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The leader-following formation problem is discussed for a team of quadrotors under directed switching topologies. To obtain a more general dynamic model, we describe the quadrotor system in a non-affine pure-feedback form with mismatched unknown nonlinearities. By employing an adaptive neural networks state observer to approximate the unknown nonlinear functions and to reconstruct the immeasurable inner states, we propose a novel distributed output feedback formation control protocol with the backstepping method combining with the dynamic surface control technique. From the Lyapunov stability theorem, all signals in the closed-loop formation system are proven to be cooperatively semiglobally uniformly ultimately bounded for any given bounded initial conditions. Finally, we proved that we verify the performance of the proposed formation control approach by a simulation study.
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http://dx.doi.org/10.1016/j.isatra.2019.02.030 | DOI Listing |
Alzheimers Res Ther
September 2025
Department of Neurology, Saarland University, Kirrberger Straße, 66421, Homburg/Saar, Germany.
Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.
View Article and Find Full Text PDFBMC Vet Res
September 2025
Veterinary Internal Medicine, Department of Animal Medicine, Faculty of Veterinary Medicine, Assiut University, Assiut, 71526, Egypt.
Background: Disturbances in lipid metabolism are usually associated with hyperlipidemia, which is commonly observed in donkeys with inappetence or anorexia. The diagnostic utility of ultrasound measurements of croup fat thickness (CFT) and relative liver echogenicity for lipomobilization in donkeys with fasting-induced hyperlipidemia was investigated. A prospective observational control study involving 25 donkeys was conducted, and the animals were randomly assigned to a fasting group (FG, n = 20) and a control group (CG, n = 5).
View Article and Find Full Text PDFJ Mol Neurosci
September 2025
Department of Physiology, School of Medicine, Dokuz Eylul University, Izmir, Turkey.
The ketogenic diet (KD), a high-fat, low-carbohydrate regimen, has been shown to exert neuroprotective effects in various neurological models. This study explored how KD-alone or combined with antibiotic-induced gut microbiota depletion-affects cognition and neuroinflammation in aging. Thirty-two male rats (22 months old) were assigned to four groups (n = 8): control diet (CD), ketogenic diet (KD), antibiotics with control diet (AB), and antibiotics with KD (KDAB).
View Article and Find Full Text PDFCommun Biol
September 2025
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.
Neuronal development and function are orchestrated by a plethora of regulatory mechanisms that control the abundance, localization, interactions, and function of proteins. A key role in this regard is assumed by post-translational protein modifications (PTMs). While some PTM types, such as phosphorylation or ubiquitination, have been explored comprehensively, PTMs involving ubiquitin-like modifiers (Ubls) have remained comparably enigmatic (Ubls).
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Neurosciences and Medicine, Brain & Behaviour (INM-7), Research Centre Juelich; Wilhelm-Johnen-Straße 1, Juelich, Germany.
Autism is a neurodevelopmental condition associated with altered resting-state brain function. An increased excitation-inhibition ratio is discussed as a pathomechanism but in-vivo evidence of disturbed neurotransmission underlying functional alterations remains scarce. We compare local resting-state brain activity and neurotransmitter co-localizations between autism (N = 405, N = 395) and neurotypical controls (N = 473, N = 474) in two independent cohorts and correlate them with excitation-inhibition changes induced by glutamatergic (ketamine) and GABAergic (midazolam) medication.
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