Physical restraint in residential child care : the experiences of young people and residential workers

There have long been concerns about the use of physical restraint in residential care. This paper presents the findings of a qualitative study which explores the experiences of children, young people and residential workers about physical restraint. The research identifies the dilemmas and ambiguities for both staff and young people, and participants discuss the situations where they feel physical restraint is appropriate as well as their concerns about unjustified or painful restraints. They describe the negative emotions involved in restraint but also those situations where, through positive relationships and trust, restraint can help young people through unsafe situations

Ethical issues, research and vulnerability : gaining the views of children and young people in residential care

Children and young people in residential care are some of the most vulnerable in our society. They may have experienced violence and physical, sexual or emotional abuse. They may be involved in offending or the misuse of drugs and alcohol. They are separated from their families and have to cope with living in a group situation with other young people and staff members. Children and young people in residential care also possess strengths, competencies and resilience. We have much to learn from their experiences and perspectives, both generally and surrounding their time in care. This paper will address the ethical issues which arise from gaining the views of children and young people in residential care, drawing on the experience of carrying out three studies in particular (Kendrick et al. 2004, The development of a residential unit working with sexually aggressive young men. In: H.G. Eriksson and T. Tjelflaat, eds. Residential care: horizons for the new century. Aldershot: Ashgate, 38-55; Docherty et al. 2006, Designing with care: interior design and residential child care. Farm7 and SIRCC. http://www.sircc.strath.ac.uk/publications/Designing_with_Care.pdf; Steckley, L. and Kendrick, A., 2005. Physical restraint in residential child care: the experiences of young people and residential workers. Childhoods 2005: Children and Youth in Emerging and Transforming Societies, University of Oslo, Norway, 29 June-3 July 2005, Steckley and Kendrick 2007, Young people's experiences of physical restraint in residential care: subtlety and complexity in policy and practice. In: M. Nunno, L. Bullard and D. Day, eds. For our own safety: examining the safety of high-risk interventions for children and young people. Washington, DC: Child Welfare League of America, forthcoming). The paper will discuss: information, consent and choice about involvement in the research; confidentiality, privacy and safety. It will also explore some of the more complex issues of ethical good practice which arise from researching children in their own living space. The negotiation of children's time and space must be approached carefully, with consideration of their rights and wishes. Sensitivity to children and young people's priorities and preoccupations must be paramount

Variation in The Vitamin D Receptor Gene is Associated With Multiple Sclerosis in an Australian Population

Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) resulting in accumulating neurological disability. The disorder is more prevalent at higher latitudes. To investigate VDR gene variation using three intragenic restriction fragment length polymorphisms (Apa I, Taq I and Fok I) in an Australian MS case-control population, one hundred and four Australian MS patients were studied with patients classified clinically as Relapsing Remitting MS (RR-MS), Secondary Progressive MS (SP-MS) or Primary Progressive MS (PP-MS). Also, 104 age-, sex-, and ethnicity-matched controls were investigated as a comparative group. Our results show a significant difference of genotype distribution frequency between the case and control groups for the functional exon 9 VDR marker Taq I (p_Gen = 0.016) and interestingly, a stronger difference for the allelic frequency (p_All = 0.0072). The Apa I alleles were also found to be associated with MS (p_All = 0.04) but genotype frequencies were not significantly different from controls (p_Gen = 0.1). The Taq and Apa variants are in very strong and significant linkage disequilibrium (D' = 0.96, P < 0.0001). The genotypic associations are strongest for the progressive forms of MS (SP-MS and PP-MS). Our results support a role for the VDR gene increasing

Parallel processes:Getting it write?

This paper offers a critical reflection on the processes surrounding the writing of a book aimed at foster carers and residential workers. By utilising the concept of parallel process as well as the four modes of reflection identified by Ruch (2000), we explore the ways in which the wider context of both direct works with children and reflective practice have been impacted by the tensions between relationally based, child-centred practice and wider managerialist imperatives. The paper draws parallels between these practice tensions and those currently in play within the academy. By employing a dialogical and reflective analysis of the process and interactions surrounding the writing of a practitioner-targeted book, the paper demonstrates the ways in which critical and process reflection post-event took place, considering the heretofore unexplored parallel processes between writing for practice, and practice. In so doing, it identifies the ways in which the authors mirrored practitioners in relation to the management of anxiety, a sense of constrained autonomy and confidence, and an avoidance of recognising and challenging structural and political context. Implications for the creation of practice literature and for the academy are considered.Output Status: Forthcoming/Available Onlin

Glucose Induces Pancreatic Islet Cell Apoptosis That Requires the BH3-Only Proteins Bim and Puma and Multi-BH Domain Protein Bax

