Evolutionary-biological reasoning suggests that individuals should be differentially susceptible to environmental influences, with some people being not just more vulnerable than others to the negative effects of adversity, as the prevailing diathesis-stress view of psychopathology (and of many environmental influences) maintains, but also disproportionately susceptible to the beneficial effects of supportive and enriching experiences (or just the absence of adversity). Evidence consistent with the proposition that individuals differ in plasticity is reviewed. The authors document multiple instances in which (a) phenotypic temperamental characteristics, (b) endophenotypic attributes, and (c) specific genes function less like "vulnerability factors" and more like "plasticity factors," thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences. Discussion focuses upon limits of the evidence, statistical criteria for distinguishing differential susceptibility from diathesis stress, potential mechanisms of influence, and unknowns in the differential-susceptibility equation.

BackgroundMost gene-environment interaction (GXE) research, though based on clear, vulnerability-oriented hypotheses, is carried out using exploratory rather than hypothesis-informed statistical tests, limiting power and making formal evaluation of competing GXE propositions difficult.MethodWe present and illustrate a new regression technique which affords direct testing of theory-derived predictions, as well as competitive evaluation of alternative diathesis-stress and differential-susceptibility propositions, using data on the moderating effect of DRD4 with regard to the effect of childcare quality on children's social functioning.ResultsResults show that (a) the new approach detects interactions that the traditional one does not; (b) the discerned GXE fit the differential-susceptibility model better than the diathesis-stress one; and (c) a strong rather than weak version of differential susceptibility is empirically supported.ConclusionThe new method better fits the theoretical glove' to the empirical hand,' raising the prospect that some failures to replicate GXE results may derive from standard statistical approaches being less than ideal.

The common approach to the multiplicity problem calls for controlling the familywise error rate (FWER). This approach, though, has faults, and we point out a few. A different approach to problems of multiple significance testing is presented. It calls for controlling the expected proportion of falsely rejected hypotheses-the false discovery rate. This error rate is equivalent to the FWER when all hypotheses are true but is smaller otherwise. Therefore, in problems where the control of the false discovery rate rather than that of the FWER is desired, there is potential for a gain in power. A simple sequential Bonferroni-type procedure is proved to control the false discovery rate for independent test statistics, and a simulation study shows that the gain in power is substantial. The use of the new procedure and the appropriateness of the criterion are illustrated with examples.

Approximately 6% of school-aged children have math difficulties (MD). A neurogenetic etiology has been suggested due to the presence of MD in some genetic syndromes such as 22q11.2DS. However, the contribution of 22q11.2DS to the MD phenotype has not yet been investigated. This is the first population-based study measuring the frequency of 22q11.2DS among school children with MD. Children (1,564) were identified in the schools through a screening test for language and math. Of these children, 152 (82 with MD and 70 controls) were selected for intelligence, general neuropsychological, and math cognitive assessments and for 22q11.2 microdeletion screening using MLPA. One child in the MD group had a 22q11.2 deletion spanning the LCR22-4 to LCR22-5 interval. This child was an 11-year-old girl with subtle anomalies, normal intelligence, MD attributable to number sense deficit, and difficulties in social interactions. Only 19 patients have been reported with this deletion. Upon reviewing these reports, we were able to characterize a new syndrome, 22q11.2 DS (LCR22-4 to LCR22-5), characterized by prematurity; pre- and postnatal growth restriction; apparent hypotelorism, short/upslanting palpebral fissures; hypoplastic nasal alae; pointed chin and nose; posteriorly rotated ears; congenital heart defects; skeletal abnormalities; developmental delay, particularly compromising the speech; learning disability (including MD, in one child); intellectual disability; and behavioral problems. These results suggest that 22q11.2 DS (LCR22-4 to LCR22-5) may be one of the genetic causes of MD. 2014 Wiley Periodicals, Inc.

This paper is a quantitative synthesis of research into parental involvement and academic achievement through a meta-analysis of 37 studies in kindergarten, primary and secondary schools carried out between 2000 and 2013. Effect size estimations were obtained by transforming Fisher's correlation coefficient. An analysis has also been conducted of the heterogeneity of the magnitudes grouped according to different moderator variables, and a study of the publication bias affecting meta-analytical studies. The results show that the parental models most linked to high achievement are those focusing on general supervision of the children's learning activities. The strongest associations are found when the families have high academic expectations for their children, develop and maintain communication with them about school activities, and help them to develop reading habits.

