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Daniel S. Peterson

Researcher at Arizona State University

Publications -  82
Citations -  78804

Daniel S. Peterson is an academic researcher from Arizona State University. The author has contributed to research in topics: Medicine & Balance (ability). The author has an hindex of 22, co-authored 67 publications receiving 72201 citations. Previous affiliations of Daniel S. Peterson include Pennsylvania State University & University of Utah.

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MEGA5: Molecular Evolutionary Genetics Analysis using Maximum Likelihood, Evolutionary Distance, and Maximum Parsimony Methods

TL;DR: The newest addition in MEGA5 is a collection of maximum likelihood (ML) analyses for inferring evolutionary trees, selecting best-fit substitution models, inferring ancestral states and sequences, and estimating evolutionary rates site-by-site.
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MEGA6: Molecular Evolutionary Genetics Analysis Version 6.0

TL;DR: An advanced version of the Molecular Evolutionary Genetics Analysis software, which currently contains facilities for building sequence alignments, inferring phylogenetic histories, and conducting molecular evolutionary analysis, is released, which enables the inference of timetrees, as it implements the RelTime method for estimating divergence times for all branching points in a phylogeny.
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Effects of age and walking speed on coactivation and cost of walking in healthy adults.

TL;DR: Higher C(w) and coactivation in older adults, along with the positive relationship between C(W) andCoactivation implies coactivation contributes to, higher C( w) of older adults.
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Neural Control of Walking in People with Parkinsonism.

TL;DR: A widespread supraspinal locomotor network including the cortex, cerebellum, basal ganglia, and brain stem contributes to the control of human locomotion, and altered activity of these structures underlies gait dysfunction due to Parkinson's disease.
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Gait-Related Brain Activity in People with Parkinson Disease with Freezing of Gait

TL;DR: Results suggest FoG+ exhibit dysfunction in a number of cortical and subcortical regions, possibly with asymmetric dysfunction towards the right hemisphere, as well as trends toward lower beta weights in other right-hemisphere locomotor regions