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Studies exploring neuroanatomic correlates of reading have associated white matter tissue properties with reading disability and related componential skills (e.g., phonological and single-word reading skills). Mean diffusivity (MD) and fractional anisotropy (FA) are widely used surrogate measures of tissue microstructure with high sensitivity; however, they lack specificity for individual microstructural features. Here we investigated neurite features with higher specificity in order to explore the underlying microstructural architecture. Diffusion weighted images (DWI) and a battery of behavioral and neuropsychological assessments were obtained from 412 children (6 – 16 years of age). Neurite indices influenced by orientation and density were attained from 23 major white matter tracts. Partial correlations were calculated between neurite indices and indicators of phonological processing and single-word reading skills using age, sex, and image quality metrics as covariates. In addition, mediation analysis was performed using structural equation modeling (SEM) to evaluate the indirect effect of phonological processing on reading skills. We observed that orientation dispersion index (ODI) and neurite density index (NDI) were negatively correlated with single-word reading and phonological processing skills in several tracts previously shown to have structural correlates with reading efficiency. We also observed a significant and substantial effect in which phonological processing mediated the relationship between neurite indices and reading skills in most tracts. In sum, we established that better reading and phonological processing skills are associated with greater tract coherence (lower ODI) and lower neurite density (lower NDI). We interpret these findings as evidence that reading is associated with neural architecture and its efficiency.

\"This book is a scholarly overview of the modern concepts, definitions, and theories of intellectual giftedness, and of past and current developments in the field of gifted education. The authors consider, in some detail, the roles of intelligence, creativity, and wisdom in giftedness and the interaction between culture and giftedness, as well as how giftedness can be understood in terms of a construct of developing expertise. The authors also review and discuss a set of key studies that address the issues of identification and education of children with intellectual gifts. This volume may be used as a summary overview of the field for educators, psychologists, social workers, and other professionals who serve intellectually gifted children and their families\"-- Provided by publisher.

A whole-genome and transcriptome analysis of 20 human induced pluripotent stem-cell lines shows that reprogramming does not necessarily add de novo copy number variants to what is already present in the somatic cells from which they originated. Mixed genetic message from iPSC lines The ability to derive induced pluripotent stem cells (iPSCs) from somatic cells raises exciting possibilities for the study of human development and regenerative medicine. These applications require that the clonal cells maintain the genetic background of the individual from whom they are derived, so reports of chromosomal copy number variations (CNVs) in reprogrammed cells carry serious implications for their translational utility. Flora Vaccarino and colleagues now report a whole-genome and transcriptome analysis of 20 human iPSC lines from seven individuals. They found that reprogramming does not necessarily add de novo CNVs to those already present in the somatic genome. Interestingly, they also found a mosaic CNV pattern within individuals, confirming previous findings from cultured human fibroblasts. This work shows that iPSCs can be used as a discovery tool for the investigation of genomic mosaicism due to low-frequency CNVs in human tissues. Reprogramming somatic cells into induced pluripotent stem cells (iPSCs) has been suspected of causing de novo copy number variation 1 , 2 , 3 , 4 . To explore this issue, here we perform a whole-genome and transcriptome analysis of 20 human iPSC lines derived from the primary skin fibroblasts of seven individuals using next-generation sequencing. We find that, on average, an iPSC line manifests two copy number variants (CNVs) not apparent in the fibroblasts from which the iPSC was derived. Using PCR and digital droplet PCR, we show that at least 50% of those CNVs are present as low-frequency somatic genomic variants in parental fibroblasts (that is, the fibroblasts from which each corresponding human iPSC line is derived), and are manifested in iPSC lines owing to their clonal origin. Hence, reprogramming does not necessarily lead to de novo CNVs in iPSCs, because most of the line-manifested CNVs reflect somatic mosaicism in the human skin. Moreover, our findings demonstrate that clonal expansion, and iPSC lines in particular, can be used as a discovery tool to reliably detect low-frequency CNVs in the tissue of origin. Overall, we estimate that approximately 30% of the fibroblast cells have somatic CNVs in their genomes, suggesting widespread somatic mosaicism in the human body. Our study paves the way to understanding the fundamental question of the extent to which cells of the human body normally acquire structural alterations in their DNA post-zygotically.

يتناول كتاب (التدريس من أجل الحكمة الذكاء الإبداع والنجاح) والذي قام بتأليفه (روبرت ستيرنبرغ، ليندا جارفين، إلينا قراقينكو) في حوالي (192) صفحة من القطع المتوسط موضوع (الجوانب النفسية للتدريس والإبداع) مستعرضا المحتويات التالية : الجزء الأول : التدريس للحكمة والذكاء والإبداع والنجاح مقدمة في التدريس للحكمة والذكاء والإبداع والنجاح ما هو نموذج الحكمة، حان دورك : ماهي نقاط القوة لديك، الجزء الثاني : لماذا وكيف ندرس من أجل الذكاء الناجح ؟ مقدمة في التدريس للذكاء الناجح، كيف تعزز مهارات الذاكرة ؟، كيف تعزز مهارات التحليلية ؟.

