All Publications

  • Exploring the Impact of Partial Occlusion on Emotion Classification From Facial Expressions: A Comparative Study of XR Headsets and Face Masks IEEE Access Casas-Ortiz, A., Echeverria, J., Jimenez-Tellez, N., Santos, O. C. 2024; 12: 44613 - 44627
  • Exploring the Impact of Partial Occlusion on Emotion Classification From Facial Expressions: A Comparative Study of XR Headsets and Face Masks IEEE Access Casas-Ortiz, A., Echeverria, J., Jimenez-Tellez, N., Santos, O. C. 2024; 12: 44613 - 44627
  • Sevoflurane Exposure in Neonates Perturbs the Expression Patterns of Specific Genes That May Underly the Observed Learning and Memory Deficits. International journal of molecular sciences Jimenez-Tellez, N., Pehar, M., Visser, F., Casas-Ortiz, A., Rice, T., Syed, N. I. 2023; 24 (10)


    Exposure to commonly used anesthetics leads to neurotoxic effects in animal models-ranging from cell death to learning and memory deficits. These neurotoxic effects invoke a variety of molecular pathways, exerting either immediate or long-term effects at the cellular and behavioural levels. However, little is known about the gene expression changes following early neonatal exposure to these anesthetic agents. We report here on the effects of sevoflurane, a commonly used inhalational anesthetic, on learning and memory and identify a key set of genes that may likely be involved in the observed behavioural deficits. Specifically, we demonstrate that sevoflurane exposure in postnatal day 7 (P7) rat pups results in subtle, but distinct, memory deficits in the adult animals that have not been reported previously. Interestingly, when given intraperitoneally, pre-treatment with dexmedetomidine (DEX) could only prevent sevoflurane-induced anxiety in open field testing. To identify genes that may have been altered in the neonatal rats after sevoflurane and DEX exposure, specifically those impacting cellular viability, learning, and memory, we conducted an extensive Nanostring study examining over 770 genes. We found differential changes in the gene expression levels after exposure to both agents. A number of the perturbed genes found in this study have previously been implicated in synaptic transmission, plasticity, neurogenesis, apoptosis, myelination, and learning and memory. Our data thus demonstrate that subtle, albeit long-term, changes observed in an adult animal's learning and memory after neonatal anesthetic exposure may likely involve perturbation of specific gene expression patterns.

    View details for DOI 10.3390/ijms24108696

    View details for PubMedID 37240038

  • Dexmedetomidine Pre-Treatment of Neonatal Rats Prevents Sevoflurane-Induced Deficits in Learning and Memory in the Adult Animals. Biomedicines Jimenez-Tellez, N., Pehar, M., Iqbal, F., Casas-Ortiz, A., Rice, T., Syed, N. I. 2023; 11 (2)


    Anesthetics have been shown to cause cytotoxicity, cell death, affect neuronal growth and connectivity in animal models; however, their effects on learning and memory remain to be fully defined. Here, we examined the effects of the inhalation anesthetic sevoflurane (SEV)-both in vivo by examining learning and memory in freely behaving animals, and in vitro using cultured neurons to assess its impact on viability, mitochondrial structure, and function. We demonstrate here that neonatal exposure to sub-clinically used concentrations of SEV results in significant, albeit subtle and previously unreported, learning and memory deficits in adult animals. These deficits involve neuronal cell death, as observed in cell culture, and are likely mediated through perturbed mitochondrial structure and function. Parenthetically, both behavioural deficits and cell death were prevented when the animals and cultured neurons were pre-treated with the anesthetic adjuvant Dexmedetomidine (DEX). Taken together, our data provide direct evidence for sevoflurane-induced cytotoxic effects at the neuronal level while perturbing learning and memory at the behavioural level. In addition, our data underscore the importance of adjuvant agents such as DEX that could potentially counter the harmful effects of commonly used anesthetic agents for better clinical outcomes.

    View details for DOI 10.3390/biomedicines11020391

    View details for PubMedID 36830927

  • Intelligent systems for psychomotor learning: a systematic review and two cases of study Handbook of Artificial Intelligence in Education Casas Ortiz, A., Echeverria, ., Santos, O. C. Edward Elgar Publishing. 2023; 1: 390–421
  • Designing, Building and Evaluating Intelligent Psychomotor AIED Systems International Conference on Artificial Intelligence in Education Santos, O. C., Portaz, M., Casas-Ortiz, A., Echeverria, ., Perez-Villegas , L. F. 2023: 91–96
  • Dexmedetomidine does not compromise neuronal viability, synaptic connectivity, learning and memory in a rodent model SCIENTIFIC REPORTS Jimenez-Tellez, N., Iqbal, F., Pehar, M., Casas-Ortiz, A., Rice, T., Syed, N. 2021; 11 (1): 16153


    Recent animal studies have drawn concerns regarding most commonly used anesthetics and their long-term cytotoxic effects, specifically on the nervous tissue. It is therefore imperative that the search continues for agents that are non-toxic at both the cellular and behavioural level. One such agent appears to be dexmedetomidine (DEX) which has not only been found to be less neurotoxic but has also been shown to protect neurons from cytotoxicity induced by other anesthetic agents. However, DEX's effects on the growth and synaptic connectivity at the individual neuronal level, and the underlying mechanisms have not yet been fully resolved. Here, we tested DEX for its impact on neuronal growth, synapse formation (in vitro) and learning and memory in a rodent model. Rat cortical neurons were exposed to a range of clinically relevant DEX concentrations (0.05-10 µM) and cellular viability, neurite outgrowth, synaptic assembly and mitochondrial morphology were assessed. We discovered that DEX did not affect neuronal viability when used below 10 µM, whereas significant cell death was noted at higher concentrations. Interestingly, in the presence of DEX, neurons exhibited more neurite branching, albeit with no differences in corresponding synaptic puncta formation. When rat pups were injected subcutaneously with DEX 25 µg/kg on postnatal day 7 and again on postnatal day 8, we discovered that this agent did not affect hippocampal-dependent memory in freely behaving animals. Our data demonstrates, for the first time, the non-neurotoxic nature of DEX both in vitro and in vivo in an animal model providing support for its utility as a safer anesthetic agent. Moreover, this study provides the first direct evidence that although DEX is growth permissive, causes mitochondrial fusion and reduces oxygen reactive species production, it does not affect the total number of synaptic connections between the cortical neurons in vitro.

    View details for DOI 10.1038/s41598-021-95635-x

    View details for Web of Science ID 000683506200054

    View details for PubMedID 34373548

    View details for PubMedCentralID PMC8352930

  • KSAS: A Mobile App with Neural Networks to Guide the Learning of Motor Skills Conferencia de la Asociación Española para la Inteligencia Artificial Casas Ortiz, A., Santos, O. C. Asociación Española para la Inteligencia Artificial. 2021: 997-1000