994 resultados para Homeless pathways


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A strong link between drug use and homelessness has long since been documented in the international literature. However, much of the research has concentrated on the direction of the relationship between drug use and homelessness, seeking to establish drug use as a cause or consequence of homelessness, with far less attention to the intersection of drug and homeless ‘careers’. This paper examines the drug and homeless pathways of young people who are participants in a qualitative longitudinal study of homeless youth in Dublin, Ireland. The findings highlight downward drug transitions as associated with exiting homelessness and continued or escalated consumption as associated with remaining homeless. Analyses of the meanings young people attach to drug use over time reveal the importance of housing as an enabler to engaging with treatment and as assisting the process of becoming and remaining drug free. Young people who remained homeless did not accept their situations, as ‘acculturation’ accounts would suggest; rather, they aspired to changing their situations. However, they also face strong barriers to accessing housing which in turn hamper their efforts to address the matter of their drug use. The implications for how the homeless/drug use ‘nexus’ is conceptualised and understood, as well as implications for policy, are discussed.

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The families of homeless young people are most often portrayed as a precipitating factor in their homelessness. However, recent studies, particularly those taking a longitudinal approach, have drawn attention to the enabling role of family members and their positive influence on the housing trajectories of homeless youth. Drawing on selected findings from an ongoing longitudinal qualitative study of homeless young people in Dublin, Ireland, this paper aims to build on this relatively fertile area of research. We demonstrate the supportive role of the families of young people who experience homelessness (often as a consequence of difficult family environments) and specifically examine how family re-engagement is negotiated and achieved. The findings highlight a number of dimensions of transition and change. Prominent among these is the importance of renewed trust and communication. Young people and their parents also had to accept responsibility for areas of life that previously served to undermine their relationships and were implicated in the circumstances surrounding a young person's premature home-leaving. Tensions and resistances on the part of young people are highlighted, demonstrating the adaptive mechanisms at work as they attempt to re-engage with family members. The implications of the findings for social work intervention with homeless youth are discussed.

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In the past decade in particular, research attention has shifted from an almost exclusive focus on routes or pathways into homelessness towards the investigation of exits from homelessness. As well as demonstrating the multiple paths possible for young people who become homeless, recent research, and longitudinal studies in particular, has contributed to a more nuanced understanding of the complexity of the homeless pathways of young people. Nonetheless, knowledge and understanding of the nature of homeless exits, and of the mechanisms that facilitate the transition out of homelessness, is far from complete. This paper explores the processes surrounding the exit routes taken by young people out of homelessness and the meanings attached by them to these housing transitions based on selected findings from an ongoing qualitative longitudinal study of homeless youth in Dublin, Ireland. More broadly, the paper considers the utility of distinguishing between the types of routes that young people take out of homelessness, with particular attention to the notions of ‘independent’ and ‘dependent’ exits. The paper aims to further the discussion and debate on the conceptualisation of homeless exits and also discusses a number of policy implications arising from the study's findings.

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This literature review was commissioned by the Commissioner for Children and Young People Western Australia to provide an overview of the issues affecting the wellbeing of children who are homeless with their families. This review outlines the scholarly evidence in relation to the following issues. • The causes and extent of children’s homelessness in Western Australia (and Australia), including pathways leading to family homelessness; • The impact of homelessness on children’s near-term and long-term wellbeing; • The service and support needs of children and families at risk of or experiencing homelessness; • Strategic approaches and systems for providing services to children and families; • Successful programs that are evidence-based and have been evaluated to show positive effects on children’s wellbeing (particularly programs replicated in multiple jurisdictions or applied across diverse population groups); • Children’s own views and experiences of homelessness and support services (particularly direct consultations with children), and; • Gaps in knowledge.

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A number of critiques have been published drawing attention to the gaps in research methods applied to issues surrounding homelessness and service utilisation in Britain. This paper discusses the use of social identity, a theory drawn from the field of applied social psychology, and synthesises it with the pathways model, thereby providing a framework to further explore service utilisation. The synthesised framework was used to predict the uptake of outreach services in a prospective study of 121 homeless people in a major UK city. In general, homeless people's use of intervention services was affected by the extent to which they identified with the support services themselves. The study demonstrates the central role of social identity in understanding service utilisation patterns, and shows the importance of applying fresh techniques to fine-tune our understanding of uptake in the long term.

