677 research outputs found

    Examination of the Effects of Speech Disorders on Juvenile Delinquency and the Potential Benefits of Speech Therapy for Offenders

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    In the United States, there are currently over 50,000 juveniles housed in youth confinement facilities for delinquent acts ranging from truancy to murder. To decrease that number, it is pertinent to identify possible risk factors of juvenile delinquency, but also to establish impactful preventative strategies as well as reactive solutions. Speech disorders and speech differences have been identified as potential risk factors for juvenile delinquency. Having a speech disorder/difference has an undeniable impact on a child’s life, with potentially negative impacts ranging from poor engagement with school and bullying—both risk factors in themselves for juvenile delinquency. Unsurprisingly, researchers have found that an overwhelmingly large number of juvenile offenders show signs of speech disorders. The extensive research—which is detailed and evaluated in this literature review—demonstrates that having a speech disorder is a risk factor of becoming a juvenile delinquent. Due to this, it is imperative that possible treatment and prevention strategies are identified to help prevent these juveniles from entering the juvenile justice system, and barring that, prevent them from recidivating once released. This white paper aims to inform and present solutions to juvenile justice administrators regarding these issues, as well as serve as a means to educate the general public regarding these issues

    Modelling coevolutionary dynamics in heterogeneous SI epidemiological systems across scales

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    We develop a new structured compartmental model for the coevolutionary dynamics between susceptible and infectious individuals in heterogeneous SI epidemiological systems. In this model, the susceptible compartment is structured by a continuous variable that represents the level of resistance to infection of susceptible individuals, while the infectious compartment is structured by a continuous variable that represents the viral load of infectious individuals. We first formulate an individual-based model wherein the dynamics of single individuals is described through stochastic processes, which permits a fine-grain representation of individual dynamics and captures stochastic variability in evolutionary trajectories amongst individuals. Next we formally derive the mesoscopic counterpart of this model, which consists of a system of coupled integro-differential equations for the population density functions of susceptible and infectious individuals. Then we consider an appropriately rescaled version of this system and we carry out formal asymptotic analysis to derive the corresponding macroscopic model, which comprises a system of coupled ordinary differential equations for the proportions of susceptible and infectious individuals, the mean level of resistance to infection of susceptible individuals, and the mean viral load of infectious individuals. Overall, this leads to a coherent mathematical representation of the coevolutionary dynamics between susceptible and infectious individuals across scales. We provide well-posedness results for the mesoscopic and macroscopic models, and we show that there is excellent agreement between analytical results on the long-time behaviour of the components of the solution to the macroscopic model, the results of Monte Carlo simulations of the individual-based model, and numerical solutions of the macroscopic model

    TOSSICITA’ ED EFFETTI DELLA METANFETAMINA

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    La metanfetamina (MA) ù una sostanza d’abuso che induce una varietà di effetti tossici a livello centrale tra cui ansia, confusione e allucinazioni. L’esposizione alla MA risulta neurotossica per le cellule dopaminergiche del sistema nigro-striatale. Infatti la MA induce un immediato massivo rilascio di dopamina (DA) in striato, che produce stress ossidativo, portando a degenerazione i terminali dopaminergici striatali e alla conseguente riduzione dei livelli di DA in striato. I corpi cellulari della substantia nigra pars compacta (SNpc) vengono distrutti per dosi elevate di MA. Prima di andare incontro a morte nel loro citoplasma ù possibile osservare strutture multi lamellari e inclusioni positive per proteine quali l’ubiquitina e l’alfa-sinucleina. Quest’ultima proteina in presenza di specie reattive dell’ossigeno forma aggregati, tossici per la cellula. Inclusioni citoplasmatiche positive per l’-sinucleina e per le proteine del sistema Ubiquitina Proteasoma (UP) sono presenti anche nella malattia degenerativa nota come malattia di Parkinson (MdP) che pertanto viene parzialmente mimata dalla tossicità da MA

    Complexidade textual em textos de divulgação sobre a Doença de Parkinson e seu impacto para a tradução : um estudo baseado em corpus

