355 research outputs found

    How Neutrinos Get Mass and What Other Things May Happen Besides Oscillations

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    In this talk I address the theoretical issue of what new physics is required to make mν0m_\nu \neq 0. I then discuss what other things may happen besides neutrino oscillations. In particular I consider a possible new scenario of leptogenesis in R parity nonconserving supersymmetry.Comment: 7 pages including 1 figure, talk at WHEPP-

    Leptogenesis from R parity nonconservation

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    It is known that realistic neutrino masses for neutrino oscillations may be obtained from R parity nonconserving supersymmetry. It is also known that such interactions would erase any preexisting lepton or baryon asymmetry of the Universe because of the inevitable intervention of the electroweak sphalerons. We now show how a crucial subset of these R parity nonconserving terms may in fact create its own successful leptogenesis.Comment: 4 pages latex file with one postscript figur

    The possibility of critical realist randomised controlled trials.

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    BACKGROUND: Some realists have criticised randomised controlled trials for their inability to explain the causal relations that they identify; to take into account the influence of the social context of the interventions they evaluate; and to account for individual difference. However, among realists, there is controversy over whether it is possible to improve trials by making them realist, or whether realism and the philosophical assumptions underlying trials are incompatible. This paper contributes to the debate in Trials on this issue. The debate thus far has concentrated on the possibility of combining trial methodology with that of realist evaluation. MAIN BODY: We concur with the contention that it is not feasible to combine randomised controlled trial design with the realist evaluation approach. However, we argue that a different variant of realism, critical realism, provides a more appropriate theoretical grounding for realist trials. In contrast to realist evaluation, which regards social mechanisms as an amalgam of social resources and people's reasoning, critical realism insists on their distinction. It does so on the basis of its assertion of the need to distinguish between social structures (in which resources lie) and human agency (which is at least partly guided by reasoning). From this perspective, conceiving of social mechanisms as external to participants can be seen as a valid methodological strategy for supplementing the exclusive concentration of trials on outcomes. While accepting realist evaluation's insistence that causality in open systems involves a configuration of multiple generative mechanisms, we adopt the critical realist interpretation of the experimental method, which sees it as creating artificial closure in order to identify the effects of specific causal mechanisms. If randomised controlled trials can be regarded as epidemiological proxies that substitute probabilistic controls over extraneous factors for closed experiments, their examination of the powers of discrete mechanisms through observation of the variation of outcomes is appropriate. CONCLUSION: While there are still issues to be resolved, critical realist randomised controlled trials are possible and have the potential to overcome some of the difficulties faced by traditional trial designs in accounting for the influence of social context and individual interpretation

    Aboriginal and Torres Strait Islander Suicide in Context

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    Aboriginal and Torres Strait Islander suicide has been an issue of national public health and mental health concern for only one decade, having increased dramatically from levels that were very low in the late 1980s to levels of young adult male suicide that are now substantially higher than for the non-indigenous population. In this review the authors socially and historically contextualize these changes, identifying the causal frameworks adopted in developing interventions, and present an explanation in narrative and pictorial form that draws on critical family-centered trauma

    Longitudinal study of ‘retraining’ non-maths specialist teachers to become capable, confident teachers of mathematics

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    One of the key problems to be solved in mathematics education in England is that the demand for mathematics teachers is far in excess of the supply. Acknowledging that there are simply too few mathematics teachers, the UK government has invested significantly in retraining programmes. These programmes ‘retrain’ out-of-field teachers, that is, teachers of other subjects or from other phases, to teach secondary mathematics. The increased mathematical demand of the reformed GCSE courses coupled with the expectation that most post-16 students will engage with some mathematics (studying for A and AS levels, a Core Maths qualification or re-sitting GCSE) means many more teachers of mathematics will be needed. We consider the viability of a retraining course as an effective way of alleviating the problem of the lack of well qualified teachers for mathematics. In this four-year longitudinal study, we followed teachers during their year of ‘retraining’ and in the succeeding years. Once a participant completes their part-time one-year course, the teacher is considered ‘retrained’. However, we conclude that without ongoing professional development involving collaborative support retraining courses alone can have little impact on the problem of the lack of competent and confident teachers of mathematics in the secondary sector

    SOX2 Co-Occupies Distal Enhancer Elements with Distinct POU Factors in ESCs and NPCs to Specify Cell State

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    SOX2 is a master regulator of both pluripotent embryonic stem cells (ESCs) and multipotent neural progenitor cells (NPCs); however, we currently lack a detailed understanding of how SOX2 controls these distinct stem cell populations. Here we show by genome-wide analysis that, while SOX2 bound to a distinct set of gene promoters in ESCs and NPCs, the majority of regions coincided with unique distal enhancer elements, important cis-acting regulators of tissue-specific gene expression programs. Notably, SOX2 bound the same consensus DNA motif in both cell types, suggesting that additional factors contribute to target specificity. We found that, similar to its association with OCT4 (Pou5f1) in ESCs, the related POU family member BRN2 (Pou3f2) co-occupied a large set of putative distal enhancers with SOX2 in NPCs. Forced expression of BRN2 in ESCs led to functional recruitment of SOX2 to a subset of NPC-specific targets and to precocious differentiation toward a neural-like state. Further analysis of the bound sequences revealed differences in the distances of SOX and POU peaks in the two cell types and identified motifs for additional transcription factors. Together, these data suggest that SOX2 controls a larger network of genes than previously anticipated through binding of distal enhancers and that transitions in POU partner factors may control tissue-specific transcriptional programs. Our findings have important implications for understanding lineage specification and somatic cell reprogramming, where SOX2, OCT4, and BRN2 have been shown to be key factors

    Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

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    To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.Peer reviewe
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