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Allan L. Reiss

Researcher at Stanford University

Publications -  553
Citations -  64704

Allan L. Reiss is an academic researcher from Stanford University. The author has contributed to research in topics: Fragile X syndrome & Autism. The author has an hindex of 118, co-authored 529 publications receiving 59363 citations. Previous affiliations of Allan L. Reiss include Johns Hopkins University School of Medicine & University of California, San Diego.

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Virtual (Zoom) Interactions Alter Behavioral Cooperation, Neural Activation, and Dyadic Neural Coherence

TL;DR: Increased and sustained prefrontal activation in the virtual condition, potentially providing a neural basis of “Zoom® fatigue” and altered patterns of averaged and dynamic inter-brain coherence, in virtual interactions are found.
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Novel effects of Ras-MAPK pathogenic variants on the developing human brain and their link to gene expression and inhibition abilities

TL;DR: In this paper , structural brain MRI and cognitive-behavioral data were collected from 40 pre-pubertal children with Noonan syndrome (NS), caused by PTPN11 or SOS1 (n = 10) variants (age 8.53 ± 2.15, 25 females), and compared them to 40 age and sex-matched typically developing controls (9.24 ± 1.62, 27 females).
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Longitudinal investigation of cognition, social competence, and anxiety in children and adolescents with Turner syndrome

TL;DR: Turner syndrome (TS), a common neurogenetic disorder caused by complete or partial absence of an X chromosome in females, is characterized by distinct physical, cognitive, and social-emotional features as mentioned in this paper .
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Virtual (Zoom) Interactions Alter Conversational Behavior and Interbrain Coherence

TL;DR: In this article , the authors explored potential effects of virtual interactions on observed behavior, subjective experience, and neural "single-brain" and "interbrain" activity via functional near-infrared spectroscopy neuroimaging.
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Cortical gray matter structure in boys with Klinefelter syndrome.

TL;DR: In this paper, the brain structure in pre- or early-pubertal boys with Klinefelter syndrome was examined using surface-based analyses of cortical gray matter volume, thickness and surface area.