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    A doença de Parkinson (DP) Ă© um distĂșrbio progressivo do sistema nervoso central que afeta o movimento e, muitas vezes, provoca tremores. AlĂ©m de nĂŁo ter cura, pesquisadores preveem que no futuro o nĂșmero de pessoas com a doença irĂĄ aumentar, devido ao aumento da expectativa de vida. Como, em geral, cabe aos familiares sem preparo assumir a função de cuidadores, a internet acaba desempenhando o importante papel de servir como fonte de instrução para essas pessoas. AlĂ©m disso, essa rede pode despertar no prĂłprio paciente o desejo de saber mais sobre a sua doença, os tratamentos disponĂ­veis e os estudos que estĂŁo sendo realizados. Por esse motivo, um nĂșmero significativo de websites especializados, criados por estudiosos, doutores e especialistas, possuem o intuito de oferecer informaçÔes sobre essa doença. Apesar do aumento do uso da internet como forma de busca de informaçÔes sobre doenças, basta uma simples pesquisa em dissertaçÔes e artigos acadĂȘmicos para notarmos como hĂĄ poucas pesquisas sobre a complexidade textual desses websites. Sendo assim, nosso objetivo, nesta monografia, Ă© analisar a complexidade textual de textos de divulgação da fundação Michael J. Fox e da Parkinson's UK, suas traduçÔes para o portuguĂȘs e cinco websites de associaçÔes de Parkinson escritos originalmente em PortuguĂȘs. Utilizando a metodologia da LinguĂ­stica de Corpus, nosso intuito Ă© verificar se os textos originais em portuguĂȘs e em inglĂȘs (estadunidense e britĂąnico) sĂŁo adequados para o seu pĂșblico alvo, e se houve alteração na complexidade textual das traduçÔes para o portuguĂȘs. Para isso, concentramo-nos na voz passiva analĂ­tica – considerada critĂ©rio de complexidade textual –, presente no corpus de estudo, relacionando seu uso com os resultados do Ă­ndice Flesch. Apoiamo-nos na teoria funcionalista da tradução (NORD 2006, 2007 e 2012) para analisarmos as traduçÔes dos textos para o portuguĂȘs, pois essa teoria tem como um dos focos o pĂșblico-alvo da tradução. Por fim, apresentamos o nĂșmero de ocorrĂȘncias de voz passiva dos textos originais e suas traduçÔes. Quando comparadas com os textos originais, as traduçÔes dos textos dos websites das fundaçÔes Michael J.Fox e Parkinson's UK tiveram um aumento de sentenças na voz passiva, indicando, portanto, um aumento da complexidade textual, ao menos no que tange a esse quesito.Parkinson’s disease (PD) is a progressive nervous system disorder that affects movement and causes tremors. PD does not have a cure and researchers predict that the number of people with Parkinson will grow more in the future, due to the fact that people are living longer. Often, it is a relative without training that becomes a caregiver. Thus, the information available on the internet is used as a kind of guide. Also, the patient might want to learn more about his or her disease, treatments and studies being developed it. For this reason, an expressive number of specialized websites, created by researchers, doctor and specialists, are being developed to provide information about PD. However, although the number of people who seeks online information about the disease is increasing exponentially, few are the dissertations and thesis that focus on the subject of textual complexity on these websites. Therefore, my aim is to investigate the textual complexity of the informative texts of Michael J. Fox foundation and Parkinson's UK websites, their translations to Portuguese, and five websites of Parkinson associations, originally written in Portuguese. My objective is to verify if the original texts in Portuguese and English (American and British) are suitable for the target public. Also, I want to determine if there was any change in terms of textual complexity in the translated texts. In order to do that, I analyzed sentences in the passive voice in analytical position in the study corpora – since it is considered a criterion of textual complexity –, relating them with the scores of the Flesch index score. This study draws on the functional theory (NORD 2006, 2007 e 2012) to analyze the Portuguese translations, because this theory has the target audience of a translation text as focus. Lastly, we present the number of occurrences of the passive voice in both the original and the translated texts. When the translations are confronted with the originals texts, I could observe an increase in the use of passive voice in both the translations of the websites Michael J.Fox and Parkinson's UK texts, which leads to higher complexity, at least in what regards this criterion

    High-intensity exercise training induces morphological and biochemical changes in skeletal muscle

