NE,Day J,et al.Universal DNA microarray method for multiplex detection of low abundance point mutations[J].J Mol Biol,1999,292(2):251-262.
[174]Luo J,Bergstrom DE,Barany F.Improving the fidelity of thermos thermophilus DNA ligae[J].Nucleic Acids Res,1996,24(15):3071-3078.
[175]Consolandi C,Busti E,Pera C,et al.Detection of HLA Polymorphisms by Ligase Detection Reaction and a Universal Array Format:A Pilot Study for Low Resolution Genotyping[J].Hum Immunol.2003,64(1):168-178.
[176]谭红专.现代流行病学[M].第2版.北京:人民卫生出版社,2008.
[177]赵仲堂.流行病学研究方法与应用[M].第二版.北京:科学出版社,2005,537-538.
[178]沈靖,王润田,徐希平.代谢酶基因多态性与环境暴露交互作用的分析方法及其应用[J].中华流行病学杂志,2001,22(1):61-62.
[179]舒良,张鸿燕,汪向东,等.“复合性国际诊断交谈检查核心本”现场测试.信度效度检验[J].中国心理卫生杂志,1993,7(5):208-211.
[180]邹义壮,舒良,沈渔邨,等.CIDI对神经症诊断的现场测试[J].中国心理卫生杂志,1995.9(5):206-208.
[181]Komiti AA,Jacks on HJ,Judd FK,et al.A comparison of the Composite International Diagnostic Interview(CIDI-Auto) with clinical assessment in diagnosing mood and anxiety disorders[J].Aust N Z J Psychiatry,2001,35(2):224-230.
[182]Jordanova V,Wickramesinghe C,Gerada C,et al.Validation of two survey diagnostic interviews among primary care attendees:a comparison of CIS-R and CIDI with SCAN ICD-10 diagnostic categories[J].Psychol Med,2004,34(6):1013-1024.
[183]胡赤怡,胡纪泽,段卫东,等.复合性国际诊断访谈表的效度研究[J].中国神经精神疾病杂志,2008,34(7):385-389.
[184]张延赤.大学生神经症流行病学特征分析与防治对策研究[D].长春:吉林大学,2006.
[185]吴承红,蔡澄.大学生强迫症症状学的研究[J].扬州大学学报,2002,6(3):32-34.
[186]赵勇.大学生强迫症状况调查及其个性分析[J].中国健康心理学杂志,2005,13(6):19-20.
[187]高良会,崔利军,粟克清,等.河北省特殊恐怖性神经症的流行病学调查[J].中国全科医学,2007,10(7):1451-1452.
[188]Maggee WJ,Eaton WW,Wittchen HU,et al.Agoraphobia,simple phobia,and social phobia in the national comorbidity survery[J].Arch Gen Psychiatry,1996,53(3):159.
[189]Furmark T.Social phobia:overview of community surveys[J].Acta Psychiatr Stand,2002,105(2):84-93.
[190]李建芹.河南省大学生焦虑状况调查[J].中国健康教育,2006,22(3):112-113.
[191]申小莹,刘晓瑞,董雪.西安某高校大学生焦虑状况的调查研究[J].中国健康心理学杂志,2006,14(3):311-312.
[192]王云强,乔建中.理工科大学生焦虑状况测查研究[J].中国健康心理学杂志,2007,15(11):1007-1009.
[193]许韶君,陶芳标,张洪波.大学生抑郁、焦虑症状及其影响因素的分析[J].安徽预防医学杂志,1999,5(2):121-122.
[194]杨青侠.大学生神经衰弱患病情况的调查分析[J].贵州医药,1996,20(1):28.
[195]郭莉,娟祝雁,郝曙光.在校大学生神经衰弱病因调查分析[J].吉林大学学报(医学版),2008,33(6):1045.
[196]张在坦.烟台师范学院大学生神经衰弱的病因调查[J].中国校医,2004,18(4):333-334.
[197]黎凡.兰州地区4868名大学生神经衰弱调查报告[J].中国心理卫生杂志,1988,2(5):229-230,233.
[198]谢冰.大学生强迫症现况调查及SAPAP3基因多态性关联研究[D].长春:吉林大学,2008.
[199]张香云,刘卉兰,储耀辉,等.神经症患者的社会支持和应对方式调查[J].中国心理卫生杂志,2003,17(6):427.
[200]朱红.2型糖尿病并发肺结核病遗传和环境危险因素探讨[D].天津:天津医科大学,2006.
[201]Gray IC,Campbell DA,Spurr NK,et al.Single nucleotide polymorphisms as tools in human genetics[J].Hum Mol Genet,2000,9(16):2403-2408.
[202]杨玉凤.环境与遗传因素在胃癌发生中的交互作用研究[D].南京:东南大学,2006:41.
[203]Wallaee HM.A model of gene-gene and gene-environment interactions and its implications for targeting environmental interventions by genotype[J].Theor Biol Med Mode,2006,3:35.
[204]Wacholder S,Chatterjee N,Hartge P.Joint effect of genes and environment distorted by Selection biases:implications for hospital-based case-control studies[J].Cancer Epidemiol Biomkarers Prev,2002,11(9):885-889.
[205]Lander ES,Schork NJ.Gene dissection of complex traits[J].Science,1994,265(5184):2037-2048.
[206]Greenland S,Rothman KJ.Concepts of interaction In:Rothman KJ,Greenland S,eds.Modern Epidemiology[M].2nd ed.Philadelphia:Lippineott-Raven,1998:329-342.
