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Michael D. Edge

Researcher at University of California, Davis

Publications -  37
Citations -  1477

Michael D. Edge is an academic researcher from University of California, Davis. The author has contributed to research in topics: Population & Medicine. The author has an hindex of 18, co-authored 32 publications receiving 1254 citations. Previous affiliations of Michael D. Edge include Stanford University & University of Southern California.

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The relationship between F(ST) and the frequency of the most frequent allele

TL;DR: The relationship between FST and the frequency of the most frequent allele is examined, demonstrating that the range of values that FST can take is restricted considerably by the allele-frequency distribution and providing a conceptual basis for understanding the dependence of FST on allele frequencies and genetic diversity.
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Emotional reactivity and cognitive regulation in anxious children.

TL;DR: Children with anxiety disorders experienced greater negative emotional responses to the images, were less successful at applying reappraisals, but showed intact ability to reduce their negative emotions following reappraisal.
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The Behavioral Activation System and Mania

TL;DR: A burgeoning empirical literature on this model of bipolar disorder relates to an increased willingness to expend effort toward reward and to increases in energy and goal pursuit after an initial reward is reviewed.
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Experiential, autonomic, and neural responses during threat anticipation vary as a function of threat intensity and neuroticism.

TL;DR: The biobehavioral impact of varying levels of anticipatory anxiety is examined using a shock anticipation task in which unpredictable electric shocks were threatened and delivered to the wrist at variable intervals and intensities, to suggest that individual differences in neuroticism may influence sensitivity to anticipatory threat.
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Interpreting polygenic scores, polygenic adaptation, and human phenotypic differences

TL;DR: It is shown how genetic contributions to traits, as estimated by polygenic scores, combine with environmental contributions so that differences among populations in trait distributions need not reflect corresponding differences in genetic propensity.