496 research outputs found
Learning from people with long-term conditions: new insights for governance in primary health care
Internationally, system-wide changes to the structures and systems governing health care aim to improve outcomes for patients, quality of care and access to services. The introduction of top-down centrally driven solutions to governance of health care, at the same time as increasing policy emphasis on greater ‘bottom up’ patient and public involvement in all aspects of health care, has set up complex tensions for policy implementation and health care practice. This paper explores the interplay of these agendas in the context of changes in primary health care services provided by the National Health Service (NHS) in England. Specifically, it looks at an example of service user involvement in a study (the PEGI study) of professional response to changes in the governance and incentives in the care of people with long-term conditions. This qualitative study was conducted in three Primary Care Trust sites in England. Service users influenced and guided the study throughout. In-depth interviews with 56 health and social care professionals engaged in the development of local policies and the delivery of care for people with complex long-term illness drew on vignettes developed by 32 members from three Service User Reference Groups (SURG). Themes generated by the cross case analysis were validated through these SURG groups. The findings presented here focus on four themes about risk and comparison of professionals’/service users’ perspectives of the issues: managing risks/consistent support, the risks of letting go/feeling in control, professionalism/helping people to help themselves, and managing expectations/professionals losing out. Service user involvement added value by: validating understandings of governance, framing debates to focus on what matters at the point of care, and enabling perspective sharing and interaction. We suggest that more collaborative forms of governance in health care, that take account of service user perspectives and enable interaction with professional groups, could help to validate processes of quality assurance and provide motivation for continuous quality improvement. We offer a model for ‘opening up’ collaborative projects to evaluation and appraisal and a process for critical reflection of the interrelationships between the PEGI study context, researcher issues, methods/approach and outcomes/impact of service user involvement
Adult Social Work and High Risk Domestic Violence Cases
Summary
This article focuses on adult social work’s response in England to high-risk domestic violence cases and the role of adult social workers in Multi-Agency Risk and Assessment Conferences. (MARACs). The research was undertaken between 2013-2014 and
focused on one city in England and involved the research team attending MARACs, Interviews with 20 adult social workers, 24 MARAC attendees, 14 adult service users at time T1 (including follow up interviews after six months, T2), focus groups with IDVAs and Women’s Aid and an interview with a Women’s Aid service user.
Findings
The findings suggest that although adult social workers accept the need to be involved in domestic violence cases they are uncertain of what their role is and are confused with the need to operate a parallel domestic violence and adult safeguarding approach, which is further, complicated by issues of mental capacity. MARACS are identified as overburdened, under-represented meetings staffed by committed managers. However, they are in danger of becoming managerial processes neglecting the service users they are meant to protect.
Applications
The article argues for a re-engagement of adult social workers with domestic violence that has increasingly become over identified with child protection. It also raises the issue whether MARACS remain fit for purpose and whether they still represent the best possible response to multi-agency coordination and practice in domestic violence
Values associated with public involvement in health and social care research: a narrative review
addresses: Mood Disorders Centre, Psychology, University of Exeter, Exeter, UK.OnlineOpen articleMuch has been written about public involvement (PI) in health and social care research, but underpinning values are rarely made explicit despite the potential for these to have significant influence on the practice and assessment of PI.Medical Research Council’s
Methodology Research Programm
Stress-Induced Reinstatement of Drug Seeking: 20 Years of Progress
In human addicts, drug relapse and craving are often provoked by stress. Since 1995, this clinical scenario has been studied using a rat model of stress-induced reinstatement of drug seeking. Here, we first discuss the generality of stress-induced reinstatement to different drugs of abuse, different stressors, and different behavioral procedures. We also discuss neuropharmacological mechanisms, and brain areas and circuits controlling stress-induced reinstatement of drug seeking. We conclude by discussing results from translational human laboratory studies and clinical trials that were inspired by results from rat studies on stress-induced reinstatement. Our main conclusions are (1) The phenomenon of stress-induced reinstatement, first shown with an intermittent footshock stressor in rats trained to self-administer heroin, generalizes to other abused drugs, including cocaine, methamphetamine, nicotine, and alcohol, and is also observed in the conditioned place preference model in rats and mice. This phenomenon, however, is stressor specific and not all stressors induce reinstatement of drug seeking. (2) Neuropharmacological studies indicate the involvement of corticotropin-releasing factor (CRF), noradrenaline, dopamine, glutamate, kappa/dynorphin, and several other peptide and neurotransmitter systems in stress-induced reinstatement. Neuropharmacology and circuitry studies indicate the involvement of CRF and noradrenaline transmission in bed nucleus of stria terminalis and central amygdala, and dopamine, CRF, kappa/dynorphin, and glutamate transmission in other components of the mesocorticolimbic dopamine system (ventral tegmental area, medial prefrontal cortex, orbitofrontal cortex, and nucleus accumbens). (3) Translational human laboratory studies and a recent clinical trial study show the efficacy of alpha-2 adrenoceptor agonists in decreasing stress-induced drug craving and stress-induced initial heroin lapse
Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set
We report a measurement of the bottom-strange meson mixing phase \beta_s
using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays
in which the quark-flavor content of the bottom-strange meson is identified at
production. This measurement uses the full data set of proton-antiproton
collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment
at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity.