[207]刘玮.肺结核易感基因、环境危险因素及其交互作用研究[D].北京:中国人民解放军军事医学科学院,2005.
[208]Smith PG,Day NE.The design of case-control studies:the influence of confounding and interaction effects[J].Int J Epidemiol,1984:13(3):356-365.
[209]Andrieu N,Goldstein AM,Thomas DC,et al.Counter-matching in studies of gene-environment interaction:efficiency and feasibility[J].Am J Epidemiol,2001,153(3):265-74.
[210]Sturmer T,Brenner H.Potential gain in efficiency and power to detect gene-environment Interactions by matching in case-control studies[J].Genet Epidemiol,2000,18(1):63-80.
[2]WHO.ICD-10精神与行为障碍:临床描述与诊断要点[M].中文版.北京:人民卫生出版社,1992.
[3]中华医学会精神科分会.中国精神障碍分类与诊断标准(第三版)(CCMD-3).济南:山东科学技术出版社,2001.
[4]Krupp LB.An overview of Chronic fatigue Syndrome[J].J Clin Psychiatry,1991,52:403-410.
[5]沈渔邨.精神病学[M].第四版.北京:人民卫生出版社,2002.
[6]Henderson JG.,Pollard CA.Three types of obsessive compulsive disorder in aconununity sample[J].J Clin Psychol,1988,44(5):747-752.
[7]Akhtar S,Wig NN,Varma VK,et al.A phenomenological analysis of symptoms in obsessive-compulsive neurosis[J].Br J Psychiatry,1975,8:127-342.
[8]Wilne A,Reieh T,Robins I,et al.Obsessive Compulsive neuroses[J].Comprehensive psychiatry,1976,17:527-539.
[9]胡宜,王静舒.现代医学200词:分离性障碍(Dissociative disorders)[J].日本医学介绍,2004,25(4):191-192.
[10]郝伟.精神病学[M].第六版.北京:人民卫生出版社,2008.
[11]张春美.大学生神经衰弱的身心疗法治疗150例报告[J].中国临床康复,2004,8(3):556.
[12]Kessler,Ronald C,Ustun T,et al.The World Mental Health(WMH) Survey Initiative Version of the World Health Organization(WHO) Composite International Diagnostic Interview(CIDI)[J].Int J Methods Psychiatr Res,2004,13(2):93-121.
[13]First,Spitzer著,张波译,刘协和审校.DSM-Ⅳ轴Ⅰ障碍用临床定式检查使用指南(研究版)[M].四川大学华西医学中心附属第一医院心理卫生研究所,2001.
[14]Michael BF,Robert LS,Miriam G,et al.User's Guide for Structured Clinical Interview for DSM-Ⅳ Axis Ⅰ Disorders-Research Version[M].New York:Biometrics Research,1996.
[15]张岿.一所高校学生神经症患病状况分析[J].中国心理卫生杂志,2003,17(5):340-341.
[16]田旭.大学生神经症患者个性与应付方式探讨[J].中国校医,2002,16(6):554.
[17]Marks I,刘志中译.神经症的流行病学与病因学[J].国外医学精神病学分册,1983,10(1):1-6.
[18]王娴贤,林启瑞,江小平.大学生神经症患者的心理状况调查[J].保健医学与实践,2008,5(4):27-28.
[19]Noyes R Jr,Clarkson C,Crowe RR,et al.A family study of generalized anxiety disorder[J].Am J Psychiatry,1987,144(8):1019-1024.
[20]刘协和.神经症:夏镇夷等主编,精神医学丛书(第二卷),临床精神医学[M].长沙:湖南科学技术出版社,1994:451-455.
[21]许明定.神经症家系中几种疾病流行病学初步调查[J].遗传与疾病,1985,2(4):233-235.
[22]12地区精神疾病流行学调查协作组.向孟泽执笔.12地区神经症流行学调查[J].中华神经精神科杂志,1986,19(2):87-91.
[23]李心天.医学心理学[M].北京:中国医科大学中国协和医科大学联合出版社,1997.
[24]汪向东.心理卫生评定量表手册[J].中国心理卫生杂志,1993(增刊):202-209.
[25]林雄标,黄明生.惊恐障碍与广泛性焦虑的临床对比及血乳酸、胆碱酯酶测定[J].中华神经精神科杂志,1993,26(6):348-351.
[26]马震祥,刘玉局.广泛性焦虑遗传效应和遗传方式研究[J].临床精神医学杂志,2006,16(6):336-337.
[27]马震祥,王蕾,卞正发,等.惊恐障碍的遗传方式探讨[J].临床精神医学杂志.2004,14(3):137-138.
[28]Pauls DL,Alsobrook JP,Goodman W,et al.A family study of obsessive-compulsive disorder[J].Am J Psychiatry,1995,152(1):76-84.
[29]Samuels JF,Riddle MA,Greenberg BD,et al.The OCD Collaborative Genetic Study:methods and sample description[J].Am J Med Genet B Neuropsychiatr Genet.2006,141B(3):201-207.
[30]杨彦春,刘协和.强迫症的家系遗传研究[J].中华医学遗传学杂志,1998,15(5):303-306.
[31]Jonnal AH,Gardner CO,Prescott CA,et al.Obsessive and compulsive symptoms in a general population sample of female twins[J].Am J Med Genet,2000,96(6):791-796.
