Examinando por Autor "Reyes, A."
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Ítem Computerised Dynamic Posturography in Premanifest and Manifest individuals with Huntington’s Disease(Nature Publishing Group, 2018-12) Reyes, A.; Salomonczyk, D.; Teo, W.-P.; Medina, L.D.; Bartlett, D.; Pirogovsky-Turk, E.; Zaenker, P.; Bloom, J.C.; Simmons, R.W.; Ziman, M.; Gilbert, P.E.; Cruickshank, T.Evidence from small-scale studies indicates that impairments in postural stability are an early and disabling feature of Huntington’s disease (HD) and may be a useful clinical endpoint for disease modifying trials. Larger studies are needed to confirm these preliminary findings and the suitability of postural stability outcomes as clinical endpoints. Static and dynamic postural stability were evaluated in 54 premanifest HD, 36 manifest HD and 45 healthy individuals using the Sensory Organization Test (SOT) and Limits of Stability (LOS) test. Manifest HD displayed significantly lower scores on all SOT conditions and on the SOT composite score and had more falls than healthy and premanifest HD (p < 0.05). Premanifest and manifest HD demonstrated significantly lower endpoint excursion (p < 0.001), maximum excursion (p ≤ 0.001), and directional control (p ≤ 0.004) values than healthy individuals on the LOS test. Deficits in LOS were found to manifest on the left side of premanifest HD. Significant but low associations were observed between UHDRS-TMS, disease burden score, diagnostic confidence level, SOT conditions and SOT composite score. We confirm here that individuals with premanifest and manifest HD display significant impairments in static and dynamic postural stability. Dynamic posturography assessments should be considered as clinical endpoints for future disease modifying trials. © 2018, The Author(s).Ítem Dual tasking impairments are associated with striatal pathology in Huntington’s disease(Wiley-Blackwell, 2020-09) Lo, J.; Reyes, A.; Pulverenti, T.S.; Rankin, T.J.; Bartlett, D.M.; Zaenker, P.; Rowe, G.; Feindel, K.; Poudel, G.; Georgiou-Karistianis, N.; Ziman, M.R.; Cruickshank, T.M.Background: Recent findings suggest that individuals with Huntington’s disease (HD) have an impaired capacity to execute cognitive and motor tasks simultaneously, or dual task, which gradually worsens as the disease advances. The onset and neuropathological changes mediating impairments in dual tasking in individuals with HD are unclear. The reliability of dual tasking assessments for individuals with HD is also unclear. Objectives: To evaluate differences in dual tasking performance between individuals with HD (presymptomatic and prodromal) and matched controls, to investigate associations between striatal volume and dual tasking performance, and to determine the reliability of dual tasking assessments. Methods: Twenty individuals with HD (10 presymptomatic and 10 prodromal) and 20 healthy controls were recruited for the study. Individuals undertook four single and dual task assessments, comprising motor (postural stability or force steadiness) and cognitive (simple or complex mental arithmetic) components, with single and dual tasks performed three times each. Participants also undertook a magnetic resonance imaging assessment. Results: Compared to healthy controls, individuals with presymptomatic and prodromal HD displayed significant deficits in dual tasking, particularly cognitive task performance when concurrently undertaking motor tasks (P < 0.05). The observed deficits in dual tasking were associated with reduced volume in caudate and putamen structures (P < 0.05),however, not with clinical measures of disease burden. An analysis of the reliability of dual tasking assessments revealed moderate to high test–retest reliability [ICC: 0.61-0.99] for individuals with presymptomatic and prodromal HD and healthy controls. Conclusions: Individuals with presymptomatic and prodromal HD have significant deficits in dual tasking that are associated with striatal degeneration. Findings also indicate that dual tasking assessments are reliable in individuals presymptomatic and prodromal HD and healthy controls. © 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological AssociationÍtem Knee sensorimotor control following anterior cruciate ligament reconstruction: A comparison between reconstruction techniques(Public Library of Science, 2018-11) San Martín-Mohr, C.; Cristi-Sánchez, I.; Pincheira, P.A.; Reyes, A.; Berral, F.J.; Oyarzo, C.The