El otro cuerpo de la identidad: análisis de modelos culturales de los trastornos del cuerpo femenino

Justificación: El presente estudio se centra en la construcción de la identidad corporal en la anorexia nerviosa, desde una perspectiva social y cultural y tiene en cuenta las aportaciones de diferentes autores desde la perspectiva feminista de la salud y desde la antropología, dado que ambos planteamientos adoptan una visión mas amplia de los trastornos mentales y proponen comprenderlos en el contexto del malestar en la cultura. Objetivo: Analizar y comparar las variables que configuran los modelos culturales en nuestra sociedad sobre la identidad femenina, construida sobre todo a partir de la corporalidad y a través de la experiencia de mujeres diagnosticadas de anorexia. Metodología: Investigación cualitativa. Las técnicas básicas utilizadas han sido las entrevistas en profundidad y la observación participante. Resultados: Tras el análisis de las entrevistas se evidenciaron diferentes categorías que se han agrupado en tres grandes apartados la percepción de la identidad, la percepción social del cuerpo y la aceptabilidad del propio cuerpo. Conclusión: Podríamos decir que los modelos de identidad femenina que plantea la sociedad respecto a la imagen ideal y a los medios para conseguirlo producen un conflicto del que resulta difícil escapar tanto a las mujeres catalogadas de normales, como aquellas diagnosticadas de anorexia nerviosa

Mice with chronic GSH deficit display phenotypical anomalies that resemble key aspects of schizophrenia

