Entorn a la integració laboral del deficient mental : la tasca de l'educador. 'En torno a la integración laboral del deficiente mental : la tarea del educador'.

Considerar la integración laboral del deficiente mental como un cambio en la dinámica de la sociedad actual, creadora de la marginación. Presentar una descripción de una experiencia concreta dónde tres deficientes mentales siguen el proceso de integración laboral en dos empresas dedicadas a cocinar ara comedores escolares. Presentar el contexto legal, la solución de la institución, las empresas, la descripción individual de los sujetos y el proceso seguido. 3 disminuidos en proceso de integración que provienen de un ambiente familiar desestructurado, ubicados en barrios conflictivos. Su deficiencia se describe a partir de causas esencialmente sociales. El trabajo de formación de estos sujetos se realiza por el cocinero encargado de la empresa, en estrecha colaboración con el educador. Se trabaja tanto las destrezas específicas de cocina, cómo el cuidado personal,la higiene y el vestuario. Se atenua la decepción ante el posible fracaso de la integración anticipando la posibilidad de retornar al centro. Con los trabajadores de la empresa se lleva a cabo una desmitificación del sujeto disminuido enfocándolo desde la perspectiva social. Informa de manera constante a las familias sobre el proceso de integración. Observación participante del proceso de integración, entrevistas personales con los sujetos deficientes, reuniones informativas previas,reuniones de evaluación durante el proceso, reuniones posteriores. Se observan cambios notables en los chicos, se muestran más equilibrados y con una vida social más estructurada. En cuanto a los empleados el recelo inicial ha dado paso a un ambiente distendido de colaboración y amistad con los sujetos. A pesar de ser una experiencia valorada positivamente los factores que se deben considerar en el futuro son una dificultad a contemplar: la adecuación de las capacidades de los deficientes a las exigencias del trabajo y la idoneidad de éste desde las perspectivas personales, sociales, legales y laborales. Se debe destacar la importancia de los ayuntamientos, ya que grácias a su colaboración se pueden realizar estos proyectos.

El deficient adult i vell en la societat. 'El deficiente adulto y viejo en la sociedad'.

Trabajar los temas que giran en torno al deficiente adulto y al deficiente anciano, en especial el tema relacionado con la educación que reciben, haciendo incapié en el trabajo del educador. Residencia de paso de disminuidos adultos, ASPANIN, de la cual se estudió el caso de siete de sus miembros, y en concreto la caracterización de un sujeto en particular. La investigación se inicia con un estudio conceptual e historiográfico de la deficiencia para poder profundizar más concretamente en la edad adulta y la tercera edad. Seguidamente, se pasa a un trabajo mucho más práctico, el estudio de las salidas y dificultades que tienen estos sujetos, y más concretamente, el trabajo del educador en este sector. Por último, se procede al análisis y estudio de una residencia en particular, la residencia de paso de disminuidos adultos (ASPANIN). Observaciones, documentos del régimen interior de la institución y entrevistas. Tests de inteligencia. Haciendo un estudio del test de inteligencia se encontra que éste valora siempre los conocimientos adquiridos pero nunca la posibilidad de aprender y de asimilar que tiene una persona. Se confima la importancia que tiene el buen trabajo preventivo. Es importante el trabajo del educador especializado, educando a un sujeto adulto que más adelante será anciano, y un trabajo paralelo con toda la sociedad y más concretamente con la gente que le rodea; así pues, es importante también trabajar con los padres. Se ha de intentar pedir cada vez más un marco teórico a los educadores. El educador no puede hacer un trabajo sin conocimientos previos. Finalmente, en nuestra sociedad nunca un sujeto deficiente ni será considerado adulto ni de la tercera edad.

El mitjà per a la circulació social del deficient psíquic : l'educació. 'El medio para la circulación social del deficiente psíquico : la educación'.

