695 resultados para Corea de Huntington


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Nel presente lavoro sono state analizzate le distribuzioni quantitative dei Foraminiferi planctonici e bentonici presenti in una carota e in un box core prelevati nel Mare di Ross in Antartide durante la campagna KOPRI ANTA03 nel Febbraio 2013 nell’ambito del progetto di ricerca congiunto Corea- Italia finanziato dal Progetto Nazionale di Ricerca in Antartide (PNRA). Scopo del lavoro è stato quello di comprendere l’evoluzione ambientale dell’area in base alla distribuzione quantitativa e qualitativa delle associazioni a Foraminiferi nel tardo Quaternario. In base alla distribuzione quantitativa dei Foraminiferi identificati, la sequenza sedimentaria della carota C2 è stata suddivisa in tre intervalli corrispondenti a tre principali fasi paleoceanografiche/paleoclimatiche. La prima fase, più antica di 18 ka, caratterizzata dall’assenza o rarità di forme documenta un ambiente con presenza di copertura glaciale. La seconda, depositatasi tra 18 ka e ~8 ka è caratterizzata da una maggiore variabilità intraspecifica e riflette un miglioramento delle condizioni climatiche. La terza, corrisponde ad un periodo compreso tra ~8 ka e ~2 ka. La presenza di forme agglutinanti e l’assenza di Foraminiferi a guscio calcareo suggeriscono la presenza di condizioni di dissoluzione carbonatica sul fondale in un ambiente marino libero da copertura glaciale. La documentazione di numerosi individui allo stadio giovanile di Neogloboquadrina pachyderma durante l’intervallo B ha reso possibile avanzare ipotesi riguardo la strategia di sopravvivenza di questa specie in ambiente estremo quale il ghiaccio antartico. La somiglianza morfologica tra individui giovanili di Neogloboquadrina pachyderma riscontrata durante il nostro studio nei sedimenti a livello fossile nella carota con individui giovanili della stessa specie provenienti da campioni di ghiaccio marino antartico documentati in bibliografia, ha permesso di supportare la tesi dello sviluppo di tali forme nei pori del “microghiaccio”.

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“Immaginate di potervi rilassare a casa in una giornata d’estate tenendo le finestre aperte per lasciare passare la brezza ma senza essere disturbati dai rumori della città, oggi è possibile”. Quello che voglio fare attraverso questa tesi è di studiare la fattibilità per la realizzazione di una finestra che permetta il passaggio dell’aria ma non dei rumori. L’idea di questa particolare finestra silenziosa mi è stata fornita dallo studio fatto dal professor Sang-Hoon Kim del Mokpo National University maritime e dal professor Seong-Hyun Lee del Korea Institute of Machinery and Materials in Corea del Sud. Essi hanno utilizzato i metamateriali acustici per risolvere il problema dell’inquinamento sonoro in città. Queste finestre hanno il vantaggio di tenere i rumori fuori dalla nostra abitazione ma permettere il passaggio dell’aria attraverso dei fori aventi dimensioni e posizioni adeguate da garantire questo particolare fenomeno. I principi su cui si basano queste finestre sono: la diffrazione e i risonatori di Helmholtz, che analizzeremo nel dettaglio nei capitoli 1 e 2 di questa tesi. Dopo aver analizzato i due principi attraverso simulazione fatte mediante il programma COMSOL multiphysics, sono passata all’analisi della finestra vera e propria: ovvero alla realizzazione delle dimensioni adeguate dei risonatori di Helmholtz utilizzati, alle dimensioni dei rispettivi fori d’ingresso e alla combinazione di questi risonatori per ricavare la miglior finestra silenziosa, che trattenesse al suo esterno il maggior numero di dB.