ABSTRACTSchizophrenia is a major psychiatric disorder occurring with a prevalence of 1% in the worldwide population. It develops progressively with psychosis onset in late adolescence or earlyadulthood. The disorder can take many different facets and has a highly diffuse anddistributed neuropathology including deficits in major neurotransmitter systems,myelination, stress regulation, and metabolism. The delayed onset and the heterogeneouspathology suggest that schizophrenia is a developmental disease that arises from interplayof genetic and environmental factors during sensitive periods. Redox dysregulation due to animbalance between pro-oxidants and antioxidant defence mechanisms is among the riskfactors for schizophrenia. Glutathione (GSH) is the major cellular redox regulator andantioxidant. Levels of GSH are decreased in cerebrospinal fluid, prefrontal cortex and postmortemstriatum of schizophrenia patients. Moreover, polymorphisms of the key GSHsynthesizingenzyme, glutamate-cysteine ligase, modifier (GCLM) subunit, are associatedwith the disease, suggesting that GSH deficit is of genetic origin. Here we used miceknockout (KO) for the GCLM gene, which display chronic GSH deficit (~70 to 80% decrease)to investigate the direct link between redox dysregulation and schizophrenia. Accordingly,we evaluated whether GCLM KO compared to normal wildtype mice display behavioralchanges that relate to schizophrenia symptoms and whether their brains showmorphological, functional or metabolic alterations that resemble those in patients.Moreover, we exposed pubertal GCLM mice to repeated mild stress and measured theirhormonal and behavioral stress reactivity. Our data show that chronic GSH deficit isassociated with altered emotion- and stress-related behaviors, deficient prepulse inhibition,pronounced amphetamine-induced hyperlocomotion but normal spatial learning andworking memory. These changes represent important schizophrenia endophenotypes.Moreover, this particular pattern of change indicates impairment of the ventralhippocampus (VH) and related circuitry as opposed to the dorsal hippocampus (DH), which isimplicated in spatial information processing. This is consistent with a selective deficit ofparvalbumin positive interneurons and gamma oscillation in the VH but not DH. Increasedlevels of circulating stress hormones in KO mice following pubertal stress corroborate VHdysfunction as it is involved in negative feedback control of the stress response. VHstructural and functional deficits are frequently found in the schizophrenic brain. Metabolicevaluation of the developing GCLM KO anterior cortex using in vivo magnetic resonancespectroscopy revealed elevated glutamine (Gln), glutamate (Glu), Gln/Glu and N-acetylaspartate(NAA) during the pre-pubertal period. Similar changes are reported in earlyschizophrenia. Overall, we observe phenotypic anomalies in GSH deficient GCLM KO micethat correspond to major schizophrenia endophenotypes. This supports an important rolefor redox dysregulation in schizophrenia and validates the GCLM KO mouse as model for thedisease. Moreover, our results indicate that puberty may be a sensitive period for redoxsensitivechanges highliting the importance of early intervention. Gln, Gln/Glu, Glu and NAAmay qualify as early metabolic biomarkers to identify young at-risk individuals. Since chronictreatment with NAC normalized most metabolic changes in GCLM KO mice, NAC may be oneadjunct treatment of choice for early intervention in patients.RESUMELa schizophrénie est une maladie psychiatrique majeure avec une prévalence de 1% dans lapopulation. Son développement est progressif, les premières psychoses apparaissant àl'adolescence ou au début de l'âge adulte. La maladie a plusieurs présentations et uneneuropathologie étendue, qui inclut des déficits neurochimiques, métaboliques, de lamyélination et de la régulation du stress. L'émergence tardive et l'hétérogénéité de lapathologie suggèrent que la schizophrénie est une maladie développementale, favorisée pardes facteurs génétiques et environnementaux durant des périodes sensibles. La dérégulationrédox, due à un déséquilibre entre facteurs pro-oxidantes et défenses anti-oxidantes,constitue un facteur de risque. Le glutathion (GSH) est le principal régulateur rédox et antioxidantdes cellules, ses taux sont diminués dans le liquide céphalorachidien, le cortexpréfrontal et le striatum de patients. De plus, des variations du gène codant la sous-unitémodulatrice (GCLM) de la glutamate-cystéine ligase, enzyme de synthèse du GSH, sontassociés la maladie, suggérant que le déficit observé chez les patients est d'originegénétique. Nous avons donc utilisé des souris ayant une délétion du gène GCLM (KO), quiont un déficit chronique en GSH (70-80%), afin d'étudier le lien entre une dérégulation rédoxet la schizophrénie. Nous avons évalué si ces souris présentent des altérationscomportementales analogues aux symptômes de la maladie, et des modificationsstructurelles, fonctionnelles et métaboliques au niveau du cerveau, ressemblant à celles despatients. De plus, nous avons soumis les souris à des stresses modérés durant la puberté,puis mesuré les réponses hormonales et comportementales. Les animaux présentent undéficit pré-attentionnel du traitement des informations moto-sensorielles, un déficit pourcertains apprentissages, une réponse accrue à l'amphétamine, mais leurs mémoires spatialeet de travail sont préservées. Ces atteintes comportementales sont analogues à certainsendophénotypes de la schizophrénie. De plus, ces changements comportementaux sontlargement expliqués par une perturbation morphologique et fonctionnelle de l'hippocampeventral (HV). Ainsi, nous avons observé un déficit sélectif des interneurones immunoréactifsà la parvalbumine et une désynchronisation neuronale dans l'HV. L'hippocampe dorsal,impliqué dans l'orientation spatiale, demeure en revanche intact. L'augmentationd'hormones de stress dans le sang des souris KO suite à un stress prépubertal soutien aussil'hypothèse d'une dysfonction de l'HV, connu pour moduler ce type de réponse. Des déficitsstructurels et fonctionnels dans l'hippocampe antérieur (ventral) ont d'ailleurs été rapportéschez des patients schizophrènes. Par de résonance magnétique, nous avons également suivile profil métabolique du le cortex antérieur au cours du développement postnatal des sourisKO. Ces mesures ont révélé des taux élevés de glutamine (Gln), glutamate (Glu), du ratioGln/Glu, et de N-acétyl-aspartate (NAA) durant la période prépubertale. Des altérationssimilaires sont décrites chez les patients durant la phase précoce. Nous avons donc révélédes anomalies phénotypiques chez les souris GCLM KO qui reflètent certainsendophénotypes de la schizophrénie. Nos résultats appuient donc le rôle d'une dérégulationrédox dans l'émergence de la maladie et le potentiel des souris KO comme modèle. De plus,cette étude met en évidence la puberté comme période particulièrement sensible à unedérégulation rédox, renforçant l'importance d'une intervention thérapeutique précoce. Dansce cadre, Gln, Gln/Glu, Glu and NAA seraient des biomarqueurs clés pour identifier de jeunesindividus à risque. De part son efficacité dans notre modèle, NAC pourrait être unesubstance de choix dans le traitement précoce des patients.