[32]Liebowitz MR:Social phobia.Modern Problems of Pharmacopsychiatry[J].1987, 22:141-173.
[33]Williams RB,Marchuk DA,Gadde KM,et al.Serotonin-related gene polymorphisms and central nervous system serotonin function[J].Neuropsychopharmacology,2003,28(3):533-541.
[34]Denys D,Zohar J,Westenberg HG.The Role of Dopamine in Obsessive Compulsive Disorder:Preclinical and Clinical Evidence[J].J.Clin Psychiatry,2004,65(14):11-17.
[35]Fineberg NA,Roberts A,Montgomery SA.Brain 5-HT function in obsessive compulsive disorder[J].Br J Psychiatry,1997,171:280-282.
[36]Catalano M,Sciuto G,Di Bella D,et al.Lack of association between obsessive-compulsive disorder and the dopamine D3 receptor gene:some preliminary considerations[J].Am J Med Genet,1994,54(3):253-255.
[37]陈邵建.大学生心理卫生状况及其原因分析[J].应用心理学,1988,4:46-54.
[38]刘美娟,余华.大学生SCL-90测试研究的结果[J].心理科学,1995,18(5):289-290.
[39]郑延平,林克明.洛杉矶地区美国华人的神经衰弱流行病学研究[J].上海精神医学,1997,9(3):129-134.
[40]长虹,丛中.临床心理治疗[M].北京:人民军医出版社,2004.
[41]邹文华,张宏根.神经症与正常人的社会心理因素个性和躯体症状的对照研究[J].中国神经精神疾病杂志,1998,2(4):211-214.
[42]冯丽云,李克均.通径分析在大学生神经症危险因素研究中的应用[J].郑州大学学报·医学版,2003,38(2):239-242.
[43]陈复平.神经症的流行学调查[J].中华神经精神科杂志,1986,5:301-305.
[44]邱德胜,罗小年,金卫东.大学生精神障碍与生活事件[J].中原精神医学杂志,1997,3(1):8-10.
[45]李书平,郑烈,李映原,等.宁夏回族自治区城市居民神经症流行病学调查[J].中国心理卫生杂志,1999,13(3):160.
[46]章秀娟,胡岳松,俞承烈.余姚市神经症流行病学调查[J].临床精神医学杂志,1999,9(4):251-252.
[47]周天骍,张少平,江渝琦.社区老年神经症流行病学调查[J].上海精神医学,2000,12(3):125-128.
[48]韩岭,杨德森.机械工业人群神经症流行病学调查[J].中国心理卫生杂志,1989,3(2):55-58.61.
[49]吴传东,官尚工,朱国钦,等.三亚市牛兰镇回、黎、汉神经症流行病学调查[J].中国民政医学杂志,1994,增(1):19-20.
[50]赵虎,赵丹青,朱少毅,等.汕头市神经症流行病学调查[J].中国民政医学杂志,2000,12(2):80-81.
[51]王天根.流行病学研究方法[M].北京:人民卫生出版社,1991:83.
[52]向孟泽.神经症的流行病学调查[J].中华神经精神科杂志,1996,19(5):301.
[53]李真,胡季明,陈贻华,等.中山市神经症流行病学调查报告[J].临床精神医学杂志,2004,14(3):145-146.
[54]张毅宏,胡纪泽,胡赤怡,等.深圳市神经症流行病学调查[J].中国公共卫生,2006,22(7):866-867.
[55]唐宏.用MMPI、SCL-90调查大学生神经症结果分析[J].赣南医学院学报,2003,23(4):449-451.
[56]高作咏,陈晓姣,雷平冲.1542在校大学生神经症流行病学调查分析[J].咸宁医学院学报,1995,9(1):27-28,30.
[57]王志铭,王宇中,冯丽云,等.河南某医学院校学生神经症流行病学调查及其成因分析[J].河南医科大学学报,2000,35(5):438-441.
[58]梁执群,王建本,岳月仙,等.医科大学生神经症患病倾向调查[J].山西医学院学报,1993,24(3):274-275.
[59]黄周忠,陈小维,吴小南,等.福州市大学生神经症的患病状况的调查研究[J].四川精神卫生,1998,11(4):230-232.
[60]陈继军,武雪冰,刘清波.用SCL-90、EPQ调查某部队神经症结果分析[J].健康心理学杂志,2000,8(1):112-114.
[61]高平青,周宁,严昌安,等.武警部队神经症流行病学调查[J].武警医学,1999,10(2):100-101.
[62]林慰慈.南京市738名中小学生神经症患病情况的调查[J].中国校医,2000,14(4):283.
[63]吴传东,余慧菲,叶廷蔚,等.社区14-18岁中学生神经症流行病学调查[J].海南医学,1991,2(4):61-62.
[64]沈蕴华,张希良.大学生因病辍学情况调查[J].中国心理卫生杂志,1989,3(3):117.
[65]Hettema JM,Neale MC,Kendler KS.A review and meta-analysis of the genetic epidemiology of anxiety disorders[J].Am J Psychiatry,2001,158(10):1568-1578.
[66]陈婷婷.复杂疾病基因定位的统计学方法[J].黑龙江医药,2008,21(2):48-50.
[67]张学军.复杂疾病的遗传学研究策略[J].安徽医科大学学报,2007,42(3):237-240.
[68]Rutter M.Biological implications of gene-environment interaction[J].J Abnorm Child Psychol,2008,36(7):969-975.
