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The origins of writing -- Writing and human development -- Working memory and expertise in writing -- The teaching of writing -- Creativity and emotions in writing -- Disorder of written language: diagnostic criteria, prevalence, and biological bases -- Testimonials

This handbook helps readers to both understand and craft policies to aid the successful acculturation of immigrants in the US. It is an excellent road map for researchers in immigration and education, as well as educational and developmental psychologists, sociologists, economists, and public policy makers. An immigrant from Russia, Dr. Grigorenko weaves her first-hand experiences and strategies into this unique text. It encompasses all available research on immigration and acculturation, from new information on bilingual education to studies of low-skill versus high-skill workers. Key Topics

Intelligence cannot be fully or even meaningfully understood outside its cultural context. Work that seeks to study intelligence a contextually risks the imposition of an investigator's view of the world on the rest of the world. Moreover, work on intelligence within a single culture may fail to do justice to the range of skills and knowledge that may constitute intelligence broadly defined and risks drawing false and hasty generalizations. In this article, we consider the relevance of culture to intelligence and its investigation, assessment, and development. We describe studies from diverse continents, based on the theory of successful intelligence, that show the importance of understanding intelligence in its cultural context and conclude that intelligence must be understood in such context.

This study was designed to investigate relationships among self‐reported and spouse‐reported beliefs about parenting styles, the characteristics of the individuals manifesting these styles, and the contextual characteristics of parenting. Demographic characteristics, life circumstances, family functioning, personality traits, ability indices, and parenting‐styles indicators were collected from a sample of 452 women and 293 men, all of whom were raising adolescents in contemporary Russia. Of the families studied, 275 were intact (i.e. consisted of married and cohabiting couples). It was found that individual characteristics and contextual characteristics (e.g. family functioning) together predicted about 20% of the variance in reported beliefs about parental styles of responsiveness and demandingness. Moreover, these variables discriminated about 65% of the parents reporting indulging, neglectful, authoritarian or authoritative beliefs about parenting. The percentage of explained variance doubled when beliefs about parenting styles of partners were placed in the model. Thus, in attempts to understand the etiology of parents' beliefs about parenting styles, more attention should be given to beliefs about parenting styles of their spouses. It might be that beliefs about parenting styles emerge as a structure shared by spouses; they are mediated, but not solely determined, by the individual characteristics of parents and their children.

AbstractDifferences in learning patterns of vocabulary acquisition in children at risk (+SRD) and not at risk (−SRD) for Specific Reading Disability (SRD) were examined using a microdevelopmental paradigm applied to the multi‐trial Foreign Language Learning Task (FLLT; Baddeley et al., 1995). The FLLT was administered to 905 children from rural Chitonga‐speaking Zambia. A multi‐group Latent Growth Curve Model (LGCM) was implemented to study interindividual differences in intraindividual change across trials. Results showed that the +SRD group recalled fewer words correctly in the first trial, learned at a slower rate during the subsequent trials, and demonstrated a more linear learning pattern compared to the −SRD group. This study illustrates the promise of LGCM applied to multi‐trial learning tasks, by isolating three components of the learning process (initial recall, rate of learning, and functional pattern of learning). Implications of this microdevelopmental approach to SRD research in low‐to‐middle income countries are discussed.