Programa de atención a pacientes con Esclerosis Lateral Amiotrófica (ELA): Información para el personal sanitario de los Centros de Atención Primaria

Etimológicamente, esclerosis significa endurecimiento (skerós es "endurecmiento patológico" y osis, "enfermedad") y hace referencia al estado de la médula espinal en las fases avanzadas de la enfermedad. Lateral significa "al lado" y pone de manifiesto la ubicación del daño en la médula espinal. Por último, el término amiotrófica significa "sin nutrición muscular" y se refiere a la pérdida de señales que los nervios envían normalmente a los músculos. La Esclerosis Lateral Amiotrófica (ELA) es la enfermedad más grave de un grupo de dolencias que tienen síntomas similares y son conocidas como "enfermedades de motoneuronas": la Atrofia Muscular Juvenil o Enfermedad de Kugelberg Welander, la Atrofia Muscular Infantil o Enfermedad de Werdnig Hoffmann, la parálisis bulbar progresiva, la amiotrofia focal benigna, la esclerosis lateral primaria y la atrofia muscular espinobulbar o Enfermedad de Kennedy.

Plan integral de enfermería para la atención domiciliaria de pacientes con enfermedad neuromuscular e insuficiencia respiratoria

Las enfermedades neuromuscualres son enfermedades neurológicas, de naturaleza progresiva, normalmente hereditarias cuya principal característica clínica es la debilidad muscular. Dentro de las enfermedades que causan problemas respiratorios, existen una gran variedad de enfermedades neuromusculares que comprometen la función respiratoria, las cuales pueden dividirse en enfermedades neuromusculares neuropaticas y miopáticas, además de poder clasificarlas según la evolución. Las ENM pueden comprometer el sistema respiratorio condicionando morbilidad respiratoria de intensidad y precocidad variable dependiendo del grado de afección de los músculos respiratorios y deglutorios, así como de otros factores como el estado nutricional o la capacidad de deambulación, todos ellos factores que pueden ser incluidos dentro de un programa de enfermería de atención a domicilio.

Arte Outsider: Aproximación a la construcción artística de las manifestaciones creativas al margen del sistema del Arte

Para este trabajo se ha querido mirar afuera de los límites del arte tal y como se concibe en occidente. Dicho de otra forma, con mirar más allá no se hace referencia al arte de otras culturas, pues, de hecho, no nos movemos de la nuestra. Lo que se pretende a continuación, es la contemplación en la producción “artística” que se crea al margen de los dominios del “arte” oficial. Con esto puede parecer que nos inclinemos hacia las manifestaciones antisistemas que surgen en ambientes no institucionales como las paredes de las calles de las ciudades o en espacios de Internet. Por el contrario, se quiere tener en cuenta a aquellos individuos que, no perteneciendo al mundo del arte, pero impulsados por las mismas fuerzas expresivas que siente un artista “profesional”, generan imágenes plásticas de gran ímpetu y valor estético, tales como los niños, los pacientes y discapacitados mentales a causa de psicopatologías o trastornos, o visionarios y médiums espirituales. En definitiva, se prestará atención a individuos social y culturalmente marginados.