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Background: In dimorphic seabirds, the larger sex tends to provision more than the smaller sex. In contrast, monogamy and biparental care are often associated with equal effort between the sexes. However, the few studies that have tested sex-specific effort in monomorphic seabirds have primarily examined the details of foraging at sea. Hypotheses: Parental effort is also sex-biased in a monomorphic seabird mating system for one of two reasons: (1) If females enter the period of parental care less able to invest in care due to the cost of egg production, male-biased effort may be necessary to avoid reproductive failure. (2) Alternatively, female-biased effort may occur due to the initial disparity in gamete size, particularly in species with internal fertilization. Organism: Leach’s storm-petrel (Oceanodroma leucorhoa), a monomorphic seabird with true monogamy and obligate biparental care. Site: A breeding colony of Oceanodroma leucorhoa at the Bowdoin Scientific Station on Kent Island, Bay of Fundy, New Brunswick, Canada. Methods: Across multiple breeding seasons, we assessed incubation behaviour and chickrearing behaviour through one manipulative and multiple observational studies. We assessed energetic investment by inducing feather replacement and measuring the resulting rate of feather growth during both the incubation and chick-rearing phases of parental care. Conclusions: We observed male-biased effort. Males incubated the egg for a greater proportion of time than did females and, when faced with an egg that would not hatch, males continued to incubate past the point when females abandoned it. Males made a higher percentage of total food deliveries to chicks than did females, resulting in greater mean daily food provisioning by males than by females. During chick rearing, males grew replacement feathers more slowly than did females, indicating that males were more likely to reduce their own nutritional condition while raising chicks than were females. These results support the hypothesis that females enter the period of parental care at a nutritional deficit and males must compensate to avoid reproductive failure.

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Nitric oxide (NO) mediates a variety of physiological functions in the central nervous system and acts as an important developmental regulator. Striatal interneurons expressing neuronal nitric oxide synthase (nNOS) have been described to be relatively spared from the progressive cell loss in Huntington's disease (HD). We have recently shown that creatine, which supports the phosphagen energy system, induces the differentiation of GABAergic cells in cultured striatal tissue. Moreover, neurotrophin-4/5 (NT-4/5) has been found to promote the survival and differentiation of cultured striatal neurons. In the present study, we assessed the effects of creatine and NT-4/5 on nNOS-immunoreactive (-ir) neurons of E14 rat ganglionic eminences grown for 1 week in culture. Chronic administration of creatine [5mM], NT-4/5 [10ng/ml], or a combination of both factors significantly increased numbers of nNOS-ir neurons. NT-4/5 exposure also robustly increased levels of nNOS protein. Interestingly, only NT-4/5 and combined treatment significantly increased general viability but no effects were seen for creatine supplementation alone. In addition, NT-4/5 and combined treatment resulted in a significant larger soma size and number of primary neurites of nNOS-ir neurons while creatine administration alone exerted no effects. Double-immunolabeling studies revealed that all nNOS-ir cells co-localized with GABA. In summary, our findings suggest that creatine and NT-4/5 affect differentiation and/or survival of striatal nNOS-ir GABAergic interneurons. These findings provide novel insights into the biology of developing striatal neurons and highlight the potential of both creatine and NT-4/5 as therapeutics for HD.

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There is increasing interest in the search for therapeutic options for diseases and injuries of the central nervous system (CNS), for which currently no effective treatment strategies are available. Replacement of damaged cells and restoration of function can be accomplished by transplantation of cells derived from different sources, such as human foetal tissue, genetically modified cell lines, embryonic or somatic stem cells. Preclinical and clinical trials have shown promising results in neurodegenerative disorders, like Parkinson's and Huntington's disease, but also ischaemic stroke, intracerebral haemorrhage, demyelinating disorders, epilepsy and traumatic lesions of the brain and spinal cord. Other studies have focused on finding new ways to activate and direct endogenous repair mechanisms in the CNS, eg, by exposure to specific neuronal growth factors or by inactivating inhibitory molecules. Neuroprotective drugs may offer an additional tool for improving neuronal survival in acute or chronic CNS diseases. Importantly however, a number of scientific issues need to be addressed in order to permit the introduction of these experimental techniques in the wider clinical setting.

