Distance Education in the Professionalization of People with Disability and Prison Inmates

Recibido 21 de junio de 2012 •  Corregido 09 de octubre de 2012 • Aceptado 07 de noviembre de 2012El presente trabajo ilustra, mediante dos ejemplos, el impacto que ha tenido la Universidad Estatal a Distancia (UNED), en la atención y profesionalización de sectores marginales de la sociedad costarricense, tales como los privados de libertad, personas con discapacidad física, individuos de zonas muy alejadas del centro capitalino, entre otros. Se trata de dar respuesta a las preguntas: ¿Cómo ha sido la atención  en esos sectores? ¿Cuáles son los retos que enfrentan las universidades a distancia para ser pertinentes? ¿De qué manera ha logrado alcanzarlos?  ¿Qué impacto sobre la sociedad costarricense ejerce la UNED en la profesionalización de su población?   Para el abordaje de la temática se recurre a documentación y estadísticas existentes, y se ejemplifica mediante el testimonio de dos estudiantes egresados de la UNED, elegidos con el propósito de ilustrar algunos de los diferentes casos que atiende dicha  Universidad.This paper illustrates the impact of the Universidad Estatal a Distancia  (UNED, by its Spanish acronym) in supporting and professionalizing the vulnerable groups of the Costa Rican society, including prison inmates, persons with physical disability, individuals from remote areas, among others.  This study attempts to answer this type of questions: What kind of support has been provided to these sectors?  What are the challenges faced by distance education universities to succeed?  How does UNED have solved these challenges?  What is the impact of the Universidad Estatal a Distancia on the Costa Rican society for the professionalization of its population?  Documentation and statistics have been used in the study; in addition, two people who graduated from UNED were selected to illustrate the type of cases the University serves. (1) Translator’s note: It refers to the “Costa Rican Distance Education State University”

Deficiency of Complement Component C1Q Prevents Cerebrovascular Damage and White Matter Loss in a Mouse Model of Chronic Obesity.

Age-related cognitive decline and many dementias involve complex interactions of both genetic and environmental risk factors. Recent evidence has demonstrated a strong association of obesity with the development of dementia. Furthermore, white matter damage is found in obese subjects and mouse models of obesity. Here, we found that components of the complement cascade, including complement component 1qa (C1QA) and C3 are increased in the brain of Western diet (WD)-fed obese mice, particularly in white matter regions. To functionally test the role of the complement cascade in obesity-induced brain pathology, female and male mice deficient in C1QA, an essential molecule in the activation of the classical pathway of the complement cascade, were fed a WD and compared with WD-fed wild type (WT) mice, and t

Continuum percolation of simple fluids: Energetic connectivity criteria

During the last few years, a number of works in computer simulation have focused on the clustering and percolation properties of simple fluids based in an energetic connectivity criterion proposed long ago by T.L. Hill [J. Chem. Phys. 23, 617 (1955)]. This connectivity criterion appears to be the most appropriate in the study of gas-liquid phase transition. So far, integral equation theories have relayed on a velocity-averaged version of this criterion. We show, by using molecular dynamics simulations, that this average strongly overestimates percolation densities in the Lennard-Jones fluid making unreliable any prediction based on it. Additionally, we use a recently developed integral equation theory [Phys. Rev. E 61, R6067 (2000)] to show how this velocity-average can be overcome.Comment: 14 pages, 2 figure

Historia de la Medicina Local y la formación cultural de los estudiantes de Ciencias Médicas

The need to enhance the cultural training of the students throughout the History of Local Medicine (HLM) made possible the bibliographic search, document analysis and the review of doctoral thesis. The objective of this paper is to set the foundations of the need to apply the knowledge of HLM to contribute to the cultural training of medical students in Ciego de Ávila.La necesidad de potenciar la formación cultural de los estudiantes a través de la Historia de la Medicina Local (HML) propició la revisión bibliográfica, así como el análisis de documentos y consulta de tesis doctorales. El objetivo de este artículo es reflexionar acerca de la HML como una vía para contribuir a la formación cultural de los estudiantes de las ciencias médicas en Ciego de Ávila. &nbsp

Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer\u27s disease

Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer\u27s disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APBTg) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APBTg mice that carry only one copy of Meox2 (B6.APBTg.Mx−/+) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APBTgmice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD

Meox2 haploinsufficiency increases neuronal cell loss in a mouse model of Alzheimer\u27s disease

