Efectos de la FES en la neurorehabilitacion de la medula espinal danada

88 p.Revertir el daño neurológico provocado en la médula espinal dañada sigue siendo un objetivo difícil de alcanzar. Contrario a esto, los avances en neurorehabilitación han traducido una mejora de las funciones alteradas en las personas con lesión de la médula espinal (Ragnarsson, 2008).A falta de una cura, el uso creativo de la tecnología, junto a los logros en microelectrónica y neurociencia, han permitido la creación de la estimulación eléctrica funcional (FES del ingles functional electrical stimulation), una corriente terapéutica capaz de permitir recuperar movimientos funcionales alterados o perdidos (Popovic et al., 2004). Los mecanismos, progresos y condición actual de este método terapéutico se presentan a continuación, mediante una revisión de las investigaciones científicas actuales que emplean la FES como medio para la recuperación funcional de los pacientes con lesión medular. Se revisaron bases de datos reconocidas mediante una metodología detallada, y posterior análisis de la literatura revisada, a fin de fundamentar los efectos que posee esta técnica orientada principalmente a pacientes tetrapléjicos y parapléjicos. Se discute finalmente los hallazgos encontrados, señalando entre otros que es una técnica que no ha sido ampliamente investigada por gran variedad de estudios clínicos que aporten una elevada evidencia a ésta como método de neurorehabilitación para pacientes con lesión medular

Anomalous reactivity of supported V2O5 nanoparticles for propane oxidative dehydrogenation: influence of the vanadium oxide precursor

Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG geförderten) Allianz- bzw. Nationallizenz frei zugänglich.This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.The oxidative dehydrogenation (ODH) of propane to propylene by supported vanadia catalysts has received much attention in recent years, but different reactivity trends have been reported for this catalytic reaction system. In the present investigation, the origin of these differing trends are investigated with synthesis of supported V/SiO2, V/TiO2, and V/Al2O3 catalysts prepared with three different vanadium oxide precursors (2-propanol/vanadyl triisopropoxide [VO(O-Pri)3] (VTI), oxalic acid/ammonium metavanadate [NH4VO3] (AMV), and toluene/vanadyl acetylacetonate [VO(C5H7O2)2] (VAA)) in order to elucidate the influence of the precursor on supported vanadia phase and propane ODH activity. In situ Raman spectroscopy revealed that the choice of vanadium precursor does not affect the dispersion of the supported vanadium oxide phase below 4 V nm−2 (0.5 monolayer coverage), where only isolated and oligomeric surface VO4 species are present, and only the AMV precursor favors crystalline V2O5 nanoparticle (NP) formation below monolayer coverage (8 V nm−2). The propane ODH specific reactivity trend demonstrated that there is no significant difference in TOF for the isolated and oligomeric surface VO4 sites. Surprisingly, V2O5 NPs in the ∼1–2 nm range exhibit anomalously high propane ODH TOF values for the supported vanadia catalysts. This was found for all supported vanadium oxide catalysts examined. This comparative study with different V-precursors and synthesis methods and oxide supports finally resolves the debate in the catalysis literature about the dependence of TOF on the surface vanadium density that is related to the unusually high reactivity of small V2O5 NPs.DFG, SFB 546, Struktur, Dynamik und Reaktivität von Übergangsmetalloxid-Aggregate

Tracking the cognitive, social, and neuroanatomical profile in early neurodegeneration: Type III Cockayne syndrome

Cockayne syndrome (CS) is an autosomal recessive disease associated with premature aging, progressive multiorgan degeneration, and nervous system abnormalities including cerebral and cerebellar atrophy, brain calcifications, and white matter abnormalities. Although several clinical descriptions of CS patients have reported developmental delay and cognitive impairment with relative preservation of social skills, no previous studies have carried out a comprehensive neuropsychological and social cognition assessment. Furthermore, no previous research in individuals with CS has examined the relationship between brain atrophy and performance on neuropsychological and social cognition tests. This study describes the case of an atypical late-onset type III CS patient who exceeds the mean life expectancy of individuals with this pathology. The patient and a group of healthy controls underwent a comprehensive assessment that included multiple neuropsychological and social cognition (emotion recognition, theory of mind, and empathy) tasks. In addition, we compared the pattern of atrophy in the patient to controls and to its concordance with ERCC8 gene expression in a healthy brain. The results showed memory, language, and executive deficits that contrast with the relative preservation of social cognition skills. The cognitive profile of the patient was consistent with his pattern of global cerebral and cerebellar loss of gray matter volume (frontal structures, bilateral cerebellum, basal ganglia, temporal lobe, and occipito-temporal/occipito-parietal regions), which in turn was anatomically consistent with the ERCC8 gene expression level in a healthy donor's brain. The study of exceptional cases, such as the one described here, is fundamental to elucidating the processes that affect the brain in premature aging diseases, and such studies provide an important source of information for understanding the problems associated with normal and pathological aging.Fil: Báez Buitrago, Sandra Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Diego Portales; Chile. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires"; Argentina. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Couto, Juan Blas Marcos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Herrera, Eduar. Universidad Autónoma del Caribe; ColombiaFil: Bocanegra, Yamile. Universidad de Antioquia; Colombia. Universidad de San Buenaventura; ColombiaFil: Trujillo Orrego, Natalia. Universidad de Antioquia; ColombiaFil: Madriga Zapata, Lucia. Universidad de Antioquia; ColombiaFil: Cardona Londoño, Juan Felipe. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Manes, Facundo Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Australian Government, Australian Research Council; Australia. Universidad Diego Portales; Chile. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Ibáñez Barassi, Agustín Mariano. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Diego Portales; Chile. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Villegas, Andres. Universidad de Antioquia; Colombi