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The amino acid glutamate is the primary excitatory neurotransmitter for the CNS and is responsible for the majority of fast synaptic transmission. Glutamate receptors have been shown to be involved in multiple forms of synaptic plasticity such as LTP, LTD, and the formation of specific synaptic connections during development. In addition to contributing to the plasticity of the CNS, glutamate receptors also are involved in, at least in part, various pathological conditions such as epilepsy, ischemic damage due to stroke, and Huntington's chorea. The regulation of glutamate receptors, particularly the ionotropic NMDA and AMPA/KA receptors is therefore of great interest. In this body of work, glutamate receptor function and regulation by kinase activity was examined using the Xenopus oocyte which is a convenient and faithful expression system for exogenous proteins. Glutamate receptor responses were measured using the two-electrode voltage clamp technique in oocytes injected with rat total forebrain RNA. NMDA elicited currents that were glycine-dependent, subject to block by Mg$\sp{2+}$ in a voltage-dependent manner and sensitive to the specific NMDA antagonist APV in a manner consistent with those types of responses found in neural tissue. Similarly, KA-evoked currents were sensitive to the specific AMPA/KA antagonist CNQX and exhibited current voltage relationships consistent with the calcium permeable type II KA receptors found in the hippocampus. There is evidence to indicate that NMDA and AMPA/KA receptors are regulated by protein kinase A (PKA). We explored this by examining the effects of activators of PKA (forskolin, 1-isobutyl-3-methylxanthine (IBMX) and 8-Br-cAMP) on NMDA and KA currents in the oocyte. In buffer where Ca$\sp{2+}$ was replaced by 2 mM Ba$\sp{2+},$ forskolin plus IBMX and 8-Br-cAMP augmented currents due to NMDA application but not KA. This augmentation was abolished by pretreating the oocytes in the kinase inhibitor K252A. The use of chloride channel blockers resulted in attenuation of this effect indicating that Ba$\sp{2+}$ influx through the NMDA channel was activating the endogenous calcium-activated chloride current and that the cAMP mediated augmentation was at the level of the chloride channel and not the NMDA channel. This was confirmed by (1) the finding that 8-Br-cAMP increased chloride currents elicited via calcium channel activation while having no effect on the calcium channels themselves and (2) the fact that lowering the Ba$\sp{2+}$ concentration to 200 $\mu$M abolished the augmentation NMDA currents by 8-Br-cAMP. Thus PKA does not appear to modulate ionotropic glutamate receptors in our preparation. Another kinase also implicated in the regulation of NMDA receptors, calcium/phospholipid-dependent protein kinase (PKC), was examined for its effects on the NMDA receptor under low Ba$\sp{2+}$ (200 $\mu$M) conditions. Phorbol esters, activators of PKC, induced a robust potentiation of NMDA currents that was blockable by the kinase inhibitor K252A. Furthermore activation of metabotropic receptors by the selective agonist trans-ACPD, also potentiated NMDA albeit more modestly. These results indicate that neither NMDA nor KA-activated glutamate receptors are modulated by PKA in Xenopus oocytes whereas NMDA receptors appear to be augmented by PKC. Furthermore, the endogenous chloride current of the oocyte was found to be responsive to Ba$\sp{2+}$ and in addition is enhanced by PKA. Both of these latter findings are novel. In conclusion, the Xenopus oocyte is a useful expression system for the analysis of ligand-gated channel activity and the regulation of those channels by phosphorylation. ^

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Latrepirdine (Dimebon; dimebolin) is a neuroactive compound that was associated with enhanced cognition, neuroprotection and neurogenesis in laboratory animals, and has entered phase II clinical trials for both Alzheimer's disease and Huntington's disease (HD). Based on recent indications that latrepirdine protects cells against cytotoxicity associated with expression of aggregatable neurodegeneration-related proteins, including Aβ42 and γ-synuclein, we sought to determine whether latrepirdine offers protection to Saccharomyces cerevisiae. We utilized separate and parallel expression in yeast of several neurodegeneration-related proteins, including α-synuclein (α-syn), the amyotrophic lateral sclerosis-associated genes TDP43 and FUS, and the HD-associated protein huntingtin with a 103 copy-polyglutamine expansion (HTT gene; htt-103Q). Latrepirdine effects on α-syn clearance and toxicity were also measured following treatment of SH-SY5Y cells or chronic treatment of wild-type mice. Latrepirdine only protected yeast against the cytotoxicity associated with α-syn, and this appeared to occur via induction of autophagy. We further report that latrepirdine stimulated the degradation of α-syn in differentiated SH-SY5Y neurons, and in mouse brain following chronic administration, in parallel with elevation of the levels of markers of autophagic activity. Ongoing experiments will determine the utility of latrepirdine to abrogate α-syn accumulation in transgenic mouse models of α-syn neuropathology. We propose that latrepirdine may represent a novel scaffold for discovery of robust pro-autophagic/anti-neurodegeneration compounds, which might yield clinical benefit for synucleinopathies including Parkinson's disease, Lewy body dementia, rapid eye movement (REM) sleep disorder and/or multiple system atrophy, following optimization of its pro-autophagic and pro-neurogenic activities.

