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J. Raymond DePaulo

Researcher at Johns Hopkins University

Publications -  128
Citations -  12127

J. Raymond DePaulo is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Bipolar disorder & Genome-wide association study. The author has an hindex of 49, co-authored 122 publications receiving 10324 citations. Previous affiliations of J. Raymond DePaulo include Johns Hopkins University School of Medicine & LDS Hospital.

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Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression

Naomi R. Wray, +262 more
- 26 Apr 2018 - 
TL;DR: A genome-wide association meta-analysis of individuals with clinically assessed or self-reported depression identifies 44 independent and significant loci and finds important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia.
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Genome-wide association study identifies 30 loci associated with bipolar disorder

Eli A. Stahl, +342 more
- 01 May 2019 - 
TL;DR: Genome-wide analysis identifies 30 loci associated with bipolar disorder, allowing for comparisons of shared genes and pathways with other psychiatric disorders, including schizophrenia and depression.
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Depression following myocardial infarction.

TL;DR: Major depression is common in the acute post-myocardial infarction period and confer significant psychiatric morbidity and, if sustained, require psychiatric intervention.
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Genome scan meta-analysis of schizophrenia and bipolar disorder, part III: Bipolar disorder.

Ricardo Segurado, +79 more
TL;DR: The present results for the very narrow model are promising but suggest that more and larger data sets are needed to support linkage, as well as suggest that linkage might be detected in certain populations or subsets of pedigrees.
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Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes

Douglas M. Ruderfer, +631 more
- 14 Jun 2018 - 
TL;DR: For the first time, specific loci that distinguish between BD and SCZ are discovered and polygenic components underlying multiple symptom dimensions are identified that point to the utility of genetics to inform symptomology and potential treatment.