227 research outputs found

    When Feeling Mixed Can Be Meaningful: The Relation Between Mixed Emotions and Eudaimonic Well-Being

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    Whilst positive emotions benefit well-being, the role of other more complex emotional experiences for well-being is less well understood. This research therefore investigated the relationship between mixed emotions and eudaimonic well-being. A cross-sectional study (Study 1; N = 429) first demonstrated (using structural equation modelling) that mixed emotions are related to the presence of goal conflict. Importantly, it was also found that mixed emotions are positively related to eudaimonic well-being, and that one potential mechanism linking mixed emotions and eudaimonic well-being is via the search for meaning in life. Study 2 (N = 52) implemented a quasi-experiment regarding a naturally occurring meaningful life event (i.e., graduation day) and again demonstrated that mixed emotions are associated with a greater level of eudaimonic well-being. Implications of these findings include the importance of mixed emotions in the search for meaning in life, and the role of mixed emotions in goal conflict resolution

    Silver linings in the face of temptations: how mixed emotions promote self-control efforts in response to goal conflict

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    Choosing between conflicting goals is a frequent yet difficult problem, especially when temptations are involved because self-control effort is required to overcome them. This study investigated whether experiencing mixed emotions in response to goal conflict can facilitate the necessary self-control effort needed to resist temptations. A sample of 73 individuals participated in an intensive longitudinal study, completing several measures 4 times a day during ten consecutive days, producing over 2500 observations. Results derived from using multilevel structural equation modeling confirmed that mixed emotions mediated the relationship between perceived goal conflict and intentions to resist temptations, over and above the influence of single positive emotions or negative emotions, and trait levels of self-control. Implication of these findings for collaboration and the impact of mixed emotions in more general social dilemmas are explored

    Supporting induction: relationships count

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    This article examines the structural changes to the induction of teachers in Scotland using the perceptions of a group of final year student teachers. This group would be the first probationer teachers to experience revised arrangements for new teacher induction in 37 years. Their preferences and concerns are highlighted, as the new procedures roll out in schools nationwide, in an attempt to stress the importance of relationships to the success of the induction scheme. The argument put forward in this article is based on the notion that personal intelligence is central to effective relationships and therefore crucially important in the context of this mentoring relationship. The views of our sample provide evidence to suggest that the quality of interactions between the mentor and the probationer teacher are paramount in providing a good induction experience. These views are substantiated by experiences in England and in induction literature elsewhere. A synthesis of this evidence is used to make recommendations for those involved in supporting induction in schools, local authorities or teacher education institutions

    Accountability and responsibility: 'Rogue' school leaders and the induction of new teachers in England

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    This paper considers the professional responsibility of schools in England to provide effective induction practices in the context of a central government mandated policy. It looks at individual schools as ‘habitats’ for induction and the role of school leaders and LEAs as facilitators or inhibitors. Notions of professional responsibility and public accountability are used to analyse the small number of ‘rogue’ school leaders who, within the new legislative framework, treat new teachers unprofessionally and waste public resources. A typology of ‘rogue’ schools that are in some way deviant in transgressing induction requirements is developed and the various sanctions that can be deployed against such schools are examined. How LEAs handle their monitoring and accountability role and manage deviant schools is considered. Finally, suggestions are made for improvements, such as the need to clarify professional responsibility and refine systems of professional accountability

    Enhanced anxiety, depressive-like behaviour and impaired recognition memory in mice with reduced expression of the vesicular glutamate transporter 1 (VGLUT1)

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    Three isoforms of a vesicular glutamate transporter (VGLUT1-3) have been identified. Of these, VGLUT1 is the major isoform of the cerebral cortex and hippocampus where it is selectively located on synaptic vesicles of excitatory glutamatergic terminals. Variations in VGLUT1 expression levels have a major impact on the efficacy of glutamate synaptic transmission. Given evidence linking alterations in glutamate neurotransmission to various neuropsychiatric disorders, we investigated the possible influence of a down-regulation of VGLUT1 transporter on anxiety, depressive-like behaviour and learning. The behavioural phenotype of VGLUT1 heterozygous mice (C57BL/6) was compared to WT littermates. Moreover, VGLUT1-3 expression, hippocampal excitatory terminal ultrastructure and neurochemical phenotype were analysed. VGLUT1 heterozygous mice displayed normal spontaneous locomotor activity, increased anxiety in the light-dark exploration test and depressive-like behaviour in the forced swimming test: no differences were shown in the elevated plus-maze model of anxiety. In the novel object recognition test, VGLUT1+/- mice showed normal short-term but impaired long-term memory. Spatial memory in the Morris water maze was unaffected. Western blot analysis confirmed that VGLUT1 heterozygotes expressed half the amount of transporter compared to WT. In addition, a reduction of the reserve pool of synaptic vesicles of hippocampal excitatory terminals and a 35-45 % reduction of GABA in the frontal cortex and the hippocampus were observed in the mutant mice. These observations suggest that a VGLUT1-mediated presynaptic alteration of the glutamatergic synapses, in specific brain regions, leads to a behavioural phenotype resembling certain aspects of psychiatric and cognitive disorders