sensorimotor system helps to maintain functional joint stability during movement. After anterior cruciate ligament (ACL) injury and reconstruction, several sensorimotor deficits may arise, including altered proprioception and changes in neuromuscular control. It is still unknown whether the type of autograft used in the reconstruction may influence knee sensorimotor impairments. The aim of this study was to comparatively assess the effects of the hamstring tendon (HT) and bone-patellar tendon-bone (BPTB) ACL reconstruction techniques on knee sensorimotor control 6–12 months post-operation. A total of 83 male subjects participated in this study: 27 healthy participants, 30 BPTB-operated patients and 26 HT-operated patients. Active joint position sense in 3 ranges of motion (90–60, 60–30, and 30–0 of knee flexion), isometric steadiness, and onset of muscle activation were used to compare sensorimotor system function between groups. Both operated groups had a small (< 5) but significant joint position sense error in the 30–0 range when compared to the healthy group. No significant differences were found between the operated and the control groups for isometric steadiness or onset of muscle activation. The results of this study suggest that operated patients present knee proprioceptive deficits independently of surgical technique. Nevertheless, the clinical implications of this impairment are still unknown. It seems that selected surgical approach for ACL reconstruction do not affect functioning of the sensorimotor system to a large degree. © 2018 San Martín-Mohr et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Ítem Soybean Meal Induces Intestinal Inflammation in Zebrafish Larvae(Public Library of Science, 2013-07) Hedrera, M.; Galdames, J.; Jimenez-Reyes, M.; Reyes, A.; Avendaño-Herrera, R.; Romero, J.; Feijóo, C.The necessary replacement of fish meal with other protein source in diets of commercially important fish has prompted the study of the effect of the inclusion of different vegetable proteins sources on growth performance and on the gastro-intestinal tract. Currently, soybean meal is the primary protein source as a fish meal replacement because of its low price and high availability. Likewise, it is been documented that the ingestion of soybean meal by several fish species, such as salmonids and carp, triggers a type of intestinal inflammation called enteritis. In this paper, we analyzed the effects of the ingestion of soybean meal and two of its components, soy protein and soy saponin, on zebrafish to establish the basis for using zebrafish larvae as a model for fish nutrition. We took advantage of the existence of different transgenic lines, which allowed us to perform in vivo analysis. Our results indicated that larvae that were feed with soybean meal developed a clear intestinal inflammation as early as two day after beginning the diet. Moreover, we determined that is not the soy protein present in the diet but the soy saponin that is primarily responsible for triggering the immune response. These findings support the use of zebrafish screening assays to identify novel ingredients that would to improved current fish diets or would formulate new ones.Ítem The hypoxia factor Hif-1α controls neural crest chemotaxis and epithelial to mesenchymal transition(Rockefeller University Press, 2013-05) Barriga, E.; Maxwell, P.; Reyes, A.; Mayor, R.One of the most important mechanisms that promotes metastasis is the stabilization of Hif-1 (hypoxia-inducible transcription factor 1). We decided to test whether Hif-1α also was required for early embryonic development. We focused our attention on the development of the neural crest, a highly migratory embryonic cell population whose behavior has been likened to cancer metastasis. Inhibition of Hif-1α by antisense morpholinos in Xenopus laevis or zebrafish embryos led to complete inhibition of neural crest migration. We show that Hif-1α controls the expression of Twist, which in turn represses E-cadherin during epithelial to mesenchymal transition (EMT) of neural crest cells. Thus, Hif-1α allows cells to initiate migration by promoting the release of cell- cell adhesions. Additionally, Hif-1α controls chemotaxis toward the chemokine SDF-1 by regulating expression of its receptor Cxcr4. Our results point to Hif-1α as a novel and key regulator that integrates EMT and chemotaxis during migration of neural crest cells.