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Gene Ontology GO Terms. Gain spectra were calculated at critical wavelength degeneracy CWD in lri collinear phase-matching geometry optical parametric amplification OPA process. Alert me when this article is cited.
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Third, the within-ASD analyses showed that a autism symptom severity but not disruptive behavior was uniquely associated with less activation in the social perception regions including the posterior superior temporal sulcus and inferior frontal gyrus; b disruptive behavior but not autism symptom severity was uniquely associated with less DMN deactivation in the medial prefrontal cortex MPFC and lateral parietal cortex; and c anxiety symptoms mediated the link between disruptive behavior and less DMN deactivation in both anterior cingulate cortex ACC and MPFC, while ADHD symptoms mediated the link primarily in ACC.
Find all citations in this journal default. Journal of Neurodevelopmental Disorders [17 Jan9: Or filter your current search.
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Age and IQ were included as covariates of no interest in all analyses. Right click equation to reveal menu options.
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The current research aims to better understand the neural underpinnings of disruptive behavior in ASD, while addressing whether the neural basis is shared with or separable from that of core ASD symptoms. Equations on this page are rendered with MathJax. Abstract Gain spectra were calculated at critical wavelength degeneracy CWD in a collinear phase-matching geometry optical parametric amplification OPA 111689.
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April 30, Manuscript Accepted: March 29, Revised Manuscript: Equations 11869 Equations on this page are rendered with MathJax. In boys with ASD, disruptive behavior has a neural basis in reduced DMN deactivation, which is distinct and separable from that of core ASD symptoms, with the latter characterized by hypoactivation in the social perception circuitry.
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