Publicaciones

Neurodata Tracker: Software for computational assessment of hand motor skills based on optical motion capture in a virtual environment

López D, Casado-Fernández L, Fernández F et al. Digit Health. 2023 May 11;9:20552076231174786. doi: 10.1177/20552076231174786. eCollection 2023 Jan-Dec. PMID: 37197411

https://pubmed.ncbi.nlm.nih.gov/37197411/

Abstract:

Objectives: Deficits affecting hand motor skills negatively impact the quality of life of patients. The NeuroData Tracker platform has been developed for the objective and precise evaluation of hand motor deficits. We describe the design and development of the platform and analyse the technological feasibility and usability in a relevant clinical setting.
Methods: A software application was developed in Unity (C#) to obtain kinematic data from hand movement tracking by a portable device with two cameras and three infrared sensors (leap motion®). Four exercises were implemented: (a) wrist flexion-extension (b) finger-grip opening-closing (c) finger spread (d) fist opening-closing. The most representative kinematic parameters were selected for each exercise. A script in Python was integrated in the platform to transform realtime kinematic data into relevant information for the clinician. The application was tested in a pilot study comparing the data provided by the tool from ten healthy subjects without any motor impairment and ten patients diagnosed with a stroke with mild to moderate hand motor deficit.
Results: The NeuroData Tracker allowed the parameterization of kinematics of hand movement and the issuance of a report with the results. The comparison of the data obtained suggests the feasibility of the tool for detecting differences between patients and healthy subjects.
Conclusions: This new platform based on optical motion capturing provides objective measurement of hand movement allowing quantification of motor deficits. These findings require further validation of the tool in larger trials to verify its usefulness in the clinical setting.

Funding: The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the Invictus Plus network under grant RD16/0019/0005 and the RICORS network under grant RD21/0006/0012, Spanish Ministry of Health-Carlos III Health Institute (ISCIII) and the Next Generation EU funds (Recovery and Resilience Plan).

Dihydropyrimidinase-Related Protein 2 Is a New Partner in the Binding between 4E-BP2 and eIF4E Related to Neuronal Death after Cerebral Ischemia

Martínez-Alonso E, Escobar-Peso A, Guerra-Pérez N et al. Int J Mol Sci. 2023 May 4;24(9):8246. doi: 10.3390/ijms24098246. PMID: 37175950

https://pubmed.ncbi.nlm.nih.gov/37175950/

Abstract: Transient cerebral ischemia induces neuronal degeneration, followed in time by secondary delayed neuronal death that is strongly correlated with a permanent inhibition of protein synthesis in vulnerable brain regions, while protein translational rates are recovered in resistant areas. In the translation-regulation initiation step, the eukaryotic initiation factor (eIF) 4E is a key player regulated by its association with eIF4E-binding proteins (4E-BPs), mostly 4E-BP2 in brain tissue. In a previous work, we identified dihydropyrimidinase-related protein 2 (DRP2) as a 4E-BP2-interacting protein. Here, using a proteomic approach in a model of transient cerebral ischemia, a detailed study of DRP2 was performed in order to address the challenge of translation restoration in vulnerable regions. In this report, several DRP2 isoforms that have a specific interaction with both 4E-BP2 and eIF4E were identified, showing significant and opposite differences in this association, and being differentially detected in resistant and vulnerable regions in response to ischemia reperfusion. Our results provide the first evidence of DRP2 isoforms as potential regulators of the 4E-BP2–eIF4E association that would have consequences in the delayed neuronal death under ischemic-reperfusion stress. The new knowledge reported here identifies DRP2 as a new target to promote neuronal survival after cerebral ischemia. 

Funding: This study has been funded by Instituto de Salud Carlos III and cofunded by European Regional Development Fund (ERDF, “A way to make Europe”) through the projects PI18/00255, PI22/01381 and RICORS RD21/0006/0019 to J.M. and A.A.