812 resultados para Adult Deaths


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The goal of this article is to introduce the reader to contemporary adult multilingual acquisition research within generative linguistics. In much the same way as monolingual and bilingual acquisition studies are approached within this paradigm, generative multilingual research focuses primarily on the psycholinguistic and cognitive aspects of the acquisition process. Herein, we critically present a panoramic view of the research questions and empirical work that have dominated this nascent field, taking the reader through several interrelated epistemological discussions that are at the vanguard of contemporary multilingual morphosyntax work. We finish this article with some thoughts looking towards the near future of adult multilingual acquisition studies.

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Within generative L2 acquisition research there is a longstanding debate as to what underlies observable differences in L1/L2 knowledge/ performance. On the one hand, Full Accessibility approaches maintain that target L2 syntactic representations (new functional categories and features) are acquirable (e.g., Schwartz & Sprouse, 1996). Conversely, Partial Accessibility approaches claim that L2 variability and/or optionality, even at advanced levels, obtains as a result of inevitable deficits in L2 narrow syntax and is conditioned upon a maturational failure in adulthood to acquire (some) new functional features (e.g., Beck, 1998; Hawkins & Chan, 1997; Hawkins & Hattori, 2006; Tsimpli & Dimitrakopoulou, 2007). The present study tests the predictions of these two sets of approaches with advanced English learners of L2 Brazilian Portuguese (n = 21) in the domain of inflected infinitives. These advanced L2 learners reliably differentiate syntactically between finite verbs, uninflected and inflected infinitives, which, as argued, only supports Full Accessibility approaches. Moreover, we will discuss how testing the domain of inflected infinitives is especially interesting in light of recent proposals that Brazilian Portuguese colloquial dialects no longer actively instantiate them (Lightfoot, 1991; Pires, 2002, 2006; Pires & Rothman, 2009; Rothman, 2007).

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Native-like use of preterit and imperfect morphology in all contexts by English learners of L2 Spanish is the exception rather than the rule, even for successful learners. Nevertheless, recent research has demonstrated that advanced English learners of L2 Spanish attain a native-like morphosyntactic competence for the preterit/imperfect contrast, as evidenced by their native-like knowledge of associated semantic entailments (Goodin-Mayeda and Rothman 2007, Montrul and Slabakova 2003, Slabakova and Montrul 2003, Rothman and Iverson 2007). In addition to an L2 disassociation of morphology and syntax (e.g., Bruhn de Garavito 2003, Lardiere 1998, 2000, 2005, Prévost and White 1999, 2000, Schwartz 2003), I hypothesize that a system of learned pedagogical rules contributes to target-deviant L2 performance in this domain through the most advanced stages of L2 acquisition via its competition with the generative system. I call this hypothesis the Competing Systems Hypothesis. To test its predictions, I compare and contrast the use of the preterit and imperfect in two production tasks by native, tutored (classroom), and naturalistic learners of L2 Spanish.

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In this communication, we describe a new method which has enabled the first patterning of human neurons (derived from the human teratocarcinoma cell line (hNT)) on parylene-C/silicon dioxide substrates. We reveal the details of the nanofabrication processes, cell differentiation and culturing protocols necessary to successfully pattern hNT neurons which are each key aspects of this new method. The benefits in patterning human neurons on silicon chip using an accessible cell line and robust patterning technology are of widespread value. Thus, using a combined technology such as this will facilitate the detailed study of the pathological human brain at both the single cell and network level.

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Objectives To model the impact on chronic disease of a tax on UK food and drink that internalises the wider costs to society of greenhouse gas (GHG) emissions and to estimate the potential revenue. Design An econometric and comparative risk assessment modelling study. Setting The UK. Participants The UK adult population. Interventions Two tax scenarios are modelled: (A) a tax of £2.72/tonne carbon dioxide equivalents (tCO2e)/100 g product applied to all food and drink groups with above average GHG emissions. (B) As with scenario (A) but food groups with emissions below average are subsidised to create a tax neutral scenario. Outcome measures Primary outcomes are change in UK population mortality from chronic diseases following the implementation of each taxation strategy, the change in the UK GHG emissions and the predicted revenue. Secondary outcomes are the changes to the micronutrient composition of the UK diet. Results Scenario (A) results in 7770 (95% credible intervals 7150 to 8390) deaths averted and a reduction in GHG emissions of 18 683 (14 665to 22 889) ktCO2e/year. Estimated annual revenue is £2.02 (£1.98 to £2.06) billion. Scenario (B) results in 2685 (1966 to 3402) extra deaths and a reduction in GHG emissions of 15 228 (11 245to 19 492) ktCO2e/year. Conclusions Incorporating the societal cost of GHG into the price of foods could save 7770 lives in the UK each year, reduce food-related GHG emissions and generate substantial tax revenue. The revenue neutral scenario (B) demonstrates that sustainability and health goals are not always aligned. Future work should focus on investigating the health impact by population subgroup and on designing fiscal strategies to promote both sustainable and healthy diets.