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Disruption of proteostasis, or protein homeostasis, is often associated with aberrant accumulation of misfolded proteins or protein aggregates. Autophagy offers protection to cells by removing toxic protein aggregates and injured organelles in response to proteotoxic stress. However, the exact mechanism whereby autophagy recognizes and degrades misfolded or aggregated proteins has yet to be elucidated. Mounting evidence demonstrates the selectivity of autophagy, which is mediated through autophagy receptor proteins (e.g. p62/SQSTM1) linking autophagy cargos and autophagosomes. Here we report that proteotoxic stress imposed by the proteasome inhibition or expression of polyglutamine expanded huntingtin (polyQ-Htt) induces p62 phosphorylation at its ubiquitin-association (UBA) domain that regulates its binding to ubiquitinated proteins. We find that autophagy-related kinase ULK1 phosphorylates p62 at a novel phosphorylation site S409 in UBA domain. Interestingly, phosphorylation of p62 by ULK1 does not occur upon nutrient starvation, in spite of its role in canonical autophagy signaling. ULK1 also phosphorylates S405, while S409 phosphorylation critically regulates S405 phosphorylation. We find that S409 phosphorylation destabilizes the UBA dimer interface, and increases binding affinity of p62 to ubiquitin. Furthermore, lack of S409 phosphorylation causes accumulation of p62, aberrant localization of autophagy proteins and inhibition of the clearance of ubiquitinated proteins or polyQ-Htt. Therefore, our data provide mechanistic insights into the regulation of selective autophagy by ULK1 and p62 upon proteotoxic stress. Our study suggests a potential novel drug target in developing autophagy-based therapeutics for the treatment of proteinopathies including Huntington's disease.

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Genetic anticipation is defined as a decrease in age of onset or increase in severity as the disorder is transmitted through subsequent generations. Anticipation has been noted in the literature for over a century. Recently, anticipation in several diseases including Huntington's Disease, Myotonic Dystrophy and Fragile X Syndrome were shown to be caused by expansion of triplet repeats. Anticipation effects have also been observed in numerous mental disorders (e.g. Schizophrenia, Bipolar Disorder), cancers (Li-Fraumeni Syndrome, Leukemia) and other complex diseases. ^ Several statistical methods have been applied to determine whether anticipation is a true phenomenon in a particular disorder, including standard statistical tests and newly developed affected parent/affected child pair methods. These methods have been shown to be inappropriate for assessing anticipation for a variety of reasons, including familial correlation and low power. Therefore, we have developed family-based likelihood modeling approaches to model the underlying transmission of the disease gene and penetrance function and hence detect anticipation. These methods can be applied in extended families, thus improving the power to detect anticipation compared with existing methods based only upon parents and children. The first method we have proposed is based on the regressive logistic hazard model. This approach models anticipation by a generational covariate. The second method allows alleles to mutate as they are transmitted from parents to offspring and is appropriate for modeling the known triplet repeat diseases in which the disease alleles can become more deleterious as they are transmitted across generations. ^ To evaluate the new methods, we performed extensive simulation studies for data simulated under different conditions to evaluate the effectiveness of the algorithms to detect genetic anticipation. Results from analysis by the first method yielded empirical power greater than 87% based on the 5% type I error critical value identified in each simulation depending on the method of data generation and current age criteria. Analysis by the second method was not possible due to the current formulation of the software. The application of this method to Huntington's Disease and Li-Fraumeni Syndrome data sets revealed evidence for a generation effect in both cases. ^

