1,436 research outputs found

    Technology to Increase Peer Interactions in Preschool

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    Adding technology to the preschool classroom without interfering with social interactions is a dilemma for educators. Peer interactions are an important developmental goal in preschool age students. Increased pressure to include technology in education at earlier ages is often viewed as a hindrance to social interactions in play-based curriculum, with many educators feeling unprepared in the methods to incorporate technology. The goal of this literature review is to analyze current research to discover methods that can increase social interactions among peers with the addition of technology tools in the preschool classroom. This review looked at forty-seven studies of social interactions in children and technology uses in classrooms. Examination of this research showed the importance of social interactions, the barriers for adding technology in early childhood classrooms, and techniques in which technology use been used to show social benefits. The research demonstrates that technology has the potential to increase social interactions among preschool peers. Based on these findings, it is recommended that educators receive ongoing professional development in methods of adding technology into the social curriculum. Further research is needed to develop the most effect procedures for educator education

    Integrating genealogical and dynamical modelling to infer escape and reversion rates in HIV epitopes

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    The rates of escape and reversion in response to selection pressure arising from the host immune system, notably the cytotoxic T-lymphocyte (CTL) response, are key factors determining the evolution of HIV. Existing methods for estimating these parameters from cross-sectional population data using ordinary differential equations (ODE) ignore information about the genealogy of sampled HIV sequences, which has the potential to cause systematic bias and over-estimate certainty. Here, we describe an integrated approach, validated through extensive simulations, which combines genealogical inference and epidemiological modelling, to estimate rates of CTL escape and reversion in HIV epitopes. We show that there is substantial uncertainty about rates of viral escape and reversion from cross-sectional data, which arises from the inherent stochasticity in the evolutionary process. By application to empirical data, we find that point estimates of rates from a previously published ODE model and the integrated approach presented here are often similar, but can also differ several-fold depending on the structure of the genealogy. The model-based approach we apply provides a framework for the statistical analysis of escape and reversion in population data and highlights the need for longitudinal and denser cross-sectional sampling to enable accurate estimate of these key parameters

    How peer mentoring fosters graduate attributes

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    The most common approach to foster graduate attributes is to teach them in the curriculum of a bachelor’s degree. However, it is difficult to include every graduate attribute in every degree. In this article we consider how co-curricular peer mentoring might provide an additional approach. We examine a case study of the mentors of the Peer Assisted Study Sessions (PASS) programme at a research-intensive university in New Zealand, and we examine the process by which they developed graduate attributes. PASS mentors reported that they developed a range of graduate attributes such as communication, critical thinking, and ethical responsibility, due to the extra responsibility and leadership involved in being a mentor in an authentic work environment. We argue that co-curricular programmes such as PASS can provide useful additional opportunities for students to acquire and develop graduate attributes. While not all students will be able to participate as PASS mentors, we also argue that our findings can inform other programmes for fostering graduate attributes. If these programmes offer authentic responsibilities to participating students, they may be more effective at fostering graduate attributes

    Insights into the Evolution and Emergence of a Novel Infectious Disease

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    Many zoonotic, novel infectious diseases in humans appear as sporadic infections with spatially and temporally restricted outbreaks, as seen with influenza A(H5N1). Adaptation is often a key factor for successfully establishing sustained human-to-human transmission. Here we use simple mathematical models to describe different adaptation scenarios with particular reference to spatial heterogeneity within the human population. We present analytical expressions for the probability of emergence per introduction, as well as the waiting time to a successful emergence event. Furthermore, we derive general analytical results for the statistical properties of emergence events, including the probability distribution of outbreak sizes. We compare our analytical results with a stochastic model, which has previously been studied computationally. Our results suggest that, for typical connection strengths between communities, spatial heterogeneity has only a weak effect on outbreak size distributions, and on the risk of emergence per introduction. For example, if or larger, any village connected to a large city by just ten commuters a day is, effectively, just a part of the city when considering the chances of emergence and the outbreak size distribution. We present empirical data on commuting patterns and show that the vast majority of communities for which such data are available are at least this well interconnected. For plausible parameter ranges, the effects of spatial heterogeneity are likely to be dominated by the evolutionary biology of host adaptation. We conclude by discussing implications for surveillance and control of emerging infections

    No evidence for competition between cytotoxic T-lymphocyte responses in HIV-1 infection

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    Strong competition between cytotoxic T-lymphocytes (CTLs) specific for different epitopes in human immunodeficiency virus (HIV) infection would have important implications for the design of an HIV vaccine. To investigate evidence for this type of competition, we analysed CTL response data from 97 patients with chronic HIV infection who were frequently sampled for up to 96 weeks. For each sample, CTL responses directed against a range of known epitopes in gag, pol and nef were measured using an enzyme-linked immunospot assay. The Lotka–Volterra model of competition was used to predict patterns that would be expected from these data if competitive interactions materially affect CTL numbers. In this application, the model predicts that when hosts make responses to a larger number of epitopes, they would have diminished responses to each epitope and that if one epitope-specific response becomes dramatically smaller, others would increase in size to compensate; conversely if one response grows, others would shrink. Analysis of the experimental data reveals results that are wholly inconsistent with these predictions. In hosts who respond to more epitopes, the average epitope-specific response tends to be larger, not smaller. Furthermore, responses to different epitopes almost always increase in unison or decrease in unison. Our findings are therefore inconsistent with the hypothesis that there is competition between CTL responses directed against different epitopes in HIV infection. This suggests that vaccines that elicit broad responses would be favourable because they would direct a larger total response against the virus, in addition to being more robust to the effects of CTL escape

    Nine challenges in modelling the emergence of novel pathogens.

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    Studying the emergence of novel infectious agents involves many processes spanning host species, spatial scales, and scientific disciplines. Mathematical models play an essential role in combining insights from these investigations and drawing robust inferences from field and experimental data. We describe nine challenges in modelling the emergence of novel pathogens, emphasizing the interface between models and data.We acknowledge support from the Research and Policy for Infectious Disease Dynamics (RAPIDD) programme of the Science and Technology Directory, Department of Homeland Security, and Fogarty International Center, National Institutes of Health. JLS was also supported by the National Science Foundation (EF-0928987 and OCE-1335657) and the De Logi Chair in Biological Sciences. SF was supported by a UK Medical Research Council Career Development Award in Biostatistics. SR was supported by: Wellcome Trust Project Award 093488/Z/10/Z; R01 TW008246-01 from Fogarty International Centre; and The Medical Research Council (UK, Project Grant MR/J008761/1). JLNW was also supported by the Alborada Trust and the European Union FP7 project ANTIGONE (contract number 278976).This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.epidem.2014.09.00
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