1,200 research outputs found

    Oral tradition and Rabbinic studies

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    The literature of classical rabbinic Judaism is usually said to have been "redacted" from around 300 CE until about 700 CE in the Palestinian and Mesopotamian centers of rabbinic settlement. Rabbinic literature itself assumes that the traditions that stand behind the written texts were transmitted orally for at least several generations (and in some views, centuries) prior to the compilation of the written manuscripts that are known from the Middle Ages.Not

    Oral tradition in the writings of Rabbinic oral Torah : on theorizing Rabbinic orality

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    The present paper and the three essays following, by Yaakov Elman, Steven Fraade, and Elizabeth Alexander, will explore specific problems in theorizing the relation of written composition and oral-performative text within the various genres of Rabbinic learned tradition of Late Antiquity. For my part, I intend only to offer some introductory comments on the Rabbinic literature in general and some further observations intended to contextualize the more text-centered contributions to follow.Not

    New directions for tackling food safety risks in the informal sector of developing countries

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    Informal food markets are important sources of affordable, nutritious food for millions of people in low- and middle-income countries. However, a large part of the public health burden of foodborne disease is associated with foods that are handled and sold by informal food processors and vendors. In most low- and lower middle-income countries, informal food markets will remain important for food and nutritional security for the foreseeable future. And, under a ‘business as usual’ scenario, we might even expect the problem of unsafe food in this sector to worsen rather than improve over time. To be more effective in addressing unsafe food in informal markets, there is a need for a shift in mind-sets, and a very different, multi-sectoral, multi-dimensional and spatially focused approach which deals with the complex capacity- and incentive-related constraints associated with informal markets

    Protocol Risk factors for disruptive behaviours: protocol for a systematic review and meta-analysis of quasi-experimental evidence

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    Introduction: Disruptive behaviour disorders, including oppositional defiant disorder and conduct disorder, are a common set of diagnoses in childhood and adolescence, with global estimates of 5.7%, 3.6% and 2.1% for any disruptive disorder, oppositional defiant disorder and conduct disorder, respectively. There are high economic and social costs associated with disruptive behaviours and the prevalence of these disorders has increased in recent years. As such, disruptive behaviours represent an escalating major public health concern and it is important to understand what factors may influence the risk of these behaviours. Such research would inform interventions that aim to prevent the development of disruptive behaviours. The current review will identify the most stringent evidence of putative risk factors for disruptive behaviour from quasi-experimental studies, which enable stronger causal inference. Methods and analysis: The review will be carried out according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. An electronic search of references published between 1 January 1980 and 1 March 2020 will be conducted using Medline, Embase, PsycINFO and Web of Science. Initial abstract and title screening, full-text screening and data extraction will be completed independently by two reviewers using Evidence for Policy and Practice Information (EPPI)-Reviewer 4 software. Quasi-experimental studies in the English language examining the association between any putative risk factor and a clearly defined measure of disruptive behaviour (eg, a validated questionnaire measure) will be included. We will conduct meta-analyses if we can pool a minimum of three similar studies with the same or similar exposures and outcomes. Ethics and dissemination: The proposed review does not require ethical approval. The results will help to identify risk factors for which there is strong evidence of causal effects on disruptive behaviours and also highlight potential risk factors that require further research. The findings will be disseminated via publication in a peer-reviewed scientific journal and through presentations at international meetings and conferences

    Parental predictors of children's executive functioning from ages 6 to 10.

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    According to prominent models of child development, parental factors may contribute to individual differences in children's executive functioning (EF). Here, we examine the relative importance of parents' socio-economic status, mental health, and parenting as predictors of EF development, drawing on a large (n = 1,070) community sample of Norwegian children who received biennial EF assessments from 6 to 10 years of age. We measure EF by means of the Behavior Rating Inventory of Executive Function. We assess parenting through observer ratings of parent-child interactions and parental mental health via the Beck Anxiety Inventory, Beck Depression Inventory, and Hopkins Symptom Checklist. When we adjust for all time-invariant unmeasured confounders, higher parental education predicts superior EF development, whereas harsh parenting forecasts poorer EF development. However, parenting does not mediate the effect of parental education. These results indicate that harsh parenting should be targeted in interventions aimed at improving EF. Statement of contribution What is already known on this subject? Parental factors seem to affect child development of executive functions (EF). Specifically, parental socio-economic status, mental health, and their parenting seem to influence the developmental course of child EF. What does this study add? To what degree the parental influence on EF development is likely to be driven by time-invariant factors, for example, genetics. The relative influence of positive and negative parenting on EF development

    Why food safety matters to Africa: Making the case for policy action

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    Trafficking of High Avidity HER-2/neu-Specific T Cells into HER-2/neu-Expressing Tumors after Depletion of Effector/Memory-Like Regulatory T Cells

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    Cancer vaccines are designed to activate and enhance cancer-antigen-targeted T cells that are suppressed through multiple mechanisms of immune tolerance in cancer-bearing hosts. T regulatory cell (Treg) suppression of tumor-specific T cells is one barrier to effective immunization. A second mechanism is the deletion of high avidity tumor-specific T cells, which leaves a less effective low avidity tumor specific T cell repertoire available for activation by vaccines. Treg depleting agents including low dose cyclophosphamide (Cy) and antibodies that deplete CD25-expressing Tregs have been used with limited success to enhance the potency of tumor-specific vaccines. In addition, few studies have evaluated mechanisms that activate low avidity cancer antigen-specific T cells. Therefore, we developed high and low avidity HER-2/neu-specific TCR transgenic mouse colonies specific for the same HER-2/neu epitope to define the tolerance mechanisms that specifically affect high versus low avidity tumor-specific T cells.High and low avidity CD8(+) T cell receptor (TCR) transgenic mice specific for the breast cancer antigen HER-2/neu (neu) were developed to provide a purified source of naïve, tumor-specific T cells that can be used to study tolerance mechanisms. Adoptive transfer studies into tolerant FVB/N-derived HER-2/neu transgenic (neu-N) mice demonstrated that high avidity, but not low avidity, neu-specific T cells are inhibited by Tregs as the dominant tolerizing mechanism. High avidity T cells persisted, produced IFNγ, trafficked into tumors, and lysed tumors after adoptive transfer into mice treated with a neu-specific vaccine and low dose Cy to deplete Tregs. Analysis of Treg subsets revealed a Cy-sensitive CD4(+)Foxp3(+)CD25(low) tumor-seeking migratory phenotype, characteristic of effector/memory Tregs, and capable of high avidity T cell suppression.Depletion of CD25(low) Tregs allows activation of tumor-clearing high avidity T cells. Thus, the development of agents that specifically deplete Treg subsets should translate into more effective immunotherapies while avoiding autoimmunity
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