Evidence suggests that multiple genetic and environmental factors conspire together to increase susceptibility to Alzheimer\u27s disease (AD). The amyloid cascade hypothesis states that deposition of the amyloid-β (Aβ) peptide is central to AD; however, evidence in humans and animals suggests that Aβ buildup alone is not sufficient to cause neuronal cell loss and cognitive decline. Mouse models that express high levels of mutant forms of amyloid precursor protein and/or cleaving enzymes deposit amyloid but do not show neuron loss. Therefore, a double-hit hypothesis for AD has been proposed whereby vascular dysfunction precedes and promotes Aβ toxicity. In support of this, copy number variations in mesenchyme homeobox 2 (MEOX2), a gene involved in vascular development, are associated with severe forms of AD. However, the role of MEOX2 in AD has not been studied. Here, we tested Meox2 haploinsufficiency in B6.APP/PS1 (B6.APBTg) mice, a mouse model of AD. Despite no overt differences in plaque deposition or glial activation, B6.APBTg mice that carry only one copy of Meox2 (B6.APBTg.Mx−/+) show increased neuronal cell loss, particularly in regions containing plaques, compared with B6.APBTgmice. Neuronal cell loss corresponds with a significant decrease in plaque-associated microvessels, further supporting a synergistic effect of vascular compromise and amyloid deposition on neuronal cell dysfunction in AD

Selective pattern of motor system damage in gamma-synuclein transgenic mice mirrors the respective pathology in amyotrophic lateral sclerosis

AbstractAmyotrophic lateral sclerosis (ALS) is characterised by substantial loss of both upper and lower motor neuron function, with sensory and cognitive systems less affected. Though heritable forms of the disease have been described, the vast majority of cases are sporadic with poorly defined underlying pathogenic mechanisms. Here we demonstrate that the neurological pathology induced in transgenic mice by overexpression of γ-synuclein, a protein not previously associated with ALS, recapitulates key features of the disease, namely selective damage and loss of discrete populations of upper and lower motor neurons and their axons, contrasted by limited effects upon the sensory system

The Origin and Evolutionary Consequences of Skeletal Traits Shaped by Embryonic Muscular Activity, from Basal Theropods to Modern Birds

Embryonic muscular activity (EMA) is involved in the development of several distinctive traits of birds. Modern avian diversity and the fossil record of the dinosaur-bird transition allow special insight into their evolution. Traits shaped by EMA result from mechanical forces acting at post-morphogenetic stages, such that genes often play a very indirect role. Their origin seldom suggests direct selection for the trait, but a side-effect of other changes such as musculo-skeletal rearrangements, heterochrony in skeletal maturation, or increased incubation temperature (which increases EMA). EMA-shaped traits like sesamoids may be inconstant, highly conserved, or even disappear and then reappear in evolution. Some sesamoids may become increasingly influenced in evolution by genetic-molecular mechanisms (genetic assimilation). There is also ample evidence of evolutionary transitions from sesamoids to bony eminences at tendon insertion sites, and vice-versa. This can be explained by newfound similarities in the earliest development of both kinds of structures, which suggest these transitions are likely triggered by EMA. Other traits that require EMA for their formation will not necessarily undergo genetic assimilation, but still be conserved over tens and hundreds of millions of years, allowing evolutionary reduction and loss of other skeletal elements. Upon their origin, EMA-shaped traits may not be directly genetic, nor immediately adaptive. Nevertheless, EMA can play a key role in evolutionary innovation, and have consequences for the subsequent direction of evolutionary change. Its role may be more important and ubiquitous than currently suspected.Facultad de Ciencias Naturales y Muse

The nuclear receptor field: a historical overview and future challenges

In this article we summarize the birth of the field of nuclear receptors, the discovery ofuntransformed and transformed isoforms of ligand-binding macromolecules, the discovery of thethree-domain structure of the receptors, and the properties of the Hsp90-based heterocomplexresponsible for the overall structure of the oligomeric receptor and many aspects of the biologicaleffects. The discovery and properties of the subfamily of receptors called orphan receptors is alsooutlined. Novel molecular aspects of the mechanism of action of nuclear receptors and challengesto resolve in the near future are discussed.Fil: Mazaira, Gisela Ileana. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Zgajnar, Nadia Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Lotufo, Cecilia Maricel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Daneri Becerra, Cristina del Rosario. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Sivils, Jeffrey C.. University of Texas at El Paso; Estados UnidosFil: Soto, Olga B.. University of Texas at El Paso; Estados UnidosFil: Cox, Marc B.. University of Texas at El Paso; Estados UnidosFil: Galigniana, Mario Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentin

NPC1 deficiency impairs cerebellar postnatal development of microglia and climbing fiber refinement in a mouse model of Niemann-Pick disease type C.

Little is known about the effects of NPC1 deficiency in brain development and whether these effects contribute to neurodegeneration in Niemann-Pick disease type C (NPC). Degeneration of cerebellar Purkinje cells occurs at an earlier stage and to a greater extent in NPC; therefore, we analyzed the effect of NPC1 deficiency on microglia and on climbing fiber synaptic refinement during cerebellar postnatal development using th