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    Skeletal muscle shows an elevated plasticity and can adapt its metabolic and contractile properties in response to a variety of stimuli such as physical exercise. This implies a series of biochemical and morphological changes in the recruited muscle, in order to produce the more appropriate functional response dependent on the specific stimulation. To determine the effective role of physical exercise in the muscle plasticity, in the present study we investigated the effect of two different exercise protocols on fiber composition and metabolism of two specific muscles of mice: the quadriceps -a fast-twitch muscle- and the gastrocnemius -a typical slow-twitch muscle. Mice were run daily on a motorized treadmill for 8 weeks, at a velocity corresponding to 60% (low-intensity exercise) or 90% (high-intensity exercise) of the maximal running velocity previously determined by an incremental exercise test. We found that at the end of training the body weight was significantly increased in highintensity exercise mice (18.2 ± 1.4 %) compared to low-intensity exercise (8.7 ± 0.6 %) and control (12.7 ± 0.5 %) groups, and it was lesser in low-intensity exercise mice compared to controls. In contrast, the food intake of both exercise training mice was greater compared to control group. Whereas low-intensity exercise mice, despite consumed significantly more food compared to control mice, increased the weight lesser, the weight increase of high-intensity exercise mice, that consumed significantly more food compared to other experimental groups, was significantly greater. These effects were accompanied by a progressive reduction in blood lactate levels at the end of training in both the exercised mice compared with controls; in particular, blood lactate levels after highintensity exercise were significantly lower than those measured in low-intensity exercise mice. Moreover, in the present study we demonstrated that high-intensity exercise training produced a significant increase in the expression of mitochondrial complex enzymes (significant for the enzymes corresponding to the Complex IV, II and I of mitochondrial chain) both in gastrocnemius and quadriceps muscle, compared with controls. These changes were associated with an increase in the amount of slow fibers in both these muscle of high-intensity exercise mice. No changing in the expression of mitochondrial enzymes and in the percentage of slow fibers were found in low-intensity exercise mice

    Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light

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    The prevalent view today is that schizophrenia is a syndrome rather than a specific disease. Liability to schizophrenia is highly heritable. It appears that multiple genetic and environmental factors operate together to push individuals over a threshold into expressing the characteristic clinical picture. One environmental factor which has been curiously neglected is the evidence that certain drugs can induce schizophrenia-like psychosis. In the last 60 years, improved understanding of the relationship between drug abuse and psychosis has contributed substantially to our modern view of the disorder suggesting that liability to psychosis in general, and to schizophrenia in particular, is distributed trough the general population in a similar continuous way to liability to medical disorders such as hypertension and diabetes. In this review we examine the main hypotheses resulting from the link observed between the most common psychotomimetic drugs (lysergic acid diethylamide, amphetamines, cannabis, phencyclidine) and schizophrenia

    Morphological characterization of a single knock out double transgenic mouse model of spinal muscle atrophy

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    Spinal muscular atrophy (SMA) is a neurogenetic autosomal recessive disorder characterized by degeneration of lower motor neurons associated with muscle atrophy and paralysis. Due to a lack of an in depth knowledge on the molecular mechanisms and fine neuropathology of SMA, validation of appropriate animal models is key in fostering SMA research. Recent studies set up an animal model showing long survival and slow disease progression. This model is knocked out for mouse SMN (Smn−/−) gene and carries a human mutation of the SMN1 gene (SMN1A2G), along with human SMN2 gene. In the present study we used this knockout double transgenic mouse as a SMA III model, to characterize the spinal cord pathology along with motor deficit at prolonged survival times (18 months). This long time interval (i.e. up to 535 days) was never analyzed before especially concerning specific motor tasks. We found that the delayed disease progression was likely to maintain fair motor activity despite a dramatic loss of large motor neurons (44.77%). At this stage, spared motor neurons showed significant cell body enlargement. Moreover, similar to what was described in patients affected by SMA we found neuronal heterotopy in the anterior white matter. Motor neuron degeneration was accompanied by the loss of SMN protein in the spinal cord. In summary, the present study validates over a long time period a SMA III mouse model showing neuropathology reminiscent of human patients and provide a useful experimental model to probe novel therapeutic strategies
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