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Whilst not true in all cases, the microbial communities that chronically infect the airways of patients with CF can vary little over a year despite antibiotic perturbation. The species present tended to vary more between than within subjects, suggesting that each CF airway infection is unique, with relatively stable and resilient bacterial communities. The inverse relationship between community richness and disease severity is similar to findings reported in other mucosal infections.

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One potential source of heterogeneity within autism spectrum conditions (ASC) is language development and ability. In 80 high-functioning male adults with ASC, we tested if variations in developmental and current structural language are associated with current neuroanatomy. Groups with and without language delay differed behaviorally in early social reciprocity, current language, but not current autistic features. Language delay was associated with larger total gray matter (GM) volume, smaller relative volume at bilateral insula, ventral basal ganglia, and right superior, middle, and polar temporal structures, and larger relative volume at pons and medulla oblongata in adulthood. Despite this heterogeneity, those with and without language delay showed significant commonality in morphometric features when contrasted with matched neurotypical individuals (n = 57). In ASC, better current language was associated with increased GM volume in bilateral temporal pole, superior temporal regions, dorsolateral fronto-parietal and cerebellar structures, and increased white matter volume in distributed frontal and insular regions. Furthermore, current language–neuroanatomy correlation patterns were similar across subgroups with or without language delay. High-functioning adult males with ASC show neuroanatomical variations associated with both developmental and current language characteristics. This underscores the importance of including both developmental and current language as specifiers for ASC, to help clarify heterogeneity.

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This paper describes the methodology used to compile a corpus called MorphoQuantics that contains a comprehensive set of 17,943 complex word types extracted from the spoken component of the British National Corpus (BNC). The categorisation of these complex words was derived primarily from the classification of Prefixes, Suffixes and Combining Forms proposed by Stein (2007). The MorphoQuantics corpus has been made available on a website of the same name; it lists 554 word-initial and 281 word-final morphemes in English, their etymology and meaning, and records the type and token frequencies of all the associated complex words containing these morphemes from the spoken element of the BNC, together with their Part of Speech. The results show that, although the number of word-initial affixes is nearly double that of word-final affixes, the relative number of each observed in the BNC is very similar; however, word-final affixes are more productive in that, on average, the frequency with which they attach to different bases is three times that of word-initial affixes. Finally, this paper considers how linguists, psycholinguists and psychologists may use MorphoQuantics to support their empirical work in first and second language acquisition, and clinical and educational research.

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This paper aims to consider whether there is a link between youth happiness levels and adult life satisfaction. Our results are unequivocal that such a link exists both because demographic and socio-economic conditions are persistent over a lifetime and also because there is a persistence in personality effects. To test this link, we estimate a model of happiness for a sample of young people. This model provides us with a range of variables measuring socio-economic effects and personality effects amongst young people. These variables are then included in the adult life satisfaction model. The model is estimated using data from the British Household Panel Survey for 1994–2008. In addition to childhood happiness levels influencing adult life satisfaction significantly, we also find that the youthful personality trait for happiness has a larger effect on adult life satisfaction than demographic and socio-economic conditions.

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Background Anorexia Nervosa (AN) is a highly life-threatening disorder that is extremely difficult to treat. There is evidence that family-based therapies are effective for adolescent AN, but no treatment has been proven to be clearly effective for adult AN. The methodological challenges associated with studying the disorder have resulted in recommendations that new treatments undergo preliminary testing prior to being evaluated in a randomized clinical trial. The aim of this study was to provide preliminary evidence on the effectiveness of a treatment program based on a novel adaptation of Dialectical Behavior Therapy (DBT) for adult Anorexia Nervosa (Radically Open-DBT; RO-DBT) that conceptualizes AN as a disorder of overcontrol. Methods Forty-seven individuals diagnosed with Anorexia Nervosa-restrictive type (AN-R; mean admission body mass index = 14.43) received the adapted DBT inpatient program (mean length of treatment = 21.7 weeks). Results Seventy-two percent completed the treatment program demonstrating substantial increases in body mass index (BMI; mean change in BMI = 3.57) corresponding to a large effect size (d = 1.91). Thirty-five percent of treatment completers were in full remission, and an additional 55% were in partial remission resulting in an overall response rate of 90%. These same individuals demonstrated significant and large improvements in eating-disorder related psychopathology symptoms (d = 1.17), eating disorder-related quality of life (d = 1.03), and reductions in psychological distress (d = 1.34). Conclusions RO-DBT was associated with significant improvements in weight gain, reductions in eating disorder symptoms, decreases in eating-disorder related psychopathology and increases in eating disorder-related quality of life in a severely underweight sample. These findings provide preliminary support for RO-DBT in treating AN-R suggesting the importance of further evaluation examining long-term outcomes using randomized controlled trial methodology.

