Biology subjects

Thomas, J. B.

Publications and source records attributed to Thomas, J. B..

3 recordsLinked to original sources

bioRxiv2024

Development of a real-time neural controller using an EMG-driven musculoskeletal model

Here we present our development of a novel real-time neural controller based on an EMG-driven musculoskeletal model, designed for volitional control of robots and computers. Our controller uniquely enables motion control during both isometric and non-isometric muscle contractions. We address several key challenges in EMG control system design, including accuracy, latency, and robustness. Our approach combines EMG signal processing, neural activation dynamics, and Hill-type muscle modeling to translate neural commands into muscle forces, which can enhance robustness against electrode variability and signal noise. Additionally, we integrate muscle activation dynamics with impedance control, inspired by the human motor control system, for smooth and adaptive interactions. As an initial proof of concept, we demonstrated that our system could control a robot actuator across a range of movements, both static and dynamic, and at different operating speeds, achieving high reference tracking performance and state-of-the-art processing times of 2.9 ms, important for real-time embedded computing. This research helps lay the groundwork for next-generation neural-machine interfaces that are fast, accurate, and adaptable to diverse users and control applications.

neuroscience↗

bioRxiv2023

The nutrient sensor CRTC & Sarcalumenin / Thinman represent a new pathway in cardiac hypertrophy

Obesity and type 2 diabetes are at epidemic levels and a significant proportion of these patients are diagnosed with left ventricular hypertrophy. CREB Regulated Transcription Co-activator (CRTC) is a key regulator of metabolism in mammalian hepatocytes, where it is activated by calcineurin (CaN) to increase expression of gluconeogenic genes. CaN is known its role in pathological cardiac hypertrophy, however, a role for CRTC in the heart has not been identified. In Drosophila, CRTC null mutants have little body fat and exhibit severe cardiac restriction, myofibrillar disorganization, cardiac fibrosis and tachycardia, all hallmarks of heart disease. Cardiac-specific knockdown of CRTC, or its coactivator CREBb, mimicked the reduced body fat and heart defects of CRTC null mutants. Comparative gene expression in CRTC loss- or gain-of-function fly hearts revealed contra-regulation of genes involved in glucose, fatty acid, and amino acid metabolism, suggesting that CRTC also acts as a metabolic switch in the heart. Among the contra-regulated genes with conserved CREB binding sites, we identified the fly ortholog of Sarcalumenin, which is a Ca2+-binding protein in the sarcoplasmic reticulum. Cardiac knockdown recapitulated the loss of CRTC cardiac restriction and fibrotic phenotypes, suggesting it is a downstream effector of CRTC we named thinman (tmn). Importantly, cardiac overexpression of either CaN or CRTC in flies caused hypertrophy that was reversed in a CRTC mutant background, suggesting CRTC mediates hypertrophy downstream of CaN, perhaps as an alternative to NFAT. CRTC novel role in the heart is likely conserved in vertebrates as knockdown in zebrafish also caused cardiac restriction, as in fl ies. These data suggest that CRTC is involved in myocardial cell maintenance and that CaN-CRTC- Sarcalumenin/tmn signaling represents a novel and conserved pathway underlying cardiac hypertrophy.

cell biology↗

bioRxiv2018

A GABAergic Maf-expressing interneuron subset regulates the speed of locomotion in Drosophila

Interneurons (INs) coordinate motoneurons activity to generate adequate patterns of muscle contractions, providing animals with the ability to adjust their body posture and to move over a range of speeds. In the Drosophila larvae several IN subtypes have been morphologically described and their function well documented. However, the general lack of molecular characterization of those INs prevents the identification of evolutionary counterparts in other model animals, limiting our understanding of widespread principles ruling neuronal circuits organization and functioning. Here we characterize a highly restricted neuronal subset expressing the Maf transcription factor Traffic Jam (TJ). We found that TJ+ neurons are highly diverse and their activation using intersectional genetics disrupted larval body posture and locomotion speed. We also showed that a small subset of TJ+ GABAergic INs, singled out by the unique expression of Per, Fkh, Grain and Hlh3b, a molecular signature reminiscent to V2b INs in vertebrate, impacted the larvae crawling speed.

neuroscience↗