Involving mental health service users in quality assurance

OBJECTIVE: This study compares the process and outcomes of two approaches to engaging mental health (MH) service users in the quality assurance (QA) process. BACKGROUND: QA plays a significant role in health and care services, including those delivered in the voluntary sector. The importance of actively, rather than passively, involving service users in evaluation and service development has been increasingly recognized during the last decade. DESIGN: This retrospective small-scale study uses document analysis to compare two QA reviews of a MH Day Centre, one that took place in 1998 as a traditional inspection-type event and one that took place in 2000 as a collaborative process with a user-led QA agenda. Setting and participants The project was undertaken with staff, volunteers and service users in a voluntary sector MH Day Centre. Intervention The study compares the management, style, evaluation tools and service user responses for the two reviews; it considers staff perspectives and discusses the implications of a collaborative, user-led QA process for service development. RESULTS: The first traditional top-down inspection-type QA event had less ownership from service users and staff and served the main purpose of demonstrating that services met organizational standards. The second review, undertaken collaboratively with a user-led agenda focused on different priorities, evolving a new approach to seeking users' views and achieving a higher response rate. CONCLUSIONS: Because both users and staff had participated in most aspects of the second review they were more willing to work together and action plan to improve the service. It is suggested that the process contributed to an evolving ethos of more effective quality improvement and user involvement within the organization.     

Detection of superior mesenteric vein thrombosis following splenectomy using real-time and Doppler sonography

Superior mesenteric vein thrombosis after splenectomy is very rare. In the case described of a patient presenting with acute abdominal pain the diagnosis was made primarily by real-time and Doppler ultrasonography. This reduced the time elapsing before it was recognized that angiography and subsequent thrombectomy were indicated.     

The risk of post-operative infection after reamed intramedullary locked nailing of tibial fractures. A review of 730 cases

Summary 730 consecutive acute reamed intramedullary locked nailing of tibial fractures were studied, according to Gustilo’s classification of soft tissue lesions for the open fractures. There is a significant increase of post-operative infection rate if the tibial fracture is open, and the relative risk increases with the severity of soft tissue lesions. The comparison of these figures with those of other methods of treatment and the mechanical and clinical advantages of nailing leads us to propose this method for treatment of grade I, II and IIIa open fractures, while external the fixator seems better adapted for IIIb and c open fractures. European Bone and Joint Infection Society Meeting, München, Germany, October 7–9, 1993     

Spatiotemporal pattern of striatal ERK1/2 phosphorylation in a rat model of L-DOPA-induced dyskinesia and the role of dopamine D1 receptors.

BACKGROUND: We examined the activation pattern of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and its dependence on D1 versus D2 dopamine receptors in hemiparkinsonian rats treated with 3,4-dihydroxyphenyl-L-alanine (L-DOPA). METHODS: 6-Hydroxydopamine-lesioned rats were treated acutely or chronically with L-DOPA in combination with antagonists for D1 or D2 receptors. Development of dyskinesia was monitored in animals receiving chronic drug treatment. Phosphorylation of ERK1/2, mitogen- and stress-activated protein kinase-1 (MSK-1), and the levels of FosB/DeltaFosB expression were examined immunohistochemically. RESULTS: L-DOPA treatment caused phosphorylation of ERK1/2 in the dopamine-denervated striatum after acute and chronic administration. Similar levels were observed in matrix and striosomes, and in enkephalin-positive and dynorphin-positive neurons. The severity of dyskinesia was positively correlated with phospho-ERK1/2 levels. Phosphorylation of ERK1/2 and MSK-1 was dose-dependently blocked by SCH23390, but not by raclopride. SCH23390 also inhibited the development of dyskinesia and the induction of FosB/DeltaFosB. CONCLUSIONS: L-DOPA produces pronounced activation of ERK1/2 signaling in the dopamine-denervated striatum through a D1-receptor-dependent mechanism. This effect is associated with the development of dyskinesia. Phosphorylated ERK1/2 is localized to both dynorphinergic and enkephalinergic striatal neurons, suggesting a general role of ERK1/2 as a plasticity molecule during L-DOPA treatment.     

Fine mapping by genetic association implicates the chromosome 1q23.3 gene UHMK1, encoding a serine/threonine protein kinase, as a novel schizophrenia susceptibility gene.