Mathematics ability is a complex cognitive trait with polygenic heritability. Genome-wide association study (GWAS) has been an effective approach to investigate genetic components underlying mathematic ability. Although previous studies reported several candidate genetic variants, none of them exceeded genome-wide significant threshold in general populations. Herein, we performed GWAS in Chinese elementary school students to identify potential genetic variants associated with mathematics ability. The discovery stage included 494 and 504 individuals from two independent cohorts respectively. The replication stage included another cohort of 599 individuals. In total, 28 of 81 candidate SNPs that met validation criteria were further replicated. Combined meta-analysis of three cohorts identified four SNPs (rs1012694, rs11743006, rs17778739 and rs17777541) ofSPOCK1gene showing association with mathematics ability (minimum p value 5.6765×65106110, maximum β 612.43). TheSPOCK1gene is located on chromosome 5q31.2 and encodes a highly conserved glycoprotein testican-1 which was associated with tumor progression and prognosis as well as neurogenesis. This is the first study to report genome-wide significant association of individual SNPs with mathematics ability in general populations. Our preliminary results further supported the role ofSPOCK1during neurodevelopment. The genetic complexities underlying mathematics ability might contribute to explain the basis of human cognition and intelligence at genetic level.

Mathematics ability and disability is as heritable as other cognitive abilities and disabilities, however its genetic etiology has received relatively little attention. In our recent genome-wide association study of mathematical ability in 10-year-old children, 10 SNP associations were nominated from scans of pooled DNA and validated in an individually genotyped sample. In this paper, we use a ‘SNP set’ composite of these 10 SNPs to investigate gene-environment (GE) interaction, examining whether the association between the 10-SNP set and mathematical ability differs as a function of ten environmental measures in the home and school in a sample of 1888 children with complete data. We found two significant GE interactions for environmental measures in the home and the school both in the direction of the diathesis-stress type of GE interaction: The 10-SNP set was more strongly associated with mathematical ability in chaotic homes and when parents are negative.

Abstract Gene-by-environment interactions (G×Es) can provide important biological insights into psychiatric disorders and may consequently have direct clinical implications. In this review, we begin with an overview of the major challengesG×E studies have faced (e.g., difficulties replicating findings and high false discovery rates). In light of these challenges, this review focuses on describing examples in which we might begin to understand G×Es on the molecular, cellular, circuit, and behavioral level and link this interaction to altered risk for the development of psychiatric disorders. We also describe recent studies that utilize a polygenic approach to examine G×Es. Finally, we discuss how gaining a deeper understanding of G×Es may translate into a therapeutic practice with more targeted treatments. Expected final online publication date for the Annual Review of Psychology Volume 68 is January 03, 2017. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

Objective Both clinical and biological factors influence the course of depressive disorders. This study tested for associations between the brain-derived neurotrophic factor (BDNF) gene at the Val66Met locus and the course of major depressive disorder (MDD).Methods Three hundred ten Korean subjects (209 patients, 101 controls) were genotyped for rs6265 at nucleotide 196 (G/A), which produces an amino acid substitution at codon 66 (Val66Met) of the gene for BDNF. Course of illness was evaluated both by chronicity of current episode (episode duration >24 months) and by the lifetime history of recurrences.Results Patients with the Met/Met BDNF genotype had a significantly higher rate of chronic depression than all others. There was a significant dose effect of the Met allele on chronicity. Compared with the Val/Val genotype, the relative risk of chronicity was 1.67 for the Val/Met genotype, and 2.58 for the Met/Met genotype. Lifetime history of recurrent episodes was not related to BDNF genotypes but was significantly associated with younger age of onset and with a history of depression in first degree relatives.Conclusion BDNF genotyping may be informative for anticipating chronicity in major depression. Psychiatry Investig 2013;10:56-61

Brain-derived neurotrophic factor (BDNF), a neurotrophin, is known to promote neuronal differentiation stimulating neurite outgrowth in the developing CNS, and is also known to modulate synaptic plasticity, thereby contributing to learning and memory in the mature brain. Here, we investigated the role of increased levels of intracerebral BDNF in learning and memory function. Using genetically engineered transgenic BDNF overexpressing mice (RTG-BDNF), young adult, homozygous (+/+), heterozygous (+/61), or wild-type (61/61) littermates, we analyzed escape latency to a hidden-platform and swimming velocity in the Morris Water Maze test (MWM) with modifications for the mice. The MWM comprised 4 trials per day over 5 consecutive days (sessions) without prior or subsequent training. In a separate set of animals, BDNF protein levels in the cortex, thalamostriatum and the hippocampus were measured quantitatively using ELISA. In the BDNF (+/61) mice, the BDNF levels in the cortex, the thalamostriatum and the hippocampus were significantly high, compared to the wild-type littermates; 238%, 158%, and 171%, respectively (P<0.01, one-way ANOVA and a post-hoc test in each region). The BDNF levels in the BDNF (+/+) mice were not elevated. The BDNF (+/61), but not the (+/+) mice, demonstrated significantly shorter escape latency, shorter total path length in the MWM, and more frequent arrivals at the location where the platform had been placed previously in the probe trial, compared with the wild-type littermates (P<0.05, at each time pint). Because the maximum swimming velocity was not affected in the BDNF-transgenic mice, increased BDNF levels in the brain were found to enhance spatial learning and memory function. Although it has been postulated that excessive BDNF is deteriorating for neuronal survival or neurite outgrowth, further investigations are needed to clarify the mechanism of paradoxical lack of increase in BDNF levels in the (+/+) mouse brain.

