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Humans learn motor skills (MSs) through practice and experience and may then retain them for recruitment, which is effective as a rapid response for novel contexts. For an MS to be recruited for novel contexts, its recruitment range must be extended. In addressing this issue, we hypothesized that an MS is dynamically modulated according to the feedback context to expand its recruitment range into novel contexts, which do not involve the learning of an MS. The following two sub-issues are considered. We previously demonstrated that the learned MS could be recruited in novel contexts through its modulation, which is driven by dynamically regulating the synergistic redundancy between muscles according to the feedback context. However, this modulation is trained in the dynamics under the MS learning context. Learning an MS in a specific condition naturally causes movement deviation from the desired state when the MS is executed in a novel context. We hypothesized that this deviation can be reduced with the additional modulation of an MS, which tunes the MS-produced muscle activities by using the feedback gain signals driven by the deviation from the desired state. Based on this hypothesis, we propose a feedback gain signal-driven tuning model of a learned MS for its robust recruitment. This model is based on the neurophysiological architecture in the cortico-basal ganglia circuit, in which an MS is plausibly retained as it was learned and is then recruited by tuning its muscle control signals according to the feedback context. In this study, through computational simulation, we show that the proposed model may be used to neurophysiologically describe the recruitment of a learned MS in novel contexts.
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http://dx.doi.org/10.3389/fncom.2020.457682 | DOI Listing |
Protein Sci
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Departament de Química, Universitat Autònoma de Barcelona, Barcelona, Spain.
Cyclooxygenase-2 (COX-2) plays a crucial role in inflammation and has been implicated in cancer development. Understanding the behavior of COX-2 in different cellular contexts is essential for developing targeted therapeutic strategies. In this study, we investigate the fluorescence spectrum of a fluorogenic probe, NANQ-IMC6, when bound to the active site of human COX-2 in both its monomeric and homodimeric forms.
View Article and Find Full Text PDFJACC Adv
January 2025
Division of Cardiology, Department of Medicine, Warren Alpert Medical School of Brown University, and Lifespan Cardiovascular Institute, Providence, Rhode Island, USA.
This state-of-the-art review describes the potential etiologies, pathophysiology, and management of mixed shock in the context of a proposed novel classification system. Cardiogenic-vasodilatory shock occurs when cardiogenic shock is complicated by inappropriate vasodilation, impairing compensatory mechanisms, and contributing to worsening shock. Vasodilatory-cardiogenic shock occurs when vasodilatory shock is complicated by myocardial dysfunction, resulting in low cardiac output.
View Article and Find Full Text PDFJ Pathol Inform
January 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, United States of America.
With the increasing utilization of exome and genome sequencing in clinical and research genetics, accurate and automated extraction of human phenotype ontology (HPO) terms from clinical texts has become imperative. Traditional methods for HPO term extraction, such as PhenoTagger, often face limitations in coverage and precision. In this study, we propose a novel approach that leverages large language models (LLMs) to generate synthetic sentences with clinical context, which were semantically encoded into vector embeddings.
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December 2024
Department of Physics, University of Alberta, Edmonton, AB, Canada.
A steadily increasing number of publications support the concept of physiological networks, and how cellular bioelectrical properties drive cell proliferation and cell synchronization. All cells, especially cancer cells, are known to possess characteristic electrical properties critical for physiological behavior, with major differences between normal and cancer cell counterparts. This opportunity can be explored as a novel treatment modality in Oncology.
View Article and Find Full Text PDFFront Genet
December 2024
Department of Molecular and Medical Genetics, Tbilisi State Medical University, Tbilisi, Georgia.
Spinal muscular atrophy (SMA) is a progressive neuromuscular disorder caused by mutations in , with disease severity influenced by the number of copies. Although SMA is one of the most common autosomal recessive disorders, molecular diagnosis still presents challenges. We present a case series illustrating the variable clinical presentations and diagnostic complexities of spinal muscular atrophy (SMA).
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