Early glutathione deficit impairs parvalbumin expression in gaba interneurons and kainate-induced gamma oscillations

An increased oxidative stress and alteration of the antioxidant systems have been observed in schizophrenia. Glutathione (GSH), a major redox regulator, is decreased in patients' cerebrospinal fluid, prefrontal cortex in vivo and striatum post-mortem tissue. Most importantly, there is genetic and functional evidence for the implication of the gene of the glutamate cysteine ligase (GCL) catalytic subunit, the key GSH-synthesizing enzyme. We have developed animal models for a GSH deficit to study the consequences of such deficit on the brain development. A GSH deficit combined with elevated dopamine (DA) during development leads to reduced parvalbumin (PV) expression in a subclass of GABA interneurons in rat anterior cingulate cortex (ACC). Similar changes are observed in postmortem brain tissue of schizophrenic patients. GSH dysregulation increases vulnerability to oxidative stress, that in turn could lead to cortical circuit anomalies in the schizophrenic brain. In the present study, we use a GCL modulatory subunit (GCLM) knock-out (KO) mouse model that presents up to 80% decreased brain GSH levels. During postnatal development, a subgroup of animals from each genotype is exposed to elevated oxidative stress induced by treatment with the DA reuptake inhibitor GBR12909. Results reveal a significant genotype-specific delay International Congress on Schizophrenia Research 136 10. 10. Neuroanatomy, Animal Downloaded from http://schizophreniabulletin.oxfordjournals.org at Bibliotheque Cantonale et Universitaire on June 18, 2010 in cortical PV expression at postnatal day P10 in GCLM-KO mice, as compared to wild-type. This effect seems to be further exaggerated in animals treated with GBR12909 from P5 to P10. At P20, PV expression is no longer significantly reduced in GCLM-KO ACC without GBR but is reduced if GBR is applied from P10 to P20. However, our result show that GCLM-KO mice exhibit increased oxidative stress, cortical altered myelin development as shown by MBP marker, and more specifically impairment of the peri-neuronal net known to modulate PV connectivity. In addition, we also observe a reduced PV expression in the ventro-temporal hippocampus of adult GCLM-KO mice, suggesting that anomalies of the PV interneurons prevail at least in some brain regions throughout the adulthood. Interestingly, the power of kainate-induced gamma oscillations, known to be dependent on proper activation of PV interneuron's, is also lower in hippocampal slices of adult GCLM KO mice. These results suggest that the PV positive GABA interneurons is particularly vulnerable to increased oxidative stress

Alterações no perfil de frações nitrogenadas em calos de cana-de-açúcar induzidas por deficit hídrico

O objetivo deste trabalho foi avaliar o uso de marcadores bioquímicos e fisiológicos, na caracterização do estresse hídrico em calos de cultivares de cana-de-açúcar (Sacharum sp.), RB 72 454 (sensível) e SP 813250 (resistente), contrastantes quanto à resistência à seca em campo. O delineamento experimental foi o inteiramente casualizado, em esquema fatorial de 2x5 [cultivar x doses de polietilenoglicol (PEG)], com dez tratamentos e três repetições. Os calos foram submetidos a concentrações de PEG correspondentes aos potenciais osmóticos de 0, -0,3, -0,6, -0,9 e -1,2 MPa, por 120 horas. A variação no conteúdo relativo de água e na umidade não foi significativamente diferente entre as cultivares. Entretanto, foi observada a tendência de aumento no vazamento de eletrólitos, em conseqüência da diminuição do potencial osmótico na cultivar tolerante. Na cultivar sensível, observou-se tendência de aumento de prolina e, na resistente, diminuição, embora os níveis não tenham sido afetados pelo deficit hídrico. As concentrações de aminoácidos livres foram maiores na sensível. Houve queda nas concentrações de amônia, em ambas cultivares. Os níveis de proteínas não foram afetados pelo PEG. O perfil protéico por SDS-PAGE não mostrou aumento induzido por PEG, na intensidade das bandas correspondentes aos peptídeos entre 14 e 66 kDa. Os marcadores bioquímicos e fisiológicos não foram relacionados ao grau diferencial de resistência observado nas cultivares em condições de campo.