Gene×environment (G×E) interactions are known to predict susceptibility to disorders such as depression and anxiety. Adverse experiences in childhood and number of stressful life events (SLEs) have been widely studied as environmental risk factors; however, SLE response has not yet been studied. Here we present a first attempt at the analysis of the interaction between the response to personal and academic stressful events during different life stages and the gene polymorphisms 5-HTTLPR, 5-HTTVNTR (STin2), HTR1A C(611019)G, and BDNF Val66Met in the prediction of negative affectivity (NA). Standardized questionnaires (ST-DEP and STAI) were used to measure negative affectivity derived from depression and anxiety in a sample of 303 undergraduate students. Response to stressful events during childhood, high school and college years was evaluated together with a self-report personal history form. Multiple logistic regression analysis was used to perform association and G×E analysis. Negative affectivity is strongly associated with childhood maltreatment and stress response. Gene associations were observed between 5-HTTVNTR allele 12 and the S_12 haplotype with NA derived from high scores in both depression and anxiety. The BDNF gene variant was not associated with NA derived from depression or anxiety alone, but it was associated with the comorbid presentation. A significant G×E interaction was observed between the BDNF Val66Met and stress response during childhood and college years although the risk for negative affectivity conferred by stress response during childhood was only significant among the Met allele carriers, while stress response during college years was a significant risk factor regardless of the BDNF Val66Met genotype. A significant G×E interaction was also found between the HTR1A C(611019)G variant and childhood maltreatment. The study has two main limitations, sample size is low and retrospective recognition of SLEs is a concern. Altogether, our results demonstrate that the BDNF Val66Met variant moderates the effect of stress during both childhood and college years; although this effect seems to be more critical during childhood given that the risk conferred by childhood stress was restricted to the Met allele carriers. We also found that the HTR1A C(611019)G variant moderates the effect of childhood maltreatment in our study population.

(2006). Parents' Educational Involvement: A Developmental Ecology Perspective. Parenting: Vol. 6, No. 1, pp. 1-48. doi: 10.1207/s15327922par0601_1

Abstract Re-parameterized regression models may enable tests of crucial theoretical predictions involving interactive effects of predictors that cannot be tested directly using standard approaches. First, we present a re-parameterized regression model for the Linear Linear interaction of 2 quantitative predictors that yields point and interval estimates of 1 key parameter-the crossover point of predicted values-and leaves certain other parameters unchanged. We explain how resulting parameter estimates provide direct evidence for distinguishing ordinal from disordinal interactions. We generalize the re-parameterized model to Linear Qualitative interactions, where the qualitative variable may have 2 or 3 categories, and then describe how to modify the re-parameterized model to test moderating effects. To illustrate our new approach, we fit alternate models to social skills data on 438 participants in the National Institute of Child Health and Human Development Study of Early Child Care. The re-parameterized regression model had point and interval estimates of the crossover point that fell near the mean on the continuous environment measure. The disordinal form of the interaction supported 1 theoretical model-differential-susceptibility-over a competing model that predicted an ordinal interaction. PsycINFO Database Record (c) 2013 APA, all rights reserved.

？基于我国特定的教育文化背景，整合已有理论和实证研究，提出了小学生父母教育卷入行为结构的理论模型。通过家长访谈、专家评定，对该模型进行了完善，并据此编制了家长报告问卷加以验证。对965位小学生家长所填问卷进行分析后，形成小学生父母教育卷入行为问卷（父母回答版）。问卷共29个项目，包括了五个维度，分别为：家庭监控，指父母对子女学习、生活及交往等的监督、控制行为；学业辅导，指家长按照教师要求或自行在家中对子女的学习进行辅导的行为；亲子沟通，指家长在日常生活中就子女学习、生活、交往以及学校事务进行沟通和交流的行为，以达到共同理解、信任的过程；共同活动，指为开阔视野、促进身心发展，家长与孩子共同进行的一些文体、社会实践活动等；家校沟通，指家长为了获取子女在校表现的信息和了解学校当前进行的工作而进行的家校之间的沟通与交流。经过探索性因素分析和交叉验证分析，问卷的结构与理论模型拟合较好，能够作为考察我国小学生父母教育卷入行为的测量工具。

Raven's Standard Progressive Matrices (R. SPM) was revised by a research group colaborated with people came from 17 places all over the country. Based upon the data of 1982 census, a group of 5108 people aged from 5-to over 70 was sampled for establishing the norm. Through a series of standardized procedures, the Chinese norm (city version) of R. SPM was complished with appropriate reliability and validity. It meets the need of group test for measuring intelligence. The result shows that there is no significant sex difference except the group aged 40-49. The Chinese norm was also compared with those came from H. K., U. K. and New Jealand.