E
Edwin H. Cook
Researcher at University of Illinois at Chicago
Publications - 339
Citations - 61045
Edwin H. Cook is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Autism & Heritability of autism. The author has an hindex of 102, co-authored 337 publications receiving 54518 citations. Previous affiliations of Edwin H. Cook include University of Chicago & University of Illinois at Urbana–Champaign.
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Journal ArticleDOI
Self-injury in autism spectrum disorder: an effect of serotonin transporter gene promoter variants.
Alexander Kolevzon,Teresa Lim,James Schmeidler,Toni Martello,Edwin H. Cook,Jeremy M. Silverman +5 more
TL;DR: Self-injury in ASD may be associated with a specific genotype of the serotonin transporter gene promoter region, and future studies should continue to explore subgroups to clarify the underlying clinical and genetic heterogeneity in ASD.
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Tryptophan loading in hyperserotonemic and normoserotonemic adults
Edwin H. Cook,George M. Anderson,George R. Heninger,Kathlyn E. Fletcher,Daniel X. Freedman,Bennett L. Leventhal +5 more
TL;DR: The mechanism(s) for elevations of platelet 5-HT in autistic children and their family members has not been determined, but a possible mechanism is increased5-HT synthesis in the enterochromaffin cell of the intestine, leading to increased platelet exposure to 5-1-|T.
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Global gene expression as a function of germline genetic variation
Deborah L. French,Mark R. Wilkinson,Wenjian Yang,Luc de Chaisemartin,Edwin H. Cook,Soma Das,Mark J. Ratain,William E. Evans,James R. Downing,Ching-Hon Pui,Mary V. Relling +10 more
TL;DR: Although their expression is limited to specific tissues, both GSTM1 and UGT1A1 are involved in the conjugation of a broad range of endobiotics and xenobiotics, which could plausibly have consequences for gene expression in different tissues.
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Case series: Adderall augmentation of serotonin reuptake inhibitors in childhood-onset obsessive compulsive disorder.
TL;DR: Four patients with childhood-onset obsessive compulsive disorder, and with partial or no response to SSRI treatment, who subsequently had a reduction of their symptoms with Adderall augmentation are described.
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The impact of genotype calling errors on family-based studies
TL;DR: It is concluded that non-symmetric genotype calling errors need careful consideration in the analysis of family-based sequence data and practical guidance on ameliorating the test bias is provided.