Brazilian maize genotypes sensitivity to water deficit estimated through a simple crop yield model

The objective of this work was to determine the sensitivity of maize (Zea mays) genotypes to water deficit, using a simple agrometeorological crop yield model. Crop actual yield and agronomic data of 26 genotypes were obtained from the Maize National Assays carried out in ten locations, in four Brazilian states, from 1998 to 2006. Weather information for each experimental location and period were obtained from the closest weather station. Water deficit sensitivity index (Ky) was determined using the crop yield depletion model. Genotypes can be divided into two groups according to their resistance to water deficit. Normal resistance genotypes had Ky ranging from 0.4 to 0.5 in vegetative period, 1.4 to 1.5 in flowering, 0.3 to 0.6 in fruiting, and 0.1 to 0.3 in maturing period, whereas the higher resistance genotypes had lower values, respectively 0.2-0.4, 0.7-1.2, 0.2-0.4, and 0.1-0.2. The general Ky for the total growing season was 2.15 for sensitive genotypes and 1.56 for the resistant ones. Model performance was acceptable to evaluate crop actual yield, whose average errors estimated for each genotype ranged from -5.7% to +5.8%, and whose general mean absolute error was 960 kg ha-1 (10%).

Sistema de administración y reportes para calificadores electrónicos de atención al cliente

El sistema desarrollado es una aplicación web que permite obtener reportes estadísticos a partir de calificaciones registradas por dispositivos electrónicos para la empresa ecuatoriana SILTTEC. Aquí se muestra el desarrollo del sistema, empezando por las fases de análisis y requerimientos, para luego continuar con el diseño y la construcción de la aplicación; se culmina con las pruebas del sistema y la implementación en un servidor de aplicaciones. Cabe mencionar que las herramientas y plataformas utilizadas en el desarrollo de este proyecto son de software libre.

Indicadores fisiológicos da interação entre deficit hídrico e acidez do solo em cana-de-açúcar

O objetivo deste trabalho foi avaliar os indicadores fisiológicos da interação entre deficit hídrico e acidez do solo em plantas jovens de cana-de-açúcar. As plantas foram submetidas a três tratamentos de disponibilidade hídrica, medidos em percentagem de capacidade de campo (CC) - sem estresse (70% CC), estresse moderado (55% CC) e estresse severo (40% CC); e três tratamentos de acidez no solo, medidos em termos de saturação por bases (V) - baixa acidez (V = 55%), média acidez (V = 33%) e alta acidez (V = 23%). O experimento foi realizado em casa de vegetação a 29,7±4,3ºC e 75±10% UR. O delineamento experimental utilizado foi o de blocos ao acaso, em esquema fatorial 3x3, com quatro repetições. Após 60 dias, foram determinados os teores de solutos compatíveis - trealose, glicina betaína e prolina - na folha diagnóstico e o crescimento inicial da parte aérea. Os solutos compatíveis trealose, glicina betaína e prolina são indicadores do efeito da interação dos estresses hídrico e ácido no solo. O acúmulo dos solutos compatíveis nos tecidos foliares das plantas não é capaz de impedir a redução na produção de matéria seca da cana-de-açúcar, resultante do agravamento nas condições de disponibilidade hídrica e de acidez no solo.

Metabolic alterations in the cortex of a mouse model with glutathione deficit - relevance to schizophrenia