Dyslexia is a common learning impairment with a genetic basis that affects word reading and spelling. An increasing list of loci and genes have been implicated, but analyses to-date have investigated only limited genomic variation within each locus with no confirmed pathogenic variants identified. Our study is the first to comprehensively sequence both coding and cis-acting regulatory regions of such genes in a large study sample. In a collection of >2000 participants in families from three independent sites, we performed targeted capture and comprehensive sequencing of all exons and some regulatory elements of five candidate risk genes ( DNAAF4 , CYP19A1 , DCDC2 , KIAA0319 and GRIN2B ) for which prior evidence for a role in dyslexia exists from more than one sample. We evaluated evidence for association in each of six dyslexia-related quantitative phenotypes (traits) using both individual common single nucleotide polymorphisms and aggregated rare variants. We detected no promoter alterations and few deleterious variants in the coding exons, none of which showed evidence of association with any trait. Single variant and aggregate testing of DNAAF4 failed to detect significant evidence of association with any of the traits. The other four genes provided evidence of association with one or more traits. A common variant downstream of CYP19A1 showed significant evidence of association with multiple traits with or without verbal IQ (VIQ) adjustment. A haplotype that stretches from the downstream region of KIAA0319 to the second intron of DCDC2 was associated with reduced performance on timed real word reading. Finally, rare exonic variants in GRIN2B were associated with performance on spelling, with or without adjustment for VIQ. Our findings from this large-scale sequencing study complement those from genome-wide association studies, argue against the causative involvement of large-effect coding variants in these five candidate genes, support a multigenic etiology, and suggest a role of transcriptional regulation.

In this essay, I will briefly sample different instances of the utilization of the concept of resilience, attempting to complement a comprehensive representation of the field in the special issue of Development and Psychopathology inspired by the 42nd Minnesota Symposium on Child Psychology, hosted by the Institute of Child Development at the University of Minnesota and held in October of 2022. Having established the general context of the field, I will zoom in on some of its features, which I consider “low-hanging fruit” and which can be harvested in a systematic way to advance the study of resilience in the context of the future of developmental psychopathology.

With the present paper, we sought to use research findings to illustrate the following thesis: the evolution of language follows the principles of human evolution. We argued that language does not exist for its own sake, it is one of a multitude of skills that developed to achieve a shared communicative goal, and all its features are reflective of this. Ongoing emerging language adaptations strive to better fit the present state of the human species. Theories of language have evolved from a single-modality to multimodal, from human-specific to usage-based and goal-driven. We proposed that language should be viewed as a multitude of communication techniques that have developed and are developing in response to selective pressure. The precise nature of language is shaped by the needs of the species (arguably, uniquely H. sapiens) utilizing it, and the emergence of new situational adaptations, as well as new forms and types of human language, demonstrates that language includes an act driven by a communicative goal. This article serves as an overview of the current state of psycholinguistic research on the topic of language evolution.

Although learning disorders (LD) and developmental language disorder (DLD) can be linked to overlapping psychological and behavioral deficits, such as phonological, morphological, orthographic, semantic, and syntactic deficits, as well as academic (e.g., reading) difficulties, they are currently separate diagnoses in the DSM-5 with explicit phenotypic differences. At a neural level, it is yet to be determined to what extent they have overlapping or distinct signatures. The identification of such neural markers/endophenotypes could be important for the development of physiological diagnostic tools, as well as an understanding of disorders across different dimensions, as recommended by the Research Domain Criteria Initiative (RDoC). The current systematic review and meta-analysis examined whether the two disorders can be differentiated based on the auditory brainstem response (ABR). Even though both diagnoses require hearing problems to be ruled out, a number of articles have demonstrated associations of these disorders with the auditory brainstem response. We demonstrated that both LD and DLD are associated with longer latencies in ABR Waves III, V, and A, as well as reduced amplitude in Waves V and A. However, multilevel subgroup analyses revealed that LD and DLD do not significantly differ for any of these ABR waves. Results suggest that less efficient early auditory processing is a shared mechanism underlying both LD and DLD.

Early social deprivation (i.e., an insufficiency or lack of parental care) has been identified as a significant adverse early experience that may affect multiple facets of child development and cause long-term outcomes in physical and mental health, cognition and behavior. Current research provides growing evidence that epigenetic reprogramming may be a mechanism modulating these effects of early adversities. This work aimed to investigate the impact of early institutionalization-the immersion in an extreme socially depriving environment in humans-on the epigenome and adaptive behavior of young children up to 4 years of age. We conducted a cross-sectional study involving two comparison groups: 29 children raised in orphanages and 29 children raised in biological families. Genome-wide DNA methylation profiles of blood cells were obtained using the Illumina MethylationEPIC array; the level of child adaptive functioning was assessed using the Vineland Adaptive Behavior Scales-II. In comparison to children raised in families, children residing in orphanages had both statistically significant deficits in multiple adaptive behavior domains and statistically significant differences in DNA methylation states. Moreover, some of these methylation states may directly modulate the behavioral deficits; according to preliminary estimates, about 7-14% of the deviation of adaptive behavior between groups of children may be determined by their difference in DNA methylation profiles. The duration of institutionalization had a significant impact on both the adaptive level and DNA methylation status of institutionalized children.