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PURPOSE: To explore the effects of glaucoma and aging on low-spatial-frequency contrast sensitivity by using tests designed to assess performance of either the magnocellular (M) or parvocellular (P) visual pathways. METHODS: Contrast sensitivity was measured for spatial frequencies of 0.25 to 2 cyc/deg by using a published steady- and pulsed-pedestal approach. Sixteen patients with glaucoma and 16 approximately age-matched control subjects participated. Patients with glaucoma were tested foveally and at two midperipheral locations: (1) an area of early visual field loss, and (2) an area of normal visual field. Control subjects were assessed in matched locations. An additional group of 12 younger control subjects (aged 20-35 years) were also tested. RESULTS: Older control subjects demonstrated reduced sensitivity relative to the younger group for the steady (presumed M)- and pulsed (presumed P)-pedestal conditions. Sensitivity was reduced foveally and in the midperiphery across the spatial frequency range. In the area of early visual field loss, the glaucoma group demonstrated further sensitivity reduction relative to older control subjects across the spatial frequency range for both the steady- and pulsed-pedestal tasks. Sensitivity was also reduced in the midperipheral location of "normal" visual field for the pulsed condition. CONCLUSIONS: Normal aging results in a reduction of contrast sensitivity for the low-spatial-frequency-sensitive components of both the M and P pathways. Glaucoma results in a further reduction of sensitivity that is not selective for M or P function. The low-spatial-frequency-sensitive channels of both pathways, which are presumably mediated by cells with larger receptive fields, are approximately equivalently impaired in early glaucoma.

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A discussion of 2008/2009 developments in Australian educational policy, with specific reference to the adoption of US and UK trends in accountability, testing and school reform.

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We aim to assess the effects of end-of-life care pathways, compared with usual care or with care guided by another end-of-life care pathway across all healthcare settings (hospitals, residential aged care facilities, community). In particular, we aim to assess the effects on symptom severity and quality of life of people who are dying and/or those related to the care such as families, caregivers and health professionals.

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Background In many clinical areas, integrated care pathways are utilised as structured multidisciplinary care plans which detail essential steps in caring for patients with specific clinical problems. Particularly, care pathways for the dying have been developed as a model to improve the end-of-life care of all patients. They aim to ensure that the most appropriate management occurs at the most appropriate time and that it is provided by the most appropriate health professional. Clinical pathways for end-of-life care management are used widely around the world and have been regarded as the gold standard. Therefore, there is a significant need for clinicians to be informed about the utilisation of end-of-life care pathways with a systematic review. Objectives To assess the effects of end-of-life care pathways, compared with usual care (no pathway) or with care guided by another end-of-life care pathway across all healthcare settings (e.g. hospitals, residential aged care facilities, community). Search strategy The Cochrane Register of controlled Trials (CENTRAL), the Pain, Palliative and Supportive Care Review group specialised register,MEDLINE, EMBASE, review articles and reference lists of relevant articles were searched. The search was carried out in September 2009. Selection criteria All randomised controlled trials (RCTs), quasi-randomised trial or high quality controlled before and after studies comparing use versus non-use of an end-of-life care pathway in caring for the dying. Data collection and analysis Results of searches were reviewed against the pre-determined criteria for inclusion by two review authors. Main results The search identified 920 potentially relevant titles, but no studies met criteria for inclusion in the review. Authors’ conclusions Without further available evidence, recommendations for the use of end-of-life pathways in caring for the dying cannot be made. RCTs or other well designed controlled studies are needed for evaluating the use of end-of-life care pathways in caring for dying people.

