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Previous research has shown that children demonstrate similar sentence processing reflexes to those observed in adults, but they have difficulties revising an erroneous initial interpretation when they process garden-path sentences, passives, and wh-questions. We used the visual-world paradigm to examine children's use of syntactic and non-syntactic information to resolve syntactic ambiguity by extending our understanding of number features as a cue for interpretation to which-subject and which-object questions. We compared children's and adults’ eye-movements to understand how this information shapes children's commitment to and revision of possible interpretations of these questions. The results showed that English-speaking adults and children both exhibit an initial preference to interpret an object-which question as a subject question. While adults quickly override this preference, children take significantly longer, showing an overall processing difficulty for object questions. Crucially, their recovery from an initially erroneous interpretation is speeded when disambiguating number agreement features are present.
Language processing plays a crucial role in language development, providing the ability to assign structural representations to input strings (e.g., Fodor, 1998). In this paper we aim at contributing to the study of children's processing routines, examining the operations underlying the auditory processing of relative clauses in children compared to adults. English-speaking children (6;0–8;11) and adults participated in the study, which employed a self-paced listening task with a final comprehension question. The aim was to determine (i) the role of number agreement in object relative clauses in which the subject and object NPs differ in terms of number properties, and (ii) the role of verb morphology (active vs. passive) in subject relative clauses. Even though children's off-line accuracy was not always comparable to that of adults, analyses of reaction times results support the view that children have the same structural processing reflexes observed in adults.
Geometric uncertainties limit the accuracy of three-dimensional conformal radiotherapy treatments. This study aims to evaluate typical random and systematic set-up errors and analyse the impact of no action level (NAL) correction protocol on systematic set-up errors and clinical target volume (CTV)–planning target volume (PTV) margins.
Materials and methods
A total 668 pairs of orthogonal electronic portal images were compared with digitally reconstructed radiographs from computed tomography planning scans for 100 patients consecutively treated during 2011. Patients were divided into groups depending on the treated anatomical region. Patient-specific and population random and systematic set-up errors were calculated. Impact of application of NAL correction protocol on systematic set-up errors and CTV–PTV expansions were evaluated.
Results
Population set-up errors resulted from about 1 mm in head and neck to 2–3 mm in prostate, rectum, lung, breast and gynaecological districts. Patient-specific systematic set-up errors were higher for breast and gynaecological districts and application of NAL correction protocol gave significant reductions, even higher than 30%. Calculated CTV–PTV margins ranged from 10 mm on left–right direction for prostate to 20 mm on superior–inferior direction for lung.
Conclusions
Set-up errors resulted reasonably controlled and application of NAL correction protocol could further improve the level of accuracy. However, the NAL application alone did not seem to add any substantial benefit on CTV–PTV total margins without the adoption of corrective strategies to reduce other important uncertainties limiting accuracy of three-dimensional conformal radiotherapy.
In this introductory chapter, a classification of the etiology of epilepsy is proposed, and this forms the basis of the sectional divisions in the rest of the book. In constructing such a classification, it is necessary to take cognisance of five particular points: Definitions, Multifactorial cause of epilepsy, Cause versus mechanism, Focal versus generalized epilepsy and Flexibility. The chapter presents the definitions of the epilepsies which are divided into four main categories: Idiopathic epilepsy, Symptomatic epilepsy, Provoked epilepsy and Cryptogenic epilepsy. The ILAE Commission recommended that a classification should be a database forming the basis of a diagnostic manual; the etological schema in this chapter should be viewed as such for instance in relation to the benign focal epilepsies or even the idiopathic generalized epilepsies. It is clear that in the future, as further knowledge accrues, some of these epilepsies may be reclassified and revised.
There is often disagreement about what constitutes "epileptogenesis" and what is meant by "symptomatic epilepsy". In considering various mechanistic hypotheses, investigators have often divided potential participants in epileptogenesis into two categories: changes that are a direct result of the insult and serve to initiate the epileptogenic process, and processes that give rise to an altered brain condition that is capable of generating/supporting aberrant (hyperexcitable, hypersynchronous) neuronal discharge. These two sets of mechanisms may overlap (or turn out to be functionally inseparable). However, given the assumed temporal distinction (immediate vs. delayed) between these two categories of processes, it makes some sense to discuss them separately. The need to identify mechanisms of epileptogenesis in symptomatic epilepsies arises from a conviction that a better understanding of these processes will lead to effective antiepileptogenic therapies.
This chapter provides an overview of the known and unknown heritability of the pure epilepsies. The research method used to detect a causal gene variant varies according to the relative risk conferred by the risk allele and its frequency in the population. The considerable progress in identifying genes for Mendelian epilepsy is in sharp contrast to the absence of progress in identifying genetic susceptibility to more common sporadic forms of the disease. The alternative hypothesis to the common variant explanation of a common disease like epilepsy proposes that instead of a few common variants, a large number of rare variants with large effects underlie genetic susceptibility. Exciting developments in very-high-throughput DNA sequencing technology will soon offer the potential for whole-genome resequencing that will ultimately define all the rare variant contributions to epilepsy. The challenge will be how to translate these understandings to better therapies and improved patient care.
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