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BACKGROUND: Government health care policy urges service providers to involve service users in the decision-making process. Research studies have recommended changes to current health care practice to facilitate this involvement. However, carers' organizations continue to highlight a gap between policy and practice in relation to involvement. AIM: The aim of the study reported on in this paper was to investigate involvement in a specific health care context with a view to identifying both opportunities for change and practical, realistic ways of bringing about that change. This was a qualitative case study using a case study design. The field site selected was a respite and assessment (23 bedded) ward within the Psychiatric Unit of a hospital specializing in the care of older people. Informal carers (n=20) and members of the multidisciplinary team (n=29) were interviewed about their views and experiences. The interviews were audiorecorded and transcribed. Family meetings, multidisciplinary team meetings and ward routines were the focus of non-participant observation. Field notes from these observations, together with the interview data were analysed using constant comparative method. RESULTS AND CONCLUSIONS. The reported experiences of carers in this study highlighted four markers of satisfactory involvement: feeling that information is shared; feeling included in decision making; feeling that there is someone you can contact when you need to; and feeling that the service is responsive to your needs. The majority of carers felt dissatisfied with the level of involvement. The situation we found echoed that found in other studies, i.e. the majority of informal carers (henceforth 'carers') interviewed were dissatisfied with the level of their involvement. However, our investigation, in which the views of health care professionals as well as those of carers were sought, provided invaluable insight into why this might be the case. Two main sources of difficulty were found: hospital systems and processes, and the relationship between nursing staff and carers. The argument made is that practitioners themselves must notice and challenge these barriers if carer involvement is to be facilitated. [ABSTRACT FROM AUTHOR]

This paper examines the research process in the context of an evaluation of work-based learning. The findings of the evaluation are used to illustrate issues around roles and relationships within interpretivist research where a separation is maintained between the researcher, as investigator, and the participants, as the subject of their investigation. The discussion focuses on: the threatening nature of evaluation and the way in which that affects the process of inquiry and learning; the ways in which people's perceptions of research can act as barriers to the implementation of change; and the consequences of this role separation for practice development. In exploring these issues the paper argues for an approach to evaluation research which (a) emphasizes collaboration, (b) is orientated to change and (c) treats the evaluation process as a learning opportunity through which professionals acquire the skills and knowledge to investigate and advance their own practice. [ABSTRACT FROM AUTHOR]

This paper reports on an evaluation of work-based learning within a postregistration community health nursing degree programme. Work-based learning is primarily concerned with the process of learning and with encouraging the individual to be explicit about how and what they learn so that their experiential learning may be assessed and accredited. The methodology of Illuminative Evaluation was adopted, with case studies (n=6) used as the means of exploring in depth the different perspectives of the major stakeholders (that is, the students, their workplace supervisors and their academic supervisors). The data comprised documentation, participant and nonparticipant observation, interviews and focus groups. The initial aim was to examine the potential benefits of work-based learning to students and to describe its impact on their practice. However, what emerged through the course of inquiry was a gap between the educational philosophy of work-based learning and the way in which work-based learning was delivered within the department concerned. Work-based learning provides educators with an opportunity to debate openly fundamental issues about the nature of educational practice; in particular, about the role of the supervisor in facilitating students' learning. As the evaluation highlights, if this debate does not occur, existing educational practice remains unchanged and the potential benefits to students of this new educational philosophy are not realized. Furthermore, it is by engaging in a reflective process in relation to their own experience that educators can begin to understand how to facilitate that process in others. [ABSTRACT FROM AUTHOR]

Last month Belinda Dewar and colleagues gave the background and policy context of a research study looking at the views of recipients of free care. This month they consider older people's accounts of care tasks important to them and suggest priorities for change. [ABSTRACT FROM AUTHOR]