Background: Glutathione (GSH) is a major redox regulator and antioxidant and is decreased in cerebrospinal fluid and prefrontal cortex of schizophrenia patients [Do et al. (2000) Eur J Neurosci 12:3721]. The genes of the key GSH-synthesizing enzyme, glutamate- cysteine ligase catalytic (GCLC) and modifier (GCLM) subunits, are associated with schizophrenia, suggesting that the deficit in GSH synthesis is of genetic origin [Gysin et al. (2007) PNAS 104:16621]. GCLM knock-out (KO) mice, which display an 80% decrease in brain GSH levels, have abnormal brain morphology and function [Do et al. (2009) Curr Opin Neurobiol 19:220]. Developmental redox deregulation by impaired GSH synthesis and environmental risk factors generating oxidative stress may have a central role in schizophrenia. Here, we used GCLM KO mice to investigate the impact of a genetically dysregulated redox system on the neurochemical profile of the developing brain. Methods: The neurochemical profile of the anterior and posterior cortical areas of male and female GCLM KO and wild-type mice was determined by in vivo 1H NMR spectroscopy on postnatal days 10, 20, 30, 60 and 90, under 1 to 1.5% isoflurane anaesthesia. Localised 1H NMR spectroscopy was performed on a 14.1 T, 26 cm VNMRS spectrometer (Varian, Magnex) using a home-built 8 mm diameter quadrature surface coil (used both for RF excitation and signal reception). Spectra were acquired using SPECIAL with TE of 2.8 ms and TR of 4 s from VOIs placed in anterior or posterior regions of the cortex [Mlynárik et al. (2006) MRM 56:965]. LCModel analysis allowed in vivo quantification of a neurochemical profile composed of 18 metabolites. Results: GCLM KO mice displayed nearly undetectable GSH levels as compared to WT mice, demonstrating their drastic redox deregulation. Depletion of GSH triggered alteration of metabolites related to its synthesis, namely increase of glycine and glutamate levels during development (P20 and P30). Concentrations of glutamine and aspartate that are produced from glutamate were also increased in GCLM KO animals relative to WT. In addition, GCLM KO mice also showed higher levels of N-acetylaspartate that originates from the acetylation of aspartate. These metabolites are particularly implicated in neurotransmission processes and in mitochondrial oxidative metabolism. Their increase may indicate impaired mitochondrial metabolism with concomitant accumulation of lactate in the adult mice (P60 and P90). In addition, the GSH depletion triggers reduction of GABA concentration in anterior cortex of the P60 mice, which is in accordance with known impairment of GABAergic interneurons in that area. Changes were generally more pronounced in males than in females at P60, which is consistent with earlier disease onset in male patients. Discussion: In conclusion, the observed metabolic alterations in the cortex of a mouse model of redox deregulation suggest impaired mitochondrial metabolism and altered neurotransmission. The results also highlight the age between P20 and P30 as a sensitive period during the development for these alterations.

Respostas biométricas e fisiológicas ao deficit hídrico em cana-de-açúcar em diferentes fases fenológicas

O objetivo deste trabalho foi avaliar as respostas biométricas e fisiológicas de cana-de-açúcar (Saccharum spp.) ao deficit hídrico (DH), em diferentes fases fenológicas. Os genótipos IACSP 94-2094 e IACSP 96-2042 foram submetidos a DH nas fases de crescimento inicial, crescimento máximo e de acúmulo de sacarose no colmo. O delineamento experimental foi inteiramente casualizado. A suscetibilidade ao DH foi determinada pela redução de matéria seca do colmo e do conteúdo de sólidos solúveis no caldo. O deficit hídrico causou redução nas trocas gasosas, nas três fases fenológicas, em ambos os genótipos. Foi observada menor altura das plantas, menor acúmulo de matéria seca do colmo e de sólidos solúveis, e redução no número e comprimento de entrenós, apenas na fase de crescimento inicial, no clone IACSP 96-2042. Na fase de crescimento inicial, observou-se tolerância ao DH no genótipo IACSP 94-2094, com evidências de aclimatação fisiológica, e redução na produção de fitomassa e de sólidos solúveis no genótipo IACSP 96-2042, como resposta à menor condutância estomática e à menor eficiência aparente de carboxilação da fotossíntese. Independentemente da fase fenológica, o genótipo IACSP 94-2094 foi tolerante ao deficit hídrico, pois manteve a produção de fitomassa mesmo com redução das trocas gasosas.