[69]Caspi A,Moffitt TE,Cannon M,et al.Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene:longitudinal evidence of a gene X environment interaction[J].Biol Psychiatry,2005,57(10):1117-1127.
[70]Gatt JM,Nemeroff CB,Dobson-Stone C,et al.Interactions between BDNF Va166Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety[J].Biol Psychiatry,2009,doi:10.1038/mp.2008.143.
[71]Wagner S,Baskaya O,Lieb K,et al.The 5-HTTLPR Polymorphism modulates the association of serious life events(SLE) and impulsivity in patients with Borderline Personality Disorder[J].J Psychiatr Res,2009,doi:10.1016/j.jpsychires.2009.03.004
[72]Chattopadhyay A,Rukmini R,Mukherjee S.Photophysics of a neurotransmitter:ionization and spectroscopic properties of serotonin[J].Biophys J,1996,71(4):1952-1960.
[73]Artigas F,Romero L,de Montigny C,et al.Acceleration of the effect of selected antidepressant drugs in major depression by 5-HT1A antagonists[J].Trends Neurosci,1996,19(9):378-383.
[74]Ramboz S,Oosting R,Amara DA,et al.Serotonin receptor 1A knockout:an animal model of anxiety-related disorder[J].Proc Natl Acad Sci U S A,1998,95(24):14476-14481.
[75]Chavarria-Siles I,Walss-Bass C,Quezada P,et al.TGFB-induced factor(TGIF):a candidate gene for psychosis on chromosome 18p[J].Mol Psychiatry,2007,12(11):1033-1041.
[76]Choudhury K,McQuillin A,Purl V,et al.A genetic association study of chromosome 11q22-24 in two different samples implicates the FXYD6 gene,encoding phosphohippolin,in susceptibility to schizophrenia[J].Am J Hum Genet,2007,80(4):664-672.
[77]Albert PR,Lemonde S.5-HT1A receptors,gene repression,and depression:guilt by association[J].Neuroscientist,2004,10(6):575-593.
[78]Drago A,Ronchi DD,Serretti A.5-HT1A gene variants and psychiatric disorders:a review of current literature and selection of SNPs for future studies[J].Int J Neuropsychopharmacol,2008,11(5):701-721.
[79]Lin PY.Links Meta-analysis of the association of serotonin transporter gene polymorphism with obsessive-compulsive disorder[J].Prog Neuropsychopharmacol,2007,31(3):683-689.
[80]Lopez-Figueroa AL,Norton CS,Lopez-Figueroa MO,et al.Serotonin 5-HT1A,5-HT1B,and 5-HT2A receptor mRNA expression in subjects with major depression,bipolar disorder,and schizophrenia[J].Biol Psychiatry,2004,55(3):225-233.
[81]郭慧荣,肖泽萍.强迫症候选基因研究进展[J].国外医学遗传学分册,2003,26(5):303-306.
[82]Bloch MH,Landeros-Weisenberger A,Sen S,et al.Association of the serotonin transporter polymorphism and obsessive-compulsive disorder:systematic review[J].Am J Med Genet B Neuropsychiatr Genet,2008,147B(6):850-858.
[83]张岚,刘协和,李涛,等.不同发病年龄强迫症患者6种功能基因的分子遗传学研究[J].中华精神科杂志,2004,37(4):198-201.
[84]Murphy DL,Brodie HK,Goodwin FK,et al.Regular induction of hypomania by L-DOPA in 'bipolar' manic-depressive patients[J].Nature,1971,229(5280):135-136.
[85]Frederickson A.The dopamine hypothesis of schizophrenia[M].Second Web Rep,1998.
[86]Bonhomme N,Esposito E.Involvement of serotonin and dopamine in the mechanism of action of novel antidepressant drugs:a review[J].J Clin Psychopharmacol,1998,18(6):447-454.
[87]Georgieva L,Dimitrova A,Nikolov I,et al.Dopamine transporter gene(DAT1) VNTR polymorphism in major psychiatric disorders:family-based association study in the Bulgarian population[J].Acta Psychiatr Scand,2002,105(5):396-399.
[88]周云飞,张亚林,胡纪泽,等.多巴胺转运体基因多态性与强迫症的关联[J].中国行为医学科学,2006,15(7):586-587.
[89]徐勇,王振,肖泽萍,等.多巴胺D4受体基因与强迫症的关联[J].上海交通大学学报(医学版),2006,26(4):362-364.
[90]Olsson CA,Byrnes GB,Anney RJ,et al.COMT Val(158)Met and 5HTTLPR functional loci interact to predict persistence of anxiety across adolescence:results from the Victorian Adolescent Health Cohort Study[J].Genes Brain Behav,2007, 6(7):647-652.
[91]张野,江三多,钱伊萍,等.情感性精神障碍与儿茶酚邻位甲基转移酶基因的关联性研究[J].中华精神科杂志,2002,5(4):206-208.
[92]Stein DJ,Daniels WM,Savitz J,et al.Brain-derived neurotrophic factor:the neurotrophin hypothesis of psychopathology[J].CNS Spectr,2008,13(11):945-949.
[93]谭树凯,袁琼兰.脑源性神经营养因子(BDNF)与脑缺血性损伤[J].四川解剖学杂志,2008,16(4):39-41.