OBJECTIVE: High concentrations of circulating glucose are believed to contribute to defective insulin secretion and beta-cell function in diabetes and at least some of this effect appears to be caused by glucose-induced beta-cell apoptosis. In mammalian cells, apoptotic cell death is controlled by the interplay of proapoptotic and antiapoptotic members of the Bcl-2 family. We investigated the apoptotic pathway induced in mouse pancreatic islet cells after exposure to high concentrations of the reducing sugars ribose and glucose as a model of beta-cell death due to long-term metabolic stress. RESEARCH DESIGN AND METHODS: Islets isolated from mice lacking molecules implicated in cell death pathways were exposed to high concentrations of glucose or ribose. Apoptosis was measured by analysis of DNA fragmentation and release of mitochondrial cytochrome c. RESULTS: Deficiency of interleukin-1 receptors or Fas did not diminish apoptosis, making involvement of inflammatory cytokine receptor or death receptor signaling in glucose-induced apoptosis unlikely. In contrast, overexpression of the prosurvival protein Bcl-2 or deficiency of the apoptosis initiating BH3-only proteins Bim or Puma, or the downstream apoptosis effector Bax, markedly reduced glucose- or ribose-induced killing of islets. Loss of other BH3-only proteins Bid or Noxa, or the Bax-related effector Bak, had no impact on glucose-induced apoptosis. CONCLUSIONS: These results implicate the Bcl-2 regulated apoptotic pathway in glucose-induced islet cell killing and indicate points in the pathway at which interventional strategies can be designed

Phospholipid Composition Modulates Carbon Nanodiamond-Induced Alterations in Phospholipid Domain Formation

This document is the Accepted Manuscript version of a Published Work that appeared in final form in Langmuir, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see http://doi.org/10.1021/la504923j.The focus of this work is to elucidate how phospholipid composition can modulate lipid nanoparticle interactions in phospholipid monolayer systems. We report on alterations in lipid domain formation induced by anionically engineered carbon nanodiamonds (ECNs) as a function of lipid headgroup charge and alkyl chain saturation. Using surface pressure vs area isotherms, monolayer compressibility, and fluorescence microscopy, we found that anionic ECNs induced domain shape alterations in zwitterionic phosphatidylcholine lipids, irrespective of the lipid alkyl chain saturation, even when the surface pressure vs area isotherms did not show any significant changes. Bean-shaped structures characteristic of dipalmitoylphosphatidylcholine (DPPC) were converted to multilobed, fractal, or spiral domains as a result of exposure to ECNs, indicating that ECNs lower the line tension between domains in the case of zwitterionic lipids. For membrane systems containing anionic phospholipids, ECN-induced changes in domain packing were related to the electrostatic interactions between the anionic ECNs and the anionic lipid headgroups, even when zwitterionic lipids are present in excess. By comparing the measured size distributions with our recently developed theory derived by minimizing the free energy associated with the domain energy and mixing entropy, we found that the change in line tension induced by anionic ECNs is dominated by the charge in the condensed lipid domains. Atomic force microscopy images of the transferred anionic films confirm that the location of the anionic ECNs in the lipid monolayers is also modulated by the charge on the condensed lipid domains. Because biological membranes such as lung surfactants contain both saturated and unsaturated phospholipids with different lipid headgroup charges, our results suggest that when studying potential adverse effects of nanoparticles on biological systems the role of lipid compositions cannot be neglected

Working with challenging behaviour

This section offers some ways of thinking about behaviour, our immediate objective in managing that behaviour, and our primary task in working with young people; these ways of thinking can bring greater clarity and effectiveness. This section also addresses self and relationship as inextricable components of working with challenging behaviour. Physical restraint is briefly discussed as the extreme end of working with challenging behaviour, and finally, some practical advice and further reading are offered

Acetylation of the Pro-Apoptotic Factor, p53 in the Hippocampus following Cerebral Ischemia and Modulation by Estrogen

Recent studies demonstrate that acetylation of the transcription factor, p53 on lysine(373) leads to its enhanced stabilization/activity and increased susceptibility of cells to stress. However, it is not known whether acetylation of p53 is altered in the hippocampus following global cerebral ischemia (GCI) or is regulated by the hormone, 17β-estradiol (17β-E(2)), and thus, this study examined these issues.The study revealed that Acetyl p53-Lysine(373) levels were markedly increased in the hippocampal CA1 region after GCI at 3 h, 6 h and 24 h after reperfusion, an effect strongly attenuated by 17β-E(2). 17β-E(2) also enhanced interaction of p53 with the ubiquitin ligase, Mdm2, increased ubiquitination of p53, and induced its down-regulation, as well as attenuated elevation of the p53 transcriptional target, Puma. We also observed enhanced acetylation of p53 at a different lysine (Lys(382)) at 3 h after reperfusion, and 17β-E(2) also markedly attenuated this effect. Furthermore, administration of an inhibitor of CBP/p300 acetyltransferase, which acetylates p53, was strongly neuroprotective of the CA1 region following GCI. In long-term estrogen deprived (LTED) animals, the ability of 17β-E(2) to attenuate p53 acetylation was lost, and intriguingly, Acetyl p53-Lysine(373) levels were markedly elevated in sham (non-ischemic) LTED animals. Finally, intracerebroventricular injections of Gp91ds-Tat, a specific NADPH oxidase (NOX2) inhibitor, but not the scrambled tat peptide control (Sc-Tat), attenuated acetylation of p53 and reduced levels of Puma following GCI.The studies demonstrate that p53 undergoes enhanced acetylation in the hippocampal CA1 region following global cerebral ischemia, and that the neuroprotective agent, 17β-E(2), markedly attenuates the ischemia-induced p53 acetylation. Furthermore, following LTED, the suppressive effect of 17β-E(2) on p53 acetylation is lost, and p53 acetylation increases in the hippocampus, which may explain previous reports of increased sensitivity of the hippocampus to ischemic stress following LTED