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The molecular mechanisms responsible for the expansion and deletion of trinucleotide repeat sequences (TRS) are the focus of our studies. Several hereditary neurological diseases including Huntington's disease, myotonic dystrophy, and fragile X syndrome are associated with the instability of TRS. Using the well defined and controllable model system of Escherichia coli, the influences of three types of DNA incisions on genetic instability of CTG•CAG repeats were studied: DNA double-strand breaks (DSB), single-strand nicks, and single-strand gaps. The DNA incisions were generated in pUC19 derivatives by in vitro cleavage with restriction endonucleases. The cleaved DNA was then transformed into E. coli parental and mutant strains. Double-strand breaks induced deletions throughout the TRS region in an orientation dependent manner relative to the origin of replication. The extent of instability was enhanced by the repeat length and sequence (CTG•CAG vs. CGG•CCG). Mutations in recA and recBC increased deletions, mutations in recF stabilized the TRS, whereas mutations in ruvA had no effect. DSB were repaired by intramolecular recombination, versus an intermolecular gene conversion or crossover mechanism. 30 nt gaps formed a distinct 30 nt deletion product, whereas single strand nicks and gaps of 15 nts did not induce expansions or deletions. Formation of this deletion product required the CTG•CAG repeats to be present in the single-stranded region and was stimulated by E. coli DNA ligase, but was not dependent upon the RecFOR pathway. Models are presented to explain the DSB induced instabilities and formation of the 30 nucleotide deletion product. In addition to the in vitro creation of DSBs, several attempts to generate this incision in vivo with the use of EcoR I restriction modification systems were conducted. ^

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There are many diseases associated with the expansion of DNA repeats in humans. Myotonic dystrophy type 2 is one of such diseases, characterized by expansions of a (CCTG)•(CAGG) repeat tract in intron 1 of zinc finger protein 9 (ZNF9) in chromosome 3q21.3. The DM2 repeat tract contains a flanking region 5' to the tract that consists of a polymorphic repetitive sequence (TG)14-25(TCTG)4-11(CCTG) n. The (CCTG)•(CAGG) repeat is typically 11-26 repeats in persons without the disease, but can expand up to 11,000 repeats in affected individuals, which is the largest expansion seen in DNA repeat diseases to date. This DNA tract remains one of the least characterized disease-associated DNA repeats, and mechanisms causing the repeat expansion in humans have yet to be elucidated. Alternative, non B-DNA structures formed by the expanded repeats are typical in DNA repeat expansion diseases. These sequences may promote instability of the repeat tracts. I determined that slipped strand structure formation occurs for (CCTG)•(CAGG) repeats at a length of 42 or more. In addition, Z-DNA structure forms in the flanking human sequence adjacent to the (CCTG)•(CAGG) repeat tract. I have also performed genetic assays in E. coli cells and results indicate that the (CCTG)•(CAGG) repeats are more similar to the highly unstable (CTG)•(CAG) repeat tracts seen in Huntington's disease and myotonic dystrophy type 1, than to those of the more stable (ATTCT)•(AGAAT) repeat tracts of spinocerebellar ataxia type 10. This instability, however, is RecA-independent in the (CCTG)•(CAGG) and (ATTCT)•(AGAAT) repeats, whereas the instability is RecA-dependent in the (CTG)•(CAG) repeats. Structural studies of the (CCTG)•(CAGG) repeat tract and the flanking sequence, as well as genetic selection assays may reveal the mechanisms responsible for the repeat instability in E. coli, and this may lead to a better understanding of the mechanisms contributing to the human disease state. ^