Background: Imatinib mesylate (imatinib) is the first-line treatment for newly diagnosed chronic myeloid leukemia (CML) due to its remarkable hematologic and cytogenetic responses. We previously demonstrated that the imatinib-resistant CML cells (Myl-R) contained elevated Lyn activity and intracellular creatine pools compared to imatinib-sensitive Myl cells., Methods: Stable isotope metabolic labeling, media creatine depletion, and Na + /K + -ATPase inhibitor experiments were performed to investigate the origin of creatine pools in Myl-R cells. Inhibition and shRNA knockdown were performed to investigate the specific role of Lyn in regulating the Na + /K + -ATPase and creatine uptake., Results: Inhibition of the Na + /K + -ATPase pump (ouabain, digitoxin), depletion of extracellular creatine or inhibition of Lyn kinase (ponatinib, dasatinib), demonstrated that enhanced creatine accumulation in Myl-R cells was dependent on uptake from the growth media. Creatine uptake was independent of the Na + /creatine symporter (SLC6A8) expression or de novo synthesis. Western blot analyses showed that phosphorylation of the Na + /K + -ATPase on Tyr 10 (Y10), a known regulatory phosphorylation site, correlated with Lyn activity. Overexpression of Lyn in HEK293 cells increased Y10 phosphorylation (pY10) of the Na + /K + -ATPase, whereas Lyn inhibition or shRNA knockdown reduced Na + /K + -ATPase pY10 and decreased creatine accumulation in Myl-R cells. Consistent with enhanced uptake in Myl-R cells, cyclocreatine (Ccr), a cytotoxic creatine analog, caused significant loss of viability in Myl-R compared to Myl cells., Conclusions: These data suggest that Lyn can affect creatine uptake through Lyn-dependent phosphorylation and regulation of the Na + /K + -ATPase pump activity., General Significance: These studies identify kinase regulation of the Na + /K + -ATPase as pivotal in regulating creatine uptake and energy metabolism in cells., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient status. TAS1R member 3 (TAS1R3) is a bi-functional protein that recognizes amino acids such as L-glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. It was recently reported that deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass but the underlying cellular mechanism leading to this phenotype remains unclear. Here, we independently corroborate the increased thickness of cortical bone in femurs of 20-week-old male Tas1R3 mutant mice and confirm that Tas1R3 is expressed in the bone environment. Tas1R3 is expressed in undifferentiated bone marrow stromal cells (BMSCs) in vitro and its expression is maintained during BMP2-induced osteogenic differentiation. However, levels of the bone formation marker procollagen type I N-terminal propeptide (PINP) are unchanged in the serum of 20-week-old Tas1R3 mutant mice as compared to controls. In contrast, levels of the bone resorption marker collagen type I C-telopeptide are reduced greater than 60% in Tas1R3 mutant mice. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and their expression levels positively correlate with differentiation status. Collectively, these findings suggest that high bone mass in Tas1R3 mutant mice is due to uncoupled bone remodeling with reduced osteoclast function and provide rationale for future experiments examining the cell-type-dependent role for TAS1R family members in nutrient sensing in postnatal bone remodeling.

Protein kinases play key roles in oncogenic signaling and are a major focus in the development of targeted cancer therapies. Imatinib, a BCR-Abl tyrosine kinase inhibitor, is a successful front-line treatment for chronic myelogenous leukemia (CML). However, resistance to imatinib may be acquired by BCR-Abl mutations or hyperactivation of Src family kinases such as Lyn. We have used multiplexed kinase inhibitor beads (MIBs) and quantitative mass spectrometry (MS) to compare kinase expression and activity in an imatinib-resistant (MYL-R) and -sensitive (MYL) cell model of CML. Using MIB/MS, expression and activity changes of over 150 kinases were quantitatively measured from various protein kinase families. Statistical analysis of experimental replicates assigned significance to 35 of these kinases, referred to as the MYL-R kinome profile. MIB/MS and immunoblotting confirmed the over-expression and activation of Lyn in MYL-R cells and identified additional kinases with increased (MEK, ERK, IKKα, PKCβ, NEK9) or decreased (Abl, Kit, JNK, ATM, Yes) abundance or activity. Inhibiting Lyn with dasatinib or by shRNA-mediated knockdown reduced the phosphorylation of MEK and IKKα. Because MYL-R cells showed elevated NF-κB signaling relative to MYL cells, as demonstrated by increased IκBα and IL-6 mRNA expression, we tested the effects of an IKK inhibitor (BAY 65-1942). MIB/MS and immunoblotting revealed that BAY 65-1942 increased MEK/ERK signaling and that this increase was prevented by co-treatment with a MEK inhibitor (AZD6244). Furthermore, the combined inhibition of MEK and IKKα resulted in reduced IL-6 mRNA expression, synergistic loss of cell viability and increased apoptosis. Thus