Refelejar la experiencia en un Esplai Especial de Caldes de Montbui. Definir el marco teórico de intervención del educador social. Presentar 3 estudios de casos. Dos chicas y un chico, deficientes psíquicos, de entre 17 y 27 años de edad. Se realiza un recorrido por la evolución del concepto de deficiencia y el proceso de socialización de los deficientes psíquicos. Se define el espacio de la educación social en la educación en el tiempo libre, partiendo de la base de que Cataluña tiene una gran tradición en la organización de actividades lúdico-educativas. Se describen las actividades del centro de Esplai Especial de Caldes de Montbui, dónde se combinan las prácticas convencionales de los centros recreativos, con prácticas de la vida cotidiana. Se presentan 3 estudios de casos. Observación directa. Los resultados de las observaciones de los tres sujetos se pueden resumir de la siguiente manera: a) el sujeto chico de 19 años, tiene una dependencia absoluta del adulto, las intervenciones se encaminan hacia la autonomía del mismo, pero los resultados no son destacables; b) el sujeto chica de 17 años tiene parálisis cerebral y presenta deficiencia intelectual, se inicia en el trabajo adaptado, que a pesar de ser repetitivo y poco educativo representa un paso importante para la adolescente; c) el sujeto chica de 20 años no recibe el subsidio para deficientes, tiene una familia desestructurada que sobreprotege a la chica, su evolución se ve entorpecida por el entorno social en el cual vive. Concluye que la función del educador es transmitir las pautas culturales que permitan la integración social. Pone en relieve la importancia de la educación no-formal como un medio para la integración social de los sujetos.

Sox1-deficient mice suffer from epilepsy associated with abnormal ventral forebrain development and olfactory cortex hyperexcitability

Mutations in several classes of embryonically-expressed transcription factor genes are associated with behavioral disorders and epilepsies. However, there is little known about how such genetic and neurodevelopmental defects lead to brain dysfunction. Here we present the characterization of an epilepsy syndrome caused by the absence of the transcription factor SOX1 in mice. In vivo electroencephalographic recordings from SOX1 mutants established a correlation between behavioral changes and cortical output that was consistent with a seizure origin in the limbic forebrain. In vitro intracellular recordings from three major forebrain regions, neocortex, hippocampus and olfactory (piriform) cortex (OC) showed that only the OC exhibits abnormal enhanced synaptic excitability and spontaneous epileptiform discharges. Furthermore, the hyperexcitability of the OC neurons was present in mutants prior to the onset of seizures but was completely absent from both the hippocampus and neocortex of the same animals. The local inhibitory GABAergic neurotransmission remained normal in the OC of SOX1-deficient brains, but there was a severe developmental deficit of OC postsynaptic target neurons, mainly GABAergic projection neurons within the olfactory tubercle and the nucleus accumbens shell. Our data show that SOX1 is essential for ventral telencephalic development and suggest that the neurodevelopmental defect disrupts local neuronal circuits leading to epilepsy in the SOX1-deficient mice

Deficient acquisition and consolidation: intertrial free recall performance in Alzheimer's disease and mild cognitive impairment

Previous research demonstrates that dementia of the Alzheimer type (DAT) is characterised by deficits of episodic memory, especially in the acquisition of new material. As well as this deficit in acquisition, some researchers have also argued for a deficit in consolidation in DAT. We examined acquisition and consolidation by measuring the intertrial gained and lost access in DAT, Mild Cognitive Impairment (MCI) and controls. We report findings from a study of clinical data based on assessment of patients using three free recall trials of a word list. We found that both DAT and MCI groups showed a deficit in acquisition and consolidation of items between trials relative to controls. Moreover, the DAT group was significantly impaired relative to the MCI group for both acquisition and consolidation. Correlations within each group showed that there were strong relationships between intertrial measures and standard measures of memory function. Importantly in no group was there a significant correlation between our measures of acquisition and consolidation: we argue that these measures reflect different underlying processes, and the failure to consolidate in DAT and MCI is not related to the deficit in acquisition. Finally, we showed strong correlations between our measure and dementia severity, suggesting that acquisition and consolidation both get worse as the dementia progresses.

