839 research outputs found

    Parenting under adversity:birth parents' accounts of inequality and adoption

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    This paper aims to highlight inequality in current adoption processes and procedures in England and Wales. Whilst inequality has been recognised in adoption research, the role of social structures is often neglected. Inequality within social structures plays a role in the process of the permanent removal of children to be adopted and is worthy of further attention. Birth parent voices can contribute to a wider understanding of adoption, but often remain hidden. Empirical research findings highlight how birth parents may find that their adverse experiences are exacerbated by the adoption process, the emotional impact causing existing problems to increase, and through the impact of the adoption process on birth parent’s socio-economic status. Findings also illustrate how birth parents’ experiences were influenced by ideals of motherhood and ideas about ‘risk’ to children. The paper contributes to the growing area of research which illuminates the intersection of poverty, deprivation and child protection services and the wider contemporaneous debate concerning adoption in England and Wales

    The E12 experience: Students’ perceptions of a widening participation scheme

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    Engaging students from lower socioeconomic backgrounds in higher education is an ongoing issue in the tertiary education sector. Despite schemes to widen participation, low SES entry rates remain below 20% in Australia. Various factors have been posited for the low rates of success and strategies aimed at universities, high schools and individual students have been suggested. The literature on transition to university has informed a student-centred approach and the need to acknowledge dimensions of cultural capital. Resources to address difficulties in transition have been suggested. In this paper we report on qualitative research exploring the perspective of students who entered a Faculty of Health Sciences via a widening participation scheme. Our findings indicate that while transition strategies must be in place, the provision of ongoing material resources is also an integral factor in supporting student

    Anopheles stephensi p38 MAPK signaling regulates innate immunity and bioenergetics during Plasmodium falciparum infection.

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    BackgroundFruit flies and mammals protect themselves against infection by mounting immune and metabolic responses that must be balanced against the metabolic needs of the pathogens. In this context, p38 mitogen-activated protein kinase (MAPK)-dependent signaling is critical to regulating both innate immunity and metabolism during infection. Accordingly, we asked to what extent the Asian malaria mosquito Anopheles stephensi utilizes p38 MAPK signaling during infection with the human malaria parasite Plasmodium falciparum.MethodsA. stephensi p38 MAPK (AsP38 MAPK) was identified and patterns of signaling in vitro and in vivo (midgut) were analyzed using phospho-specific antibodies and small molecule inhibitors. Functional effects of AsP38 MAPK inhibition were assessed using P. falciparum infection, quantitative real-time PCR, assays for reactive oxygen species and survivorship under oxidative stress, proteomics, and biochemical analyses.ResultsThe genome of A. stephensi encodes a single p38 MAPK that is activated in the midgut in response to parasite infection. Inhibition of AsP38 MAPK signaling significantly reduced P. falciparum sporogonic development. This phenotype was associated with AsP38 MAPK regulation of mitochondrial physiology and stress responses in the midgut epithelium, a tissue critical for parasite development. Specifically, inhibition of AsP38 MAPK resulted in reduction in mosquito protein synthesis machinery, a shift in glucose metabolism, reduced mitochondrial metabolism, enhanced production of mitochondrial reactive oxygen species, induction of an array of anti-parasite effector genes, and decreased resistance to oxidative stress-mediated damage. Hence, P. falciparum-induced activation of AsP38 MAPK in the midgut facilitates parasite infection through a combination of reduced anti-parasite immune defenses and enhanced host protein synthesis and bioenergetics to minimize the impact of infection on the host and to maximize parasite survival, and ultimately, transmission.ConclusionsThese observations suggest that, as in mammals, innate immunity and mitochondrial responses are integrated in mosquitoes and that AsP38 MAPK-dependent signaling facilitates mosquito survival during parasite infection, a fact that may attest to the relatively longer evolutionary relationship of these parasites with their invertebrate compared to their vertebrate hosts. On a practical level, improved understanding of the balances and trade-offs between resistance and metabolism could be leveraged to generate fit, resistant mosquitoes for malaria control
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