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As a model for brain inflammation we previously studied transcriptional profiles of tumor necrosis factor-alpha (TNF)treated U373 astroglioma cells. In previous work we were able to demonstrate that the chemokine monocyte chemoattractant protein-1 (MCP-1, SCYA2, CCL2, MCAF) expression in U373 cells was inducible by TNF-alpha treatment. Demonstrably MCP-1 mRNA and protein expression in U373 cells was sustainable over time and at the highest level of all genes analyzed (Schwamborn et al., BMC Genomics 4, 46, 2003). In the hematopoietic system MCP-1 is a CC chemokine that attracts monocytes, memory T lymphocytes, and natural killer cells. In search of further functions in brain inflammation we tested the hypothesis that MCP-1 acts as a chemokine on neural stem cells. Here we report that MCP-1 activates the migration capacity of rat-derived neural stem cells. The migration of stem cells in a Boyden chamber analysis was elevated after stimulation with MCP-1. Time-lapse video microscopy visualized the migration of single stem cells from neurospheres in MCP-1-treated cultures, whereas untreated cultures depicted no migration at all, but showed signs of sprouting. Expression of the MCP-1 receptor CCR2 in neurosphere cultures was verified by RT-PCR and immunofluorescence microscopy. Supernatants from TNF-treated U373 cells also induced migration of neural stem cells.

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Neural stem cells are precursors of neurons and glial cells. During brain development, these cells proliferate, migrate and differentiate into specific lineages. Recently neural stem cells within the adult central nervous system were identified. Informations are now emerging about regulation of stem cell proliferation, migration and differentiation by numerous soluble factors such as chemokines and cytokines. However, the signal transduction mechanisms downstream of these factors are less clear. Here, we review potential evidences for a novel central role of the transcription factor nuclear factor kappa B (NF-kappaB) in these crucial signal transduction processes. NF-kappaB is an inducible transcription factor detected in neurons, glia and neural stem cells. NF-kappaB was discovered by David Baltimore's laboratory as a transcription factor in lymphocytes. NF-kappaB is involved in many biological processes such as inflammation and innate immunity, development, apoptosis and anti-apoptosis. It has been recently shown that members of the NF-kappaB family are widely expressed by neurons, glia and neural stem cells. In the nervous system, NF-kappaB plays a crucial role in neuronal plasticity, learning, memory consolidation, neuroprotection and neurodegeneration. Recent data suggest an important role of NF-kappaB on proliferation, migration and differentiation of neural stem cells. NF-kappaB is composed of three subunits: two DNA-binding and one inhibitory subunit. Activation of NF-kappaB takes place in the cytoplasm and results in degradation of the inhibitory subunit, thus enabling the nuclear import of the DNA-binding subunits. Within the nucleus, several target genes could be activated. In this review, we suggest a model explaining the multiple action of NF-kappaB on neural stem cells. Furthermore, we discuss the potential role of NF-kappaB within the so-called brain cancer stem cells.

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BACKGROUND: Brain inflammation has been recognized as a complex phenomenon with numerous related aspects. In addition to the very well-described neurodegenerative effect of inflammation, several studies suggest that inflammatory signals exert a potentially positive influence on neural stem cell proliferation, migration and differentiation. Tumor necrosis factor alpha (TNF-alpha) is one of the best-characterized mediators of inflammation. To date, conclusions about the action of TNF on neural stem or progenitor cells (NSCs, NPCs) have been conflicting. TNF seems to activate NSC proliferation and to inhibit their differentiation into NPCs. The purpose of the present study was to analyze the molecular signal transduction mechanisms induced by TNF and resulting in NSC proliferation. RESULTS: Here we describe for the first time the TNF-mediated signal transduction cascade in neural stem cells (NSCs) that results in increased proliferation. Moreover, we demonstrate IKK-alpha/beta-dependent proliferation and markedly up-regulated cyclin D1 expression after TNF treatment. The significant increase in proliferation in TNF-treated cells was indicated by increased neurosphere volume, increased bromodeoxyuridin (BrdU) incorporation and a higher total cell number. Furthermore, TNF strongly activated nuclear factor-kappa B (NF-kappaB) as measured by reporter gene assays and by an activity-specific antibody. Proliferation of control and TNF-treated NSCs was strongly inhibited by expression of the NF-kappaB super-repressor IkappaB-AA1. Pharmacological blockade of IkappaB ubiquitin ligase activity led to comparable decreases in NF-kappaB activity and proliferation. In addition, IKK-beta gene product knock-down via siRNA led to diminished NF-kappaB activity, attenuated cyclin D1 expression and finally decreased proliferation. In contrast, TGFbeta-activated kinase 1 (TAK-1) is partially dispensable for TNF-mediated and endogenous proliferation. Understanding stem cell proliferation is crucial for future regenerative and anti-tumor medicine. CONCLUSION: TNF-mediated activation of IKK-beta resulted in activation of NF-kappaB and was followed by up-regulation of the bona-fide target gene cyclin D1. Activation of the canonical NF-kappaB pathway resulted in strongly increased proliferation of NSCs.