[94]Krebs MO,Guillin O,Bourdell MC,et al.Brain derived neurotrophic factor(BDNF)gene variants association with age at onset and therapeutic response in schizophrenia [J].Mol Psychiatry,2000,5(5):558-562.
[95]T L Petryshen,P C Sabeti,K A Aldinger,et al.Population genetic study of the brain-derived neurotrophic factor(BDNF) gene[J].Mol Psychiatry,2009,doi:10.1038/mp.2009.24
[96]Katerberg H,Lochner C,Cath DC,et al.he role of the brain-derived neurotrophic factor(BDNF) va166met variant in the phenotypic expression of obsessive-compulsive disorder(OCD)[J].Am J Hum Genet,2003,73(2)370-376.
[97]李军,罗忠金,张吉翔.脑源性神经营养因子突变与焦虑[J].生命的化学,2008,28(2):217-219.
[98]Eser D,Leicht G,Lutz J,et al.Functional neuroanatomy of CCK-4-induced panic attacks in healthy volunteers[J].Hum Brain Mapp,2009,30(2):511-522.
[99]Karayiorgou M,Sobin C,Blundell ML,et al.Family-based association studies support a sexually dimorphic effect of COMT and MAOA on genetic susceptibility to obsessive-compulsive disorder[J].Biol Psychiatry.1999,45(9):1178-1189.
[100]Grossman MH,Littrell JB,Weinatein R.Identification of the possible molecular basis for inherited differences in human catechol-O-methyltransferase[J].Soc Neurosci,1992,18:70
[101]Lundstrom K,Tenhunen J,Tilgmann C,et al.Cloning,expression and structure of catechol-O-methyltransferase[J].Biochem Biophys Acta,1995,1251(1):1-10
[102]吴怀安.儿茶酚氧位甲基转移酶与精神障碍相关性研究[J].现代康复,2001,5(3):107-108.
[103]Kaakkola S,Ctordin A,Mannisito PT.General properties and clinical possibilities of new selective inhibitors of catechol-O-methyltransferase[J].Gen Pharmac,1994,25(5):813-824.
[104]贺斌.COMT抑制剂治疗帕金森病展望[J].国外医药·合成药生化药制剂分册,2001,22(1):29-31.
[105]Spielman RS,Weinshilboum RM.Genetics of red cell COMT activity:Analysis of thermal stability and family data[J].Am J Med Genet,1981,10(3):279-290.
[106]Lotta T,Vidgren J,Tilgmann C,et al.Kinnetic of human soluble and membrane-bound catechol-O-methyltransferase:A revised mechanism and description of the thermolabile variant of the enzyme[J].Biochemistry,1995,34(13):4202-4210.
[107]高清玲,邵明,李勇杰,等.儿茶酚胺氧位甲基转移酶基因多态性研究[J].首都医科大学学报,2002,22(2):113-115.
[108]Hoda F,Nicholl D,Bennett P,et al.No association between Parkinson's disease and low-activity alleles of catechol-O-methyltransferase[J].Biochem Biophys Res Commun,1996,228(3):780-784.
[109]王振,肖泽萍,陈珏.儿茶酚-邻-甲基转移酶基因多态性与强迫症[J].临床精神医学杂志,2004,14(6):321-323.
[110]Karayiorgou M,Altemus M,Galke BL,et al.Genotype determining low catechol-O-methyltransferase activity as a risk factor for obsessive-compulsiv disorder[J].Proc Natl Acad Sci USA,1997,94(9):4572-4575.
[111]Karayiorgou M,Sobin C,Blundell ML,et al.Family-based association studies support a sexually dimorphic effect of COMT and MAOA on genetic susceptibility to obsessive-compulsive disorder[J].Biol Psychiatry,1999,45(9):1178-1189.
[112]Alsobrook JP,Zohar AH,Leboyer M,et al.Association between the COMT locus and obsessive-compulsive disorder in females but not males[J].Am J Med Genet,2002,114(1):116-120.
[113]Schindler KM,Richter MA,Kennedy JL,et al.Association between homozygosity at the COMT gene locus and obsessive compulsive disorder[J]Am J Med Genet,2002.96(6):721-724.
[114]Niehaus DJ,Kinnear CJ,Corfield VA,et al.Association between a catechol-O-methyltransferase polymorphism and obsessive-compulsive disorder in the Afrikaner population[J].J Affect Disord,2001,65(1):61-65.
[115]Zinkstok J,van Nimwegen L,van Amelsvoort T,et al.Catechol-O-methyltransferase gene and obsessive-compulsive symptoms in patients with recent-onset schizophrenia:Preliminary results[J].Psychiatry Res,2008,157(1-3):1-8.
[116]Barr CL,Wigg KG,Sandor P.Catechol-O-methyltransferase and Gilles de la Tourette syndrome[J].Mol Psychiatry,1999,4(5):492-495.
[117]Ohara K,Nagai M,Suzuki Y,.et al.No association between anxiety disorders and catechol-o-methyltransferase polymorphism[J].Psychiatry Res,1998,80(2):145-148
[118]Azzam A,Mathews CA.Meta-Analysis of the Association Between the Catecholamine-O-Methyl-Transferase Gene and Obsessive-Compulsive Disorder[J].Am J Med Genet B Neuropsychiatr Genet,2003,123B(1):64-69
[119]邹政,李春波,方芳,等.儿茶酚邻甲基转移酶基因多态性与焦虑症的关联研究[J].上海精神医学,2005,17(3):139-141.