We report confidence regions in the two-dimensional space of \beta_s and the
B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2,
-1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in
agreement with the standard model expectation. Assuming the standard model
value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +-
0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +-
0.009 (syst) ps, which are consistent and competitive with determinations by
other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012
Polymorphism of the Fractalkine Receptor CX3CR1 and Systemic Sclerosis-associated Pulmonary Arterial Hypertension
Fractalkine (FKN) and its receptor CX3CR1 are critical mediators in the
vascular and tissue damage of several chronic diseases, including systemic
sclerosis (SSc) and pulmonary arterial hypertension (PAH). Interestingly, the V249I
and T280M genetic polymorphisms influence CX3CR1 expression and function. We
investigated whether these polymorphisms are associated with PAH secondary to
SSc. CX3CR1 genotypes were analyzed by PCR and sequencing in 76 patients with
limited SSc and 204 healthy controls. PAH was defined by colorDoppler echocardiography.
Homozygosity for 249II as well as the combined presence of 249II and 280MM were
significantly more frequent in patients with SSc compared to controls (17 vs 6%,
p = 0.0034 and 5 vs 1%, p = 0.0027, respectively). The 249I and 280M alleles were
associated with PAH (odd ratio [OR] 2.2, 95% confidence interval [CI] 1.01-4.75,
p = 0.028 and OR 7.37, 95%CI: 2.45-24.60, p = 0.0001, respectively). In conclusion,
the increased frequencies of 249I and 280M CX3CR1 alleles in a subgroup of
patients with SSc-associated PAH suggest a role for the fractalkine system in
the pathogenesis of this
condition. Further, the 249I allele might be associated with susceptibility to SSc
Downregulation of ETS Rescues Diabetes-Induced Reduction of Endothelial Progenitor Cells
Transplantation of vasculogenic progenitor cells (VPC) improves neovascularization after ischemia. However, patients with type 2 diabetes mellitus show a reduced VPC number and impaired functional activity. Previously, we demonstrated that p38 kinase inhibition prevents the negative effects of glucose on VPC number by increasing proliferation and differentiation towards the endothelial lineage in vitro. Moreover, the functional capacity of progenitor cells is reduced in a mouse model of metabolic syndrome including type 2 diabetes (Lepr(db)) in vivo.The aim of this study was to elucidate the underlying signalling mechanisms in vitro and in vivo. Therefore, we performed DNA-protein binding arrays in the bone marrow of mice with metabolic syndrome, in blood-derived progenitor cells of diabetic patients as well as in VPC ex vivo treated with high levels of glucose. The transcriptional activation of ETS transcription factors was increased in all samples analyzed. Downregulation of ETS1 expression by siRNA abrogated the reduction of VPC number induced by high-glucose treatment. In addition, we observed a concomitant suppression of the non-endothelial ETS-target genes matrix metalloproteinase 9 (MMP9) and CD115 upon short term lentiviral delivery of ETS-specific shRNAs. Long term inhibition of ETS expression by lentiviral infection increased the number of cells with the endothelial markers CD144 and CD105.These data demonstrate that diabetes leads to dysregulated activation of ETS, which blocks the functional activity of progenitor cells and their commitment towards the endothelial cell lineage
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