WOS: 000373197500020 ; PubMed ID: 27016271 ; BACKGROUND AND OBJECTIVE: Developmental language disorder (DLD) is a highly prevalent neurodevelopmental disorder associated with negative outcomes in different domains; the etiology of DLD is unknown. To investigate the genetic underpinnings of DLD, we performed genome-wide association and whole exome sequencing studies in a geographically isolated population with a substantially elevated prevalence of the disorder (ie, the AZ sample). METHODS: DNA samples were collected from 359 individuals for the genome-wide association study and from 12 severely affected individuals for whole exome sequencing. Multifaceted phenotypes, representing major domains of expressive language functioning, were derived from collected speech samples. RESULTS: Gene-based analyses revealed a significant association between SETBP1 and complexity of linguistic output (P = 5.47 x 10(-7)). The analysis of exome variants revealed coding sequence variants in 14 genes, most of which play a role in neural development. Targeted enrichment analysis implicated myocyte enhancer factor-2 (MEF2)-regulated genes in DLD in the AZ population. The main findings were successfully replicated in an independent cohort of children at risk for related disorders (n = 37). CONCLUSIONS: MEF2-regulated pathways were identified as potential candidate pathways in the etiology of DLD. Several genes (including the candidate SETBP1 and other MEF2-related genes) seem to jointly influence certain, but not all, facets of the DLD phenotype. Even when genetic and environmental diversity is reduced, DLD is best conceptualized as etiologically complex. Future research should establish whether the signals detected in the AZ population can be replicated in other samples and languages and provide further characterization of the identified pathway. ; National Institute of Health [R01 DC007665, P50 HD052120]; NIH Centers for Mendelian Genomics [5U54HG006504]; National Science Foundation Integrative Graduate Education and Research Traineeship grant [114399]; Government of the Russian Federation [14.Z50.31.0027]; National Institutes of Health (NIH) ; Supported by National Institute of Health grants R01 DC007665 (Dr Grigorenko, Principal Investigator) and P50 HD052120 (Richard Wagner, Principal Investigator), NIH Centers for Mendelian Genomics (5U54HG006504), National Science Foundation Integrative Graduate Education and Research Traineeship grant 114399 (Dr Magnuson, Principal Investigator), and grant 14.Z50.31.0027 from the Government of the Russian Federation (Dr Grigorenko, Principal Investigator). Funded by the National Institutes of Health (NIH).

WOS: 000373197500020 ; PubMed ID: 27016271 ; BACKGROUND AND OBJECTIVE: Developmental language disorder (DLD) is a highly prevalent neurodevelopmental disorder associated with negative outcomes in different domains; the etiology of DLD is unknown. To investigate the genetic underpinnings of DLD, we performed genome-wide association and whole exome sequencing studies in a geographically isolated population with a substantially elevated prevalence of the disorder (ie, the AZ sample). METHODS: DNA samples were collected from 359 individuals for the genome-wide association study and from 12 severely affected individuals for whole exome sequencing. Multifaceted phenotypes, representing major domains of expressive language functioning, were derived from collected speech samples. RESULTS: Gene-based analyses revealed a significant association between SETBP1 and complexity of linguistic output (P = 5.47 x 10(-7)). The analysis of exome variants revealed coding sequence variants in 14 genes, most of which play a role in neural development. Targeted enrichment analysis implicated myocyte enhancer factor-2 (MEF2)-regulated genes in DLD in the AZ population. The main findings were successfully replicated in an independent cohort of children at risk for related disorders (n = 37). CONCLUSIONS: MEF2-regulated pathways were identified as potential candidate pathways in the etiology of DLD. Several genes (including the candidate SETBP1 and other MEF2-related genes) seem to jointly influence certain, but not all, facets of the DLD phenotype. Even when genetic and environmental diversity is reduced, DLD is best conceptualized as etiologically complex. Future research should establish whether the signals detected in the AZ population can be replicated in other samples and languages and provide further characterization of the identified pathway. ; National Institute of Health [R01 DC007665, P50 HD052120]; NIH Centers for Mendelian Genomics [5U54HG006504]; National Science Foundation Integrative Graduate Education and Research Traineeship grant [114399]; Government of the Russian Federation [14.Z50.31.0027]; National Institutes of Health (NIH) ; Supported by National Institute of Health grants R01 DC007665 (Dr Grigorenko, Principal Investigator) and P50 HD052120 (Richard Wagner, Principal Investigator), NIH Centers for Mendelian Genomics (5U54HG006504), National Science Foundation Integrative Graduate Education and Research Traineeship grant 114399 (Dr Magnuson, Principal Investigator), and grant 14.Z50.31.0027 from the Government of the Russian Federation (Dr Grigorenko, Principal Investigator). Funded by the National Institutes of Health (NIH).

AbstractIn both children and adults there is large variability in reading skill, with approximately 5–10% of individuals characterized as having reading disability; these individuals struggle to learn to read despite adequate intelligence and opportunity. Although it is well established that a substantial portion of this variability is attributed to the genetic differences between individuals, specifics of the connections between reading and the genome are not understood. This article presents data that suggest that variation in the COMT gene, which has previously been associated with variation in higher‐order cognition, is associated with reading and reading‐related skills, at the level of both brain and behavior. In particular, we found that the COMT Val/Met polymorphism at rs4680, which results in the substitution of the ancestral Valine (Val) by Methionine (Met), was associated with better performance on a number of critical reading measures and with patterns of functional neural activation that have been linked to better readers. We argue that this polymorphism, known for its broad effects on cognition, may modulate (likely through frontal lobe function) reading skill.