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Young-Ah Rho

Researcher at University of Pittsburgh

Publications -  8
Citations -  884

Young-Ah Rho is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Resting state fMRI & Default mode network. The author has an hindex of 7, co-authored 7 publications receiving 727 citations. Previous affiliations of Young-Ah Rho include KAIST & Center for Complex Systems and Brain Sciences.

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Journal ArticleDOI

Noise during Rest Enables the Exploration of the Brain's Dynamic Repertoire

TL;DR: It is shown that comparable resting state networks emerge from a stability analysis of the network dynamics using biologically realistic primate brain connectivity, although anatomical information alone does not identify the network.
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Cortical network dynamics with time delays reveals functional connectivity in the resting brain.

TL;DR: By tuning the propagation velocity in a network based on primate connectivity, a hypothesis that time delays in the network dynamics play a crucial role in the generation of temporally coherent fluctuations is tested.
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25th Annual Computational Neuroscience Meeting: CNS-2016

Tatyana O. Sharpee, +738 more
- 18 Aug 2016 - 
Journal ArticleDOI

Subthreshold membrane currents confer distinct tuning properties that enable neurons to encode the integral or derivative of their input

TL;DR: Integration and differentiation are shown to be implemented by the slow feedback mediated by oppositely directed subthreshold currents expressed in different neurons, which predicts that sensitivity to the rate of change of stimulus intensity differs qualitatively between integrators and differentiators.
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Identification of molecular pathologies sufficient to cause neuropathic excitability in primary somatosensory afferents using dynamical systems theory.

TL;DR: It is demonstrated that multiple distinct molecular changes are sufficient to produce neuropathic changes in excitability; however, given that nerve injury elicits numerous molecular changes that may be individually sufficient to alter spike initiation, the results argue that no single molecular change is necessary to produce Neuropathic excitability.