Brucella melitensis 16M: characterisation of the galE gene and mouse immunisation studies with a galE deficient mutant

The galE gene of Streptomyces lividans was used to probe a cosmid library harbouring Brucella melitensis 16M DNA and the nucleotide sequence of a 2.5 kb ClaI fragment which hybridised was determined. An open reading frame encoding a predicted polypeptide with significant homology to UDP-galactose-4-epimerases of Brucella arbortus strain 2308 and other bacterial species was identified. DNA sequences flanking the B. melitensis galE gene shared no identity with other gal genes and, as for B. abortus, were located adjacent to a mazG homologue. A plasmid which encoded the B. melitensis galE open reading frame complemented a galE mutation in Salmonella typhimurium LB5010, as shown by the restoration of smooth lipopolysaccharide (LPS) biosynthesis, sensitivity to phage P22 infection and restoration of UDP-galactose-4-epimerase activity. The galE gene on the B. melitensis 16M chromosome was disrupted by insertional inactivation and these mutants lacked UDP-galactose-4-epimerase activity but no discernible differences in LPS structure between parent and the mutants were observed. One B. melitensis 16M galE mutant, Bm92, was assessed for virulence in CD-1 and BALB/c mice and displayed similar kinetics of invasion and persistence in tissues compared with the parent bacterial strain. CD-1 mice immunised with B. melitensis 16M galE were protected against B. melitensis 16M challenge. Crown Copyright (C) 1999 Published by Elsevier Science B.V.

A comparison of Shiga-toxin negative Escherichia coli O157 aflagellate and intimin deficient mutants in porcine in vitro and in vivo models of infection

Isolation of Shiga-toxin (Stx) positive Escherichia coli O157:H7 from commercially grown pigs has been reported. Furthermore, experimental infection studies have demonstrated that Stx-positive E. coli O157:H7 can persist in 12-week-old experimentally orally inoculated conventional pigs for up to 2 months and that persistence was not dependent upon intimin. We have shown that the flagellum of Stx-negative E. coli O157:H7 does not have a role to play in pathogenesis in ruminant models whereas, in poultry, the flagellum of E. coli O157:H7 was important for long-term persistent infection. The contribution of the flagellum of Stx-negative E. coli O157 in the colonisation of pigs was investigated by adherence assays on a porcine (IPI-21) cell line, porcine in vitro organ culture (IVOC) and experimental oral inoculation of conventional 14-week-old pigs. E. coli O157:H7 NCTC12900nal(r) and isogenic aflagellate and intimin deficient mutants adhered equally well to IPI-21 cells. In porcine IVOC association assays, E. coli O157:H7 NCTC12900nal(r) was associated in significantly higher numbers to tissues from the caecum and the terminal rectum than other sites. The aflagellate and intimin deficient mutants significantly adhered in greater numbers to more IVOC gastrointestinal tissues than the parent. Groups of 14-week-old pigs were dosed orally with 10(10) CFU/10 ml of either E. coli O157:H7 NCTC12900nal(r) or isogenic aflagellate and intimin deficient mutants and recovery of each test strain was similar. Histological analysis of pig tissues at post mortem examination revealed that E. coli O157 specifically stained bacteria were associated with the mucosa of the ascending and spiral colon. These data suggest that colonisation and persistence of Stx-negative E. coli O157:H7 in pigs, involves mechanisms that do not require the flagellum or intimin.

The du2J mouse model of ataxia and absence epilepsy has deficient cannabinoid CB1 receptor-mediated signalling

Key point summary • Cerebellar ataxias are progressive debilitating diseases with no known treatment and are associated with defective motor function and, in particular, abnormalities to Purkinje cells. • Mutant mice with deficits in Ca2+ channel auxiliary α2δ-2 subunits are used as models of cerebellar ataxia. • Our data in the du2J mouse model shows an association between the ataxic phenotype exhibited by homozygous du2J/du2J mice and increased irregularity of Purkinje cell firing. • We show that both heterozygous +/du2J and homozygous du2J/du2J mice completely lack the strong presynaptic modulation of neuronal firing by cannabinoid CB1 receptors which is exhibited by litter-matched control mice. • These results show that the du2J ataxia model is associated with deficits in CB1 receptor signalling in the cerebellar cortex, putatively linked with compromised Ca2+ channel activity due to reduced α2δ-2 subunit expression. Knowledge of such deficits may help design therapeutic agents to combat ataxias. Abstract Cerebellar ataxias are a group of progressive, debilitating diseases often associated with abnormal Purkinje cell (PC) firing and/or degeneration. Many animal models of cerebellar ataxia display abnormalities in Ca2+ channel function. The ‘ducky’ du2J mouse model of ataxia and absence epilepsy represents a clean knock-out of the auxiliary Ca2+ channel subunit, α2δ-2, and has been associated with deficient Ca2+ channel function in the cerebellar cortex. Here, we investigate effects of du2J mutation on PC layer (PCL) and granule cell (GC) layer (GCL) neuronal spiking activity and, also, inhibitory neurotransmission at interneurone-Purkinje cell(IN-PC) synapses. Increased neuronal firing irregularity was seen in the PCL and, to a less marked extent, in the GCL in du2J/du2J, but not +/du2J, mice; these data suggest that the ataxic phenotype is associated with lack of precision of PC firing, that may also impinge on GC activity and requires expression of two du2J alleles to manifest fully. du2J mutation had no clear effect on spontaneous inhibitory postsynaptic current (sIPSC) frequency at IN-PC synapses, but was associated with increased sIPSC amplitudes. du2J mutation ablated cannabinoid CB1 receptor (CB1R)-mediated modulation of spontaneous neuronal spike firing and CB1Rmediated presynaptic inhibition of synaptic transmission at IN-PC synapses in both +/du2J and du2J/du2J mutants; effects that occurred in the absence of changes in CB1R expression. These results demonstrate that the du2J ataxia model is associated with deficient CB1R signalling in the cerebellar cortex, putatively linked with compromised Ca2+ channel activity and the ataxic phenotype.