    Drivers and uncertainties of future global marine primary production in marine ecosystem models

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    Past model studies have projected a global decrease in marine net primary production (NPP) over the 21st century, but these studies focused on the multi-model mean rather than on the large inter-model differences. Here, we analyze model-simulated changes in NPP for the 21st century under IPCC's high-emission scenario RCP8.5. We use a suite of nine coupled carbon–climate Earth system models with embedded marine ecosystem models and focus on the spread between the different models and the underlying reasons. Globally, NPP decreases in five out of the nine models over the course of the 21st century, while three show no significant trend and one even simulates an increase. The largest model spread occurs in the low latitudes (between 30° S and 30° N), with individual models simulating relative changes between −25 and +40 %. Of the seven models diagnosing a net decrease in NPP in the low latitudes, only three simulate this to be a consequence of the classical interpretation, i.e., a stronger nutrient limitation due to increased stratification leading to reduced phytoplankton growth. In the other four, warming-induced increases in phytoplankton growth outbalance the stronger nutrient limitation. However, temperature-driven increases in grazing and other loss processes cause a net decrease in phytoplankton biomass and reduce NPP despite higher growth rates. One model projects a strong increase in NPP in the low latitudes, caused by an intensification of the microbial loop, while NPP in the remaining model changes by less than 0.5 %. While models consistently project increases NPP in the Southern Ocean, the regional inter-model range is also very substantial. In most models, this increase in NPP is driven by temperature, but it is also modulated by changes in light, macronutrients and iron as well as grazing. Overall, current projections of future changes in global marine NPP are subject to large uncertainties and necessitate a dedicated and sustained effort to improve the models and the concepts and data that guide their developmen

    TOM40 Mediates Mitochondrial Dysfunction Induced by α-Synuclein Accumulation in Parkinson's Disease.

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    Alpha-synuclein (α-Syn) accumulation/aggregation and mitochondrial dysfunction play prominent roles in the pathology of Parkinson's disease. We have previously shown that postmortem human dopaminergic neurons from PD brains accumulate high levels of mitochondrial DNA (mtDNA) deletions. We now addressed the question, whether alterations in a component of the mitochondrial import machinery -TOM40- might contribute to the mitochondrial dysfunction and damage in PD. For this purpose, we studied levels of TOM40, mtDNA deletions, oxidative damage, energy production, and complexes of the respiratory chain in brain homogenates as well as in single neurons, using laser-capture-microdissection in transgenic mice overexpressing human wildtype α-Syn. Additionally, we used lentivirus-mediated stereotactic delivery of a component of this import machinery into mouse brain as a novel therapeutic strategy. We report here that TOM40 is significantly reduced in the brain of PD patients and in α-Syn transgenic mice. TOM40 deficits were associated with increased mtDNA deletions and oxidative DNA damage, and with decreased energy production and altered levels of complex I proteins in α-Syn transgenic mice. Lentiviral-mediated overexpression of Tom40 in α-Syn-transgenic mice brains ameliorated energy deficits as well as oxidative burden. Our results suggest that alterations in the mitochondrial protein transport machinery might contribute to mitochondrial impairment in α-Synucleinopathies

    OPTIMUM study protocol: an adaptive randomised controlled trial of a mixed whole-cell/acellular pertussis vaccine schedule.

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    INTRODUCTION: Combination vaccines containing whole-cell pertussis antigens were phased out from the Australian national immunisation programme between 1997 and 1999 and replaced by the less reactogenic acellular pertussis (aP) antigens. In a large case-control study of Australian children born during the transition period, those with allergist diagnosed IgE-mediated food allergy were less likely to have received whole-cell vaccine in early infancy than matched population controls (OR: 0.77 (95% CI, 0.62 to 0.95)). We hypothesise that a single dose of whole-cell vaccine in early infancy is protective against IgE-mediated food allergy. METHODS AND ANALYSIS: This adaptive double-blind randomised controlled trial is investigating whether a mixed whole-cell/aP vaccine schedule prevents allergic disease in the first year of life. The primary outcome is IgE-mediated food allergy by 12 months of age. Secondary outcomes include new onset of atopic dermatitis by 6 or 12 months of age; sensitisation to at least one allergen by 12 months of age; seroconversion in anti-pertussis toxin IgG titres after vaccination with aP booster at 18 months of age; and solicited systemic and local adverse events following immunisation with pertussis-containing vaccines. Analyses will be performed using a Bayesian group sequential design. ETHICS AND DISSEMINATION: This study has been approved by the Child and Adolescent Health Service Human Research Ethics Committee, Perth, Western Australia (RGS 00019). The investigators will ensure that this trial is conducted in accordance with the principles of the Declaration of Helsinki and with the International Conference on Harmonisation Guidelines for Good Clinical Practice. Individual consent will be requested. Parents will be reimbursed reasonable travel and parking costs to attend the study visits. The dissemination of these research findings will follow the National Health and Medical Research Council of Australia Open Access Policy. TRIAL REGISTRATION NUMBER: ACTRN12617000065392p
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