[120]Woo JM,Yoon KS,Yu BH.Catechol-O-Methyltransferase Genetic Polymorphism in Panic Disorder[J].Am J Psychiatry.2002,159(10):1785-1787.
[121]Hamilton SP,SlagerSL,HeimanGA,eta.l Evidence fora susceptibility locus for panic disorder near the catecol-O-methyltransferase gene on chromosome 22[J].BiolPsychiatry,2002,51(7):591-601.
[122]Rothe C,Koszycki D,Bradwejn J,et al.Association of the Val158 Met Catechol-O-Methyltransferase Genetic Polymorphism with Panic Disorder[J].Neuropsychopharmacology,2006,31(10):2237-2242.
[123]Woo JM,Yoon KS,ChoiYH,et a.l The association between panic disorder and the L/L genotype of catechol-O-methyltransferase[J].J PsychiatrRes,2004,38(4):365-370.
[124]Stein MB,Fallin MD,Schork NJ,et al.COMT polymorphisms and anxiety-related personality traits[J].Neuropsychopharmacology,2005,30(11):2092-2102.
[125]Olsson CA,Anney RJ,Lotfi-Miri M,et al.Association between the COMT Val158Met polymorphism and propensity to anxiety in an Australian population-based longitudinal study of adolescent health.[J].Psychiatric Genetics,2005,15(2):109-115.
[126]Ohara K,Nagai M,Suzuki Y,et al.No association between anxiety disorders and cateehol-O-methyltransferase polymorphism[J].Psychiatry Res,1998,80(2):145-148.
[127]Wray NR,James MR,Dumenil T,et al.Association Study of Candidate Variants of COMT With Neuroticism,Anxiety and Depression[J].Am J Med Genet B Neuropsychiatr Genet,2008,147B(7):1314-1318.
[128]Kolassa IT,Buchmann A,Lauche R,et al.Spider phobics more easily see a spider in morphed schematic pictures [J]. Behav Brain Funct, 2007,3:59.
[129] Samochowiec J, Hajduk A, Samochowiec A, et al. Association studies of MAO-A,COMT, and 5-HTT genes polymorphisms in patients with anxiety disorders of the phobic spectrum[J]. Psychiatry Res, 2004, 128(1):21-26.
[130] McGrath M, Kawachi I, Ascherio A, et al. Association Between Catechol-O-Methyltransferase and Phobic Anxiety[J]. Psychiatry, 2004, 161(9):1703-1705.
[131] Gershon ES, Badner JA, Goldin LR, et al. Closing in on genes for manic-depressive illness and schizophrenia [J]. Neuropsychopharmacology, 1998,18(4): 233-242.
[132] Holmans P. Detecting gene-gene interactions using affected sib pair analysis with covariates [J]. Hum Hered, 2002,53(2):92-102.
[133] Weeks DE, Lange K. The affected-pedigree-member method of linkage analysis [J].Am J Hum Genet, 1988,42(2):315-326.
[134] Schaid DJ, Rowland C. Use of parents, sibs, and related controls for detection of associations between genetic markers and disease [J]. Am J Hum Genet, 1998, 63(5):1492-1506.
[135] Bellodi L, Bussoleni C, Scorza-Smeraldi R, et al. Family study of schizophrenia:exploratory analysis for relevant factors [J]. Schizopr Bull, 1986,12(1): 120-128.
[136] Thomson G Mapping disease genes: family-based association studies [J]. Am J Hum Genet, 1995, 57(2):487-498.
[137] Falk CT, Rubinstein P. Haplotype relative risks: an easy reliable way to construct a proper control sample for risk calculations [J]. Ann Hum Genet, 1987,51(Pt3):227-233.
[138] Spielman RS, McGinnis RE, Ewens WJ. Transmission test for linkage disequilibrium:the insulin gene region and insulin-dependent diabetes mellitus (IDDM) [J]. Am J Hum Genet, 1993, 52(3):506-516.
[139] Spielman RS, Ewens WJ. The TDT and other family-based for linkage disequilibrium and association [J]. Am J Hum Genet, 1996, 59(5): 983-989.
[140] Botstein D, White RI, Skolnick M, et al. Construction of genetic linkage map in man using restriction fregment length polymorphisms [J]. Am J Hum Genet, 1980,32(3):314-331.
[141] Donis-Keller H, Green P, Helms C, et al. A genetic linkage map of the human genome [J]. Cell, 1987, 51(2):319-337.
[142] Lander ES. The new genomics: global views of biology [J]. Science, 1996, 274(5287):536-539.
[143]Heid CA,Stevens J,Livak KJ,et al.Real time quantitative PCR[J].Genome Res,1996,6(10):986-994.
[144]Alderborn A,Kristofferson A,Hammerling U.Determination of single nucleotide polymorphisms by real-time pyrophosphate DNA sequencing[J].Genome Res,2000,10(8):1249-1258.
[145]Zhenxian Xiao,Junxua Xiao,Yuexing Jiang,et al.A novel method based on ligase detection reaction for low abundant YIDD mutants detection in hepatitis B virus[J].Hepatology Research,2006,34(3):150-155.
[146]肇旭,秦胜营,冯国鄞,等.基于连接酶检测反应的基因芯片分型技术的建立[J].国际遗传学杂志,2006,29(3):178-182.
[147]Makino R,Yazyu H,Kishimoto Y,et al.F-SSCP:fluorescence-based polymerase chain reaction-single-strand conformation polymorphism(PCR-SSCP) analysis[J].PCR Methods Appl,1992,2(1):10-13.
