This paper studies the distributed time-varying output formation tracking problem for heterogeneous multi-agent systems with both diverse dimensions and parameters. The output of each follower is supposed to track that of the virtual leader while accomplishing a time-varying formation configuration. First, a distributed trajectory generator is proposed based on neighboring interactions to reconstitute the state of virtual leader and provide expected trajectories with the formation incorporated. Second, an optimal tracking controller is designed by the model-free reinforcement learning technique using online off-policy data instead of requiring any knowledge of the followers' dynamics. Stabilities of the learning process and resulting controller are analyzed while solutions to the output regulator equations are equivalently obtained. Third, a compensational input is designed for each follower based on previous learning results and a derived feasibility condition. It is proved that the output formation tracking error converges to zero asymptotically with the biases to cost functions being restricted arbitrarily small. Finally, numerical simulations verify the proposed learning and control scheme.
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http://dx.doi.org/10.1016/j.isatra.2023.03.003 | DOI Listing |
Alzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: How tauopathy disrupts direct entorhinal cortex (EC) inputs to CA1 and their plasticity is understudied, despite its critical role in memory. Moreover, dysfunction of lateral EC (LEC) input is less clear, despite its relevance to early Alzheimer's disease pathogenesis. Here we examined how tau impacts long-term potentiation (LTP) of LEC→CA1 input in a transgenic model of tauopathy.
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December 2024
University of Pennsylvania, Philadelphia, PA, USA.
Background: Alzheimer's disease (AD) is the most common neurodegenerative disease, and it is characterized by aggregation of misfolded proteins in the brain. Intraneuronal accumulation of tau pathology form neurofibrillary tangles (NFT) in AD. The assessment of the severity of intraneuronal inclusions holds significance in studying the clinicopathological associations in neurodegenerative diseases.
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December 2024
Laboratory of Neuro Imaging, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Mutations in the presenilin 1 (PSEN1) gene cause early onset autosomal dominant Alzheimer's Disease (AD), and the Jalisco mutation (A431E) is a subset found in people of Mexican descent (Yescas P, 2006). The Jalisco A431E mutation has been shown to produce distinct AD neuropathology such as cotton-wool amyloid plaques as well as motor dysfunction like spastic paraparesis (Orozco-Barajas, 2022). High levels of tau neuropathology have been observed with other PSEN1 mutations, but tau neuropathology in Jalisco patients has not been examined.
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January 2025
Department of Surgery, Trinity St. James's Cancer Institute, Trinity Translational Medicine Institute, Trinity College Dublin, St. James's Hospital, Dublin 8, Ireland.
Integration of multi-omic data for the purposes of biomarker discovery can provide novel and robust panels across multiple biological compartments. Appropriate analytical methods are key to ensuring accurate and meaningful outputs in the multi-omic setting. Here, we extensively profile the proteome and transcriptome of patient pancreatic cyst fluid (PCF) (n = 32) and serum (n = 68), before integrating matched omic and biofluid data, to identify biomarkers of pancreatic cancer risk.
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January 2025
Jiangsu Key Laboratory of Brain Disease and Bioinformation, Research Center for Biochemistry and Molecular Biology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Norepinephrine (NE) released from locus coeruleus (LC) noradrenergic (NAergic) neurons plays a pivotal role in the regulation of olfactory behaviors. However, the precise circuits and receptor mechanisms underlying this function are not well understood. Here, in DBH-Cre mice model, we show that LC NAergic neurons project directly to both anterior piriform cortex (aPC) and the olfactory bulb (OB).
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