BACKGROUND: Linkage studies by us and others have confirmed that chromosome 1q23.3 is a susceptibility locus for schizophrenia. Based on this information, several research groups have published evidence that markers within both the RGS4 and CAPON genes, which are 700 kb apart, independently showed allelic association with schizophrenia. Tests of allelic association with both of these genes in our case control sample were negative. Therefore, we carried out further fine mapping between the RGS4 and CAPON genes. METHODS: Twenty-nine SNP and microsatellite markers in the 1q23.3 region were genotyped in the United Kingdom based sample of 450 cases and 450 supernormal control subjects. RESULTS: We detected positive allelic association after the eighth marker was genotyped and found that three microsatellite markers (p = .011, p = .014, p = .049) and two SNPs (p = .004, p = .043) localized in the 700 kb region between the RGS4 and CAPON genes, within the UHMK1 gene, were associated with schizophrenia. Tests of significance for marker rs10494370 remained significant following Bonferroni correction (alpha = .006) for multiple tests. Tests of haplotypic association were also significant for UHMK1 (p = .009) using empirical permutation tests, which make it unnecessary to further correct for both multiple alleles and multiple markers. CONCLUSIONS: These results provide preliminary evidence that the UHMK1 gene increases susceptibility to schizophrenia. Further confirmation in adequately powered samples is needed. UHMK1 is a serine threonine kinase nuclear protein and is highly expressed in regions of the brain implicated in schizophrenia.     

Alterations in cholinergic and non-cholinergic neurotransmitter receptor densities in transgenic Tg2576 mouse brain with beta-amyloid plaque pathology.

Cholinergic deficits in Alzheimer's disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. To address the question whether beta-amyloid may contribute to these deficits, brain tissue from transgenic Tg2576 mice with Alzheimer plaque pathology at ages of 5 (still no significant plaque load) and 17 months (moderate to high cortical beta-amyloid plaque load) were examined for a number of cholinergic and non-cholinergic markers. Transgenic mice with no significant plaque load demonstrated reduced hemicholinium-3 (HCh-3) binding to choline uptake sites in anterior brain regions as compared to non-transgenic littermates, while in aged transgenic mice with high number of plaque deposits decreased HCh-3 binding levels were accompanied by increased vesicular acetylcholine transporter binding in selected cortical brain regions. In aged transgenic mice GABA(A), NMDA, AMPA, kainate, and beta-adrenergic as well 5-HT(1A)- and 5-HT(2A)-receptor binding levels were hardly affected, whereas alpha(1)- and alpha(2)-adrenoceptor binding was increased in selected cerebral cortical regions as compared to non-transgenic littermates. The development of changes in both cholinergic and non-cholinergic markers in transgenic Tg2576 mouse brain already before the onset of progressive plaque deposition provides in vivo evidence of a modulatory role of soluble beta-amyloid on cortical neurotransmission and may be referred to the deficits in learning and memory observed in these mice also before significant plaque load.     

Interactions between membrane IgM and the cytoskeleton involve the cytoplasmic domain of the immunoglobulin receptor

Cross-linking induced interactions between the membrane form of immunoglobulin (mIg) and the cytoskeletal matrix have been described by several groups. To date, the function of mIgM association with the cytoskeleton is not yet understood. Delineation of the molecular basis of these interactions will be instrumental in elucidating their function. We have previously shown that the Igα/β heterodimer is not required for ligand-induced mIgM binding to the cytoskeleton. In this study, we have investigated the role of other B cell-specific proteins in mediating these interactions. For this, we expressed mIgM in the non-hematopoietic human cervical carcinoma cell line HeLa S3 and verified the capacity of the surface-expressed IgM to interact with the cytoskeletal matrix upon cross-linking with anti-μ chain antibodies. We show here that only the mIgM molecule itself and no other B cell-specific protein(s) is required in mediating mIgM interactions with actin filaments. In an attempt to determine the cytoskeleton-binding site of mIgM we investigated the role of the cytoplasmic tail of mIgM (KVK) in binding the receptor to actin-based microfilaments. Using mutated forms of mIgM expressed in J558L cells, we show here that KVK plays a role in mediating these interactions. The absence of KVK did not, however, completely abrogate mIgM-cytoskeletal interactions, suggesting that there are additional molecular requirements for the ligand-induced mIgM binding to the cytoskeletal matrix.     

Reflective inquiry in nursing practice or 'revealing images'

Reflective inquiry in nursing practice or 'revealing images' Nurses live and work in complex practice worlds; worlds of shrinking resources and expanding needs. Reflection through journaling offers unique opportunities to gain insight into practice. What might we learn from one's journal? A reflective journal can be a source of interplay between the self as written and the self as other. Likewise, the journal may act to situate ourselves in practice, while at the same time enabling us to illuminate how and in what ways our understandings have become distorted. The extent to which one's journal is educative depends upon the manner in which one chooses to use it as a transformative tool, a tool that might well be described as a process of healing and enlightenment. In order to illustrate the reflexive nature of journaling, this paper is presented as a play reading, where a conversation about practice stories between the different aspects of the nurse's self is depicted. In adopting a play reading, an alternative pedagogical tool is used to illustrate different methodologies exemplifying the emergence of how and in what ways we develop and reconstruct our understanding in nursing.