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Public health educational pathways in Australia have traditionally been the province of Universities, with the Master of Public Health (MPH) recognised as the flagship professional entry program. Public health education also occurs within the fellowship training of the Faculty of Public Health Medicine, but within Australia this remains confined to medical graduates. In recent years, however, we have seen a proliferation of undergraduate degrees as well as an increasing public health presence in the Vocational Education and Training (VET) sector. ----- Following the 2007 Australian Federal election, the new Labour government brought with it a refreshing commitment to a more inclusive and strategic style of government. An important example of this was the 2020 visioning process that identified key issues of public health concern, including an acknowledgment that it was unacceptable to allocate less than 2% of the health budget towards disease prevention. This led to the recommendation for the establishment of a national preventive health agency (Australia: the healthiest country by 2020 National Preventative Health Strategy, Prepared by the Preventative Health Taskforce 2009). ----- The focus on disease prevention places a spotlight on the workforce that will be required to deliver the new investment in health prevention, and also on the role of public health education in developing and upskilling the workforce. It is therefore timely to reflect on trends, challenges and opportunities from a tertiary sector perspective. Is it more desirable to focus education efforts on selected lead issues such as the “obesity epidemic”, climate change, Indigenous health and so on, or on the underlying theory and skills that build a flexible workforce capable of responding to a range of health challenges? Or should we aspire to both? ----- This paper presents some of the key discussion points from 2008 – 2009 of the Public Health Educational Pathways workshops and working group of the Australian Network of Public Health Institutions. We highlight some of the competing tensions in public health tertiary education, their impact on public health training programs, and the educational pathways that are needed to grow, shape and prepare the public health workforce for future challenges.

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The homeless have been subject to considerable scrutiny, historically and within current social, political and public discourse. The aetiology of homelessness has been the focus of a large body of economic, sociological, historical and political investigation. Importantly, efforts to conceptualise, explain and measure, the phenomenon of homelessness and homeless people has occurred largely within the context of defining “the problem of the homeless” and the generation of solutions to the ‘problem’. There has been little consideration of how and why homelessness has come to be seen, or understood, as a problem, or how this can change across time and/or place. This alternative stream of research has focused on tracing and analysing the relationship between how people experiencing homeless have become a matter of government concern and the manner in which homelessness itself has been problematised. With this in mind this study has analysed the discourses - political, social and economic rationalities and knowledges - which have provided the conditions of possibility for the identification of the homeless and homelessness as a problem needing to be governed and the means for translating these discourses into the applied domain. The aim of this thesis has been to contribute to current knowledge by developing a genealogy of the conditions and rationalities that have underpinned the problematisation of homelessness and the homeless. The outcome of this analysis has been to open up the opportunity to consider alternative governmental possibilities arising from the exposure of the way in which contemporary problematisation and responses have been influenced by the past. An understanding of this process creates an ability to appreciate the intended and unintended consequences for the future direction of public policy and contemporary research.