Gene expression changes in phosphorus deficient potato (Solanum tuberosum L.) leaves and the potential for diagnostic gene expression markers

Background: There are compelling economic and environmental reasons to reduce our reliance on inorganic phosphate (Pi) fertilisers. Better management of Pi fertiliser applications is one option to improve the efficiency of Pi fertiliser use, whilst maintaining crop yields. Application rates of Pi fertilisers are traditionally determined from analyses of soil or plant tissues. Alternatively, diagnostic genes with altered expression under Pi limiting conditions that suggest a physiological requirement for Pi fertilisation, could be used to manage Pifertiliser applications, and might be more precise than indirect measurements of soil or tissue samples. Results: We grew potato (Solanum tuberosum L.) plants hydroponically, under glasshouse conditions, to control their nutrient status accurately. Samples of total leaf RNA taken periodically after Pi was removed from the nutrient solution were labelled and hybridised to potato oligonucleotide arrays. A total of 1,659 genes were significantly differentially expressed following Pi withdrawal. These included genes that encode proteins involved in lipid, protein, and carbohydrate metabolism, characteristic of Pi deficient leaves and included potential novel roles for genes encoding patatin like proteins in potatoes. The array data were analysed using a support vector machine algorithm to identify groups of genes that could predict the Pi status of the crop. These groups of diagnostic genes were tested using field grown potatoes that had either been fertilised or unfertilised. A group of 200 genes could correctly predict the Pi status of field grown potatoes. Conclusions: This paper provides a proof-of-concept demonstration for using microarrays and class prediction tools to predict the Pi status of a field grown potato crop. There is potential to develop this technology for other biotic and abiotic stresses in field grown crops. Ultimately, a better understanding of crop stresses may improve our management of the crop, improving the sustainability of agriculture.

The Impact of Vitamin A Supplementation on the Immune System of Vitamin A-deficient Children

Background & Aims: To investigate the effect of vitamin A supplementation on parameters of the immune system of vitamin A-deficient children. Methods: The study was carried out in four phases: 1) determination of serum retinol in 631 children from 36 to 83 months of age; 2) assessment of immunological markers [immunoglobulins and complement fractions, immunophenotyping of T and B lymphocytes, and natural killer (NK) cells], blood count, and serum ferritin of 52 vitamin A-deficient children (serum retinol <0.70 mu mol/L); 3) supplementation of the 52 deficient children with 200,000 IU of vitamin A; 4) determination of serum retinol and the immunological parameters 2 months after vitamin A supplementation. Results: Before vitamin A supplementation, 24.0% of the children were anemic and 4.3 %had reduced ferritin concentrations. There was no significant difference between mean values of retinol according to the presence/absence of anemia. The mean values of the humoral and cellular immunological parameters did not show a statistically significant difference before and after supplementation with vitamin A. Children with concomitant hypovitaminosis A and anemia presented a significant increase in absolute CD4 and CD8 T-cell counts after vitamin A supplementation (p < 0.05). Conclusion: Vitamin A had an effect on the recruitment of T and B lymphocytes to the circulation of children with hypovitaminosis A and anemia.