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Eduardo Aliverti visitó nuestra universidad, es locutor, periodista y profesor universitario. Condujo algunos de los programas de radio con mayor impacto de las últimas dos décadas, tales como: Anticipos -poco menos que la única voz periodística de oposición a la dictadura, por Radio Continental-; Sin Anestesia -por Radio Belgrano, en los primeros años de la transición democrática- y Protagonistas, en varias emisoras porteñas desde 1988 hasta 1996. Actualmente dirige y conduce Marca de Radio, por Rivadavia, durante la mañana de los sábados. Es ganador de 7 premios Martín Fierro. En el año 2002 recibe el Galardón Susini como reconocimiento a su trayectoria en radio, otorgado por Argentores. Dirigió tres videos de periodismo documental: Tango de un Lagarto, sobre la realidad cubana; Volviendo a Washington, acerca de la historia de la moneda argentina, y Malajunta, en torno de la última dictadura militar. Esta última realización fue galardonada en los festivales internacionales de Nueva York, Ginebra, San Salvador de Bahía, La Habana, San Francisco y Houston. Además de innumerables premios en el ámbito nacional, la proyección de Malajunta, en Suiza, motivó el surgimiento en Europa de la agrupación HIJOS, integrada por los descendientes de detenidos-desaparecidos exiliados en el Viejo Continente. Fue productor ejecutivo de Sol de Noche, largometraje testimonial que refleja la relación entre el poder económico y la última dictadura militar. Esta película participó de festivales en Alemania, España, Francia, Italia y Buenos Aires, entre otros. Aliverti efectuó coberturas periodísticas en Estados Unidos, Rusia, América Latina, Europa y la península de Corea. En Buenos Aires fundó, dirige y es docente de ETER, Escuela Terciaria de Estudios Radiofónicos (la primera escuela de radio de Latinoamérica). Hace 18 años es titular del taller radiofónico en la carrera de Ciencias de la Comunicación de la Universidad Nacional de Buenos Aires y es dueño del que está considerado como uno de los archivos periodísticos personales más importantes del país.

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Las mujeres que buscan servicios de urgencia por complicaciones de un aborto (hemorragia, infección y lesiones del tracto reproductivo) deberían ser un grupo prioritario para los programas de salud reproductiva. Frecuentemente, estas mujeres reciben atención de mala calidad que no cubre sus múltiples necesidades de salud. En ocasiones se les da de alta sin haber recibido consejería en recuperación postoperatoria, planificación familiar y otros aspectos de salud reproductiva

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Este trabajo trata sobre las perspectivas históricas, sociales y religiosas de Corea del Sur, y del funcionamiento e impacto nacional de los conglomerados empresariales coreanos. Además, se realiza una descripción del tipo de organizaciones y de estados proteccionistas. Por último, se estudia la actualidad nacional y regional de Corea.