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Prostate cancer is an important male health issue. The strategies used to diagnose and treat prostate cancer underscore the cell and molecular interactions that promote disease progression. Prostate cancer is histologically defined by increasingly undifferentiated tumour cells and therapeutically targeted by androgen ablation. Even as the normal glandular architecture of the adult prostate is lost, prostate cancer cells remain dependent on the androgen receptor (AR) for growth and survival. This project focused on androgen-regulated gene expression, altered cellular differentiation, and the nexus between these two concepts. The AR controls prostate development, homeostasis and cancer progression by regulating the expression of downstream genes. Kallikrein-related serine peptidases are prominent transcriptional targets of AR in the adult prostate. Kallikrein 3 (KLK3), which is commonly referred to as prostate-specific antigen, is the current serum biomarker for prostate cancer. Other kallikreins are potential adjunct biomarkers. As secreted proteases, kallikreins act through enzyme cascades that may modulate the prostate cancer microenvironment. Both as a panel of biomarkers and cascade of proteases, the roles of kallikreins are interconnected. Yet the expression and regulation of different kallikreins in prostate cancer has not been compared. In this study, a spectrum of prostate cell lines was used to evaluate the expression profile of all 15 members of the kallikrein family. A cluster of genes was co-ordinately expressed in androgenresponsive cell lines. This group of kallikreins included KLK2, 3, 4 and 15, which are located adjacent to one another at the centromeric end of the kallikrein locus. KLK14 was also of interest, because it was ubiquitously expressed among the prostate cell lines. Immunohistochemistry showed that these 5 kallikreins are co-expressed in benign and malignant prostate tissue. The androgen-regulated expression of KLK2 and KLK3 is well-characterised, but has not been compared with other kallikreins. Therefore, KLK2, 3, 4, 14 and 15 expression were all measured in time course and dose response experiments with androgens, AR-antagonist treatments, hormone deprivation experiments and cells transfected with AR siRNA. Collectively, these experiments demonstrated that prostatic kallikreins are specifically and directly regulated by the AR. The data also revealed that kallikrein genes are differentially regulated by androgens; KLK2 and KLK3 were strongly up-regulated, KLK4 and KLK15 were modestly up-regulated, and KLK14 was repressed. Notably, KLK14 is located at the telomeric end of the kallikrein locus, far away from the centromeric cluster of kallikreins that are stimulated by androgens. These results show that the expression of KLK2, 3, 4, 14 and 15 is maintained in prostate cancer, but that these genes exhibit different responses to androgens. This makes the kallikrein locus an ideal model to investigate AR signalling. The increasingly dedifferentiated phenotype of aggressive prostate cancer cells is accompanied by the re-expression of signalling molecules that are usually expressed during embryogenesis and foetal tissue development. The Wnt pathway is one developmental cascade that is reactivated in prostate cancer. The canonical Wnt cascade regulates the intracellular levels of β-catenin, a potent transcriptional co-activator of T-cell factor (TCF) transcription factors. Notably, β-catenin can also bind to the AR and synergistically stimulate androgen-mediated gene expression. This is at the expense of typical Wnt/TCF target genes, because the AR:β-catenin and TCF:β-catenin interactions are mutually exclusive. The effect of β-catenin on kallikrein expression was examined to further investigate the role of β-catenin in prostate cancer. Stable knockdown of β-catenin in LNCaP prostate cancer cells attenuated the androgen-regulated expression of KLK2, 3, 4 and 15, but not KLK14. To test whether KLK14 is instead a TCF:β-catenin target gene, the endogenous levels of β-catenin were increased by inhibiting its degradation. Although KLK14 expression was up-regulated by these treatments, siRNA knockdown of β-catenin demonstrated that this effect was independent of β-catenin. These results show that β-catenin is required for maximal expression of KLK2, 3, 4 and 15, but not KLK14. Developmental cells and tumour cells express a similar repertoire of signalling molecules, which means that these different cell types are responsive to one another. Previous reports have shown that stem cells and foetal tissues can reprogram aggressive cancer cells to less aggressive phenotypes by restoring the balance to developmental signalling pathways that are highly dysregulated in cancer. To investigate this phenomenon in prostate cancer, DU145 and PC-3 prostate cancer cells were cultured on matrices pre-conditioned with human embryonic stem cells (hESCs). Soft agar assays showed that prostate cancer cells exposed to hESC conditioned matrices had reduced clonogenicity compared with cells harvested from control matrices. A recent study demonstrated that this effect was partially due to hESC-derived Lefty, an antagonist of Nodal. A member of the transforming growth factor β (TGFβ) superfamily, Nodal regulates embryogenesis and is re-expressed in cancer. The role of Nodal in prostate cancer has not previously been reported. Therefore, the expression and function of the Nodal signalling pathway in prostate cancer was investigated. Western blots confirmed that Nodal is expressed in DU145 and PC-3 cells. Immunohistochemistry revealed greater expression of Nodal in malignant versus benign glands. Notably, the Nodal inhibitor, Lefty, was not expressed at the mRNA level in any prostate cell lines tested. The Nodal signalling pathway is functionally active in prostate cancer cells. Recombinant Nodal treatments triggered downstream phosphorylation of Smad2 in DU145 and LNCaP cells, and stably-transfected Nodal increased the clonogencity of LNCaP cells. Nodal was also found to modulate AR signalling. Nodal reduced the activity of an androgen-regulated KLK3 promoter construct in luciferase assays and attenuated the endogenous expression of AR target genes including prostatic kallikreins. These results demonstrate that Nodal is a novel example of a developmental signalling molecule that is reexpressed in prostate cancer and may have a functional role in prostate cancer progression. In summary, this project clarifies the role of androgens and changing cellular differentiation in prostate cancer by characterising the expression and function of the downstream genes encoding kallikrein-related serine proteases and Nodal. Furthermore, this study emphasises the similarities between prostate cancer and early development, and the crosstalk between developmental signalling pathways and the AR axis. The outcomes of this project also affirm the utility of the kallikrein locus as a model system to monitor tumour progression and the phenotype of prostate cancer cells.