[148]彭翠英,廖端芳,张佳,等.单核苷酸多态性及其检测方法[J].中华检验医学杂志,2004,27(10):703-705.
[149]Myers RM,Maniatis T,Leman LS.Detection and localization of single base changs by denaturing gradient gel electrophoresis[J].Methods Enzymol,1987,155:501-527.
[150]O'Donovan MC,Oefner PJ,Roberts SC,et al.Blind analysis of denaturing hing-performance liquid chromatography as a tool for mutation detection[J].Genomics,1998,52(1):44-49.
[151]赵春霞,石先哲,吕申,等.人类基因组的单核苷酸多态性及其研究进展[J].色谱,2003,21(2):110-114.
[152]赵广荣,扬帆,元英进,等.单核苷酸多态性的检测方法的新进展[J].遗传,2005,27(1):123-129.
[153]Pease AC,Solas D,Sullivan EJ,et al.Light-generated oligonucleotide arrays for rapid DNA sequence analysis[J].Proc Natl Acad Sci USA,1994,91(11):5022-5026.
[154]Lipshutz RJ,Morris D,Chee M,et al.Using oligonucleotide probe arrays to access genetic diversity[J].Biotechniques,1995,19(3):442-447.
[155]Griffin TJ,Tang W,Smith LM.Genetic analysis by peptide nucleic acid affinity MALDI-TOF mass spectrometry[J].Nat Biotechnol,1997,15(13):1368-1372.
[156]Monforte JA,Becker CH.High-throughout DNA analysis by Time-of-Flight mass spectrometry[J].Nature Medicine,1997,3(3):360-362.
[157]Kofiadi IA,Rebrikov DV.Methods for detecting single nucleotide polymorphisms: Allele-specific PCR and hybridization with oligonucleotide probe[J].Genetika,2006,42(1):16-26.
[158]Lucarelli F,Marrazza G,Mascini M.Design of an optimal allele-specific oligonucleotide probe for the efficient discrimination of a thermadynamically stable (G-T) mismatch[J].Anal Chim Acta,2007,603(1):82-86.
[159]高秀丽,景奉香,杨建波,等.单核苷酸多态性检测分析技术[J].遗传,2005,27(1):110-122.
[160]Prince JA,Brookes AJ.Towards high-throughput genotyping of SNPs by dynamic allele-specific hybridization[J].Expert Rev Mol Diagn,2001,1(3):352-358.
[161]Ottman R.Gene-environment interaction;definitions and study designs[J].Preventive Medicine,1996,25(6):764-770.
[162]Murtaugh MA,Sweeney C,Ma KN,et al.The CYP1A1 genotype may alter the association of Meat consumption patterns and preparation with the risk of colorectal cancer in men and women[J].J Nutr,2005,135(2):179-186.
[163]黄悦勤.临床流行病学[M].北京:人民卫生出版社,2002:143-146.
[164]王培桦,沈洪兵,陈峰,等.叉生分析在基因-环境交互研究中的应用与意义[J].中华流行病学杂志,2005,26(1):54-57.
[165]Rubinstein P,Ginsberg-Fellner F,Falk C.Genetic of Type Ⅰ diabetes mellitus:a single.recessive predisposition gene mapping between HLA-B and GLO.with an appendix on the estimation of selection bias[J].Am J Hum Genet,1981,33(6):865-882.
[166]Schaid DJ.Case-parents design for gene-environment interaction[J].Genet Epidemiol,1999,16(3):261-273.
[167]杨仕贵.病例父母对照研究在遗传性疾病中的应用[J].疾病控制杂志,2002,6(2):143-145.
[168]Yang Q,Khoury MJ.Evolving methods in genetic epidemiology Ⅲ Gene-environment interaction in epidemiologic research[J].Epidemiol Rev,1997,19(1):33-43.
[169]Piegorsch WW,Weinbegr CR,Taylor JA.Non-hierarchical logistic models and case-only designs for assessing susceptibility in population-based case-control studies[J].Stat Med,1994,13(2):153-162.
[170]Hmaajima N,Yuasa H,Matsuo K,et al.Detection of gene-environment inieraction by case-only studies[J].JPn J Clin Oneol,1999,29(10):490-493.
[171]李大林,李立明.基因-环境交互作用研究方法:无对照病例研究[J].中华流行病学杂志,2002,23(4):304-307.
[172]柏建岭,荀鹏程,赵扬,等.不完全病例对照研究基因环境交互作用研究的应用与意义[J].中华流行病学杂志,2006,27(1):72-75.
[173]Gerry NP,Witowski NE,Day J,et al.Universal DNA microarray method for multiplex detection of low abundance point mutations[J].J Mol Biol,1999,292(2):251-262.
[174]Luo J,Bergstrom DE,Barany F.Improving the fidelity of thermos thermophilus DNA ligae[J].Nucleic Acids Res,1996,24(15):3071-3078.
[175]Consolandi C,Busti E,Pera C,et al.Detection of HLA Polymorphisms by Ligase Detection Reaction and a Universal Array Format:A Pilot Study for Low Resolution Genotyping[J].Hum Immunol.2003,64(1):168-178.
[176]谭红专.现代流行病学[M].第2版.北京:人民卫生出版社,2008.
[177]赵仲堂.流行病学研究方法与应用[M].第二版.北京:科学出版社,2005,537-538.