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La presente investigación es de carácter cualitativo-exploratorio realizada desde un Equipo de Orientación Escolar (E.O.E.) que funciona en una Escuela de gestión privada católica de la Ciudad de La Plata, provincia de Buenos Aires. La novedad de este trabajo radica en que la pertenencia de un psicólogo a un E.O.E. es poco habitual ya que el cargo de Psicólogo no está previsto en la Dirección General de Escuelas y se comparte el trabajo con otros profesionales -psicopedagogos, asistentes sociales, fonoaudiólogos, médicos y maestros recuperadores- con miradas e intervenciones muy diferentes sobre cuestiones disciplinarias de los alumnos. A partir de diversas demandas -como de iniciativas propias del E.O.E.- hemos realizado intervenciones en el nivel secundario con alumnos y sus familias en el transcurso de los años 2004-2011 debido a la reiteración de problemas disciplinarios en los que se sospechaba que el adecuado sentido para su comprensión se lograba al pensar en perspectiva vincular. Es una realidad conocida, que la familia como institución formadora de hijos, atraviesa experiencias actuales de inconsistencias y confusiones sobre el qué hacer diario con sus hijos como así también la institución educativa camina en la incertidumbre crónica y es escenario de múltiples estallidos sociales (Duschatzky & Corea 2002). Aunque el abandono escolar estrictamente se liga a la idea de la interrupción definitiva de la asistencia del alumno a la Institución Educativa Pública, existen desvíos de las trayectorias educativas en el ámbito privado que pasan desapercibidos: los cambios reiterados de colegio por cuestiones de 'mala conducta'. Por esta razón, a la Escuela se le presenta como desafío impostergable propiciar un espacio de pensamiento para la remoción de los obstáculos, asumiéndose como escenario dónde se expresa el mismo, corriéndose del lugar del saber para pensar desde el paradigma de la complejidad. El problema que motiva la investigación gira en torno al observable que a menudo se presenta en los adolescentes, respecto al riesgo de perder su continuidad en la escuela por reiteradas medidas disciplinarias instrumentadas por la Institución. Históricamente el E.O.E. ha planteado estrategias del estilo de prescribir conductas esperables a los padres, derivaciones a profesionales externos y diagnósticos singulares que no proponen alguna alternativa eficaz ante la urgencia del obstáculo. Mediante el estudio de cinco casos representativos por su diversidad, se han realizado entrevistas con el directivo del nivel, padres, alumnos, otros actores institucionales, a profesionales externos y entrevistas vinculares padre/s-hijo. Los objetivos propuestos han sido explorar sobre bibliografía existente sobre la inserción del psicólogo en la Escuela para luego presentar un novedoso dispositivo de intervención fundado en el agotamiento de estrategias tradicionales en el abordaje de alumnos con sistemáticas conductas que transgreden la legalidad escolar. Ha sido significativo encontrar nuevos sentidos sobre el problema devenido obstáculo (Lewkowicz 2004) al mirar la problemática desde el Psicoanálisis Vincular (Berenstein & Puget 1997-2011), cuerpo teórico que revoluciona la lectura de las conductas individuales asociadas a determinaciones intersubjetivas que complementan las intrapsíquicas. Ninguna explicación individual y parcial del problema, ha sobrevivido al desfiladero de la producción vincularLa presente investigación es de carácter cualitativo-exploratorio realizada desde un Equipo de Orientación Escolar (E.O.E.) que funciona en una Escuela de gestión privada católica de la Ciudad de La Plata, provincia de Buenos Aires. La novedad de este trabajo radica en que la pertenencia de un psicólogo a un E.O.E. es poco habitual ya que el cargo de Psicólogo no está previsto en la Dirección General de Escuelas y se comparte el trabajo con otros profesionales -psicopedagogos, asistentes sociales, fonoaudiólogos, médicos y maestros recuperadores- con miradas e intervenciones muy diferentes sobre cuestiones disciplinarias de los alumnos. A partir de diversas demandas -como de iniciativas propias del E.O.E.- hemos realizado intervenciones en el nivel secundario con alumnos y sus familias en el transcurso de los años 2004-2011 debido a la reiteración de problemas disciplinarios en los que se sospechaba que el adecuado sentido para su comprensión se lograba al pensar en perspectiva vincular. Es una realidad conocida, que la familia como institución formadora de hijos, atraviesa experiencias actuales de inconsistencias y confusiones sobre el qué hacer diario con sus hijos como así también la institución educativa camina en la incertidumbre crónica y es escenario de múltiples estallidos sociales (Duschatzky & Corea 2002). Aunque el abandono escolar estrictamente se liga a la idea de la interrupción definitiva de la asistencia del alumno a la Institución Educativa Pública, existen desvíos de las trayectorias educativas en el ámbito privado que pasan desapercibidos: los cambios reiterados de colegio por cuestiones de 'mala conducta'. Por esta razón, a la Escuela se le presenta como desafío impostergable propiciar un espacio de pensamiento para la remoción de los obstáculos, asumiéndose como escenario dónde se expresa el mismo, corriéndose del lugar del saber para pensar desde el paradigma de la complejidad. El problema que motiva la investigación gira en torno al observable que a menudo se presenta en los adolescentes, respecto al riesgo de perder su continuidad en la escuela por reiteradas medidas disciplinarias instrumentadas por la Institución. Históricamente el E.O.E. ha planteado estrategias del estilo de prescribir conductas esperables a los padres, derivaciones a profesionales externos y diagnósticos singulares que no proponen alguna alternativa eficaz ante la urgencia del obstáculo. Mediante el estudio de cinco casos representativos por su diversidad, se han realizado entrevistas con el directivo del nivel, padres, alumnos, otros actores institucionales, a profesionales externos y entrevistas vinculares padre/s-hijo. Los objetivos propuestos han sido explorar sobre bibliografía existente sobre la inserción del psicólogo en la Escuela para luego presentar un novedoso dispositivo de intervención fundado en el agotamiento de estrategias tradicionales en el abordaje de alumnos con sistemáticas conductas que transgreden la legalidad escolar. Ha sido significativo encontrar nuevos sentidos sobre el problema devenido obstáculo (Lewkowicz 2004) al mirar la problemática desde el Psicoanálisis Vincular (Berenstein & Puget 1997-2011), cuerpo teórico que revoluciona la lectura de las conductas individuales asociadas a determinaciones intersubjetivas que complementan las intrapsíquicas. Ninguna explicación individual y parcial del problema, ha sobrevivido al desfiladero de la producción vincular