[178]沈靖,王润田,徐希平.代谢酶基因多态性与环境暴露交互作用的分析方法及其应用[J].中华流行病学杂志,2001,22(1):61-62.
[179]舒良,张鸿燕,汪向东,等.“复合性国际诊断交谈检查核心本”现场测试.信度效度检验[J].中国心理卫生杂志,1993,7(5):208-211.
[180]邹义壮,舒良,沈渔邨,等.CIDI对神经症诊断的现场测试[J].中国心理卫生杂志,1995.9(5):206-208.
[181]Komiti AA,Jacks on HJ,Judd FK,et al.A comparison of the Composite International Diagnostic Interview(CIDI-Auto) with clinical assessment in diagnosing mood and anxiety disorders[J].Aust N Z J Psychiatry,2001,35(2):224-230.
[182]Jordanova V,Wickramesinghe C,Gerada C,et al.Validation of two survey diagnostic interviews among primary care attendees:a comparison of CIS-R and CIDI with SCAN ICD-10 diagnostic categories[J].Psychol Med,2004,34(6):1013-1024.
[183]胡赤怡,胡纪泽,段卫东,等.复合性国际诊断访谈表的效度研究[J].中国神经精神疾病杂志,2008,34(7):385-389.
[184]张延赤.大学生神经症流行病学特征分析与防治对策研究[D].长春:吉林大学,2006.
[185]吴承红,蔡澄.大学生强迫症症状学的研究[J].扬州大学学报,2002,6(3):32-34.
[186]赵勇.大学生强迫症状况调查及其个性分析[J].中国健康心理学杂志,2005,13(6):19-20.
[187]高良会,崔利军,粟克清,等.河北省特殊恐怖性神经症的流行病学调查[J].中国全科医学,2007,10(7):1451-1452.
[188]Maggee WJ,Eaton WW,Wittchen HU,et al.Agoraphobia,simple phobia,and social phobia in the national comorbidity survery[J].Arch Gen Psychiatry,1996,53(3):159.
[189]Furmark T.Social phobia:overview of community surveys[J].Acta Psychiatr Stand,2002,105(2):84-93.
[190]李建芹.河南省大学生焦虑状况调查[J].中国健康教育,2006,22(3):112-113.
[191]申小莹,刘晓瑞,董雪.西安某高校大学生焦虑状况的调查研究[J].中国健康心理学杂志,2006,14(3):311-312.
[192]王云强,乔建中.理工科大学生焦虑状况测查研究[J].中国健康心理学杂志,2007,15(11):1007-1009.
[193]许韶君,陶芳标,张洪波.大学生抑郁、焦虑症状及其影响因素的分析[J].安徽预防医学杂志,1999,5(2):121-122.
[194]杨青侠.大学生神经衰弱患病情况的调查分析[J].贵州医药,1996,20(1):28.
[195]郭莉,娟祝雁,郝曙光.在校大学生神经衰弱病因调查分析[J].吉林大学学报(医学版),2008,33(6):1045.
[196]张在坦.烟台师范学院大学生神经衰弱的病因调查[J].中国校医,2004,18(4):333-334.
[197]黎凡.兰州地区4868名大学生神经衰弱调查报告[J].中国心理卫生杂志,1988,2(5):229-230,233.
[198]谢冰.大学生强迫症现况调查及SAPAP3基因多态性关联研究[D].长春:吉林大学,2008.
[199]张香云,刘卉兰,储耀辉,等.神经症患者的社会支持和应对方式调查[J].中国心理卫生杂志,2003,17(6):427.
[200]朱红.2型糖尿病并发肺结核病遗传和环境危险因素探讨[D].天津:天津医科大学,2006.
[201]Gray IC,Campbell DA,Spurr NK,et al.Single nucleotide polymorphisms as tools in human genetics[J].Hum Mol Genet,2000,9(16):2403-2408.
[202]杨玉凤.环境与遗传因素在胃癌发生中的交互作用研究[D].南京:东南大学,2006:41.
[203]Wallaee HM.A model of gene-gene and gene-environment interactions and its implications for targeting environmental interventions by genotype[J].Theor Biol Med Mode,2006,3:35.
[204]Wacholder S,Chatterjee N,Hartge P.Joint effect of genes and environment distorted by Selection biases:implications for hospital-based case-control studies[J].Cancer Epidemiol Biomkarers Prev,2002,11(9):885-889.
[205]Lander ES,Schork NJ.Gene dissection of complex traits[J].Science,1994,265(5184):2037-2048.
[206]Greenland S,Rothman KJ.Concepts of interaction In:Rothman KJ,Greenland S,eds.Modern Epidemiology[M].2nd ed.Philadelphia:Lippineott-Raven,1998:329-342.
[207]刘玮.肺结核易感基因、环境危险因素及其交互作用研究[D].北京:中国人民解放军军事医学科学院,2005.
[208]Smith PG,Day NE.The design of case-control studies:the influence of confounding and interaction effects[J].Int J Epidemiol,1984:13(3):356-365.
[209]Andrieu N,Goldstein AM,Thomas DC,et al.Counter-matching in studies of gene-environment interaction:efficiency and feasibility[J].Am J Epidemiol,2001,153(3):265-74.
[210]Sturmer T,Brenner H.Potential gain in efficiency and power to detect gene-environment Interactions by matching in case-control studies[J].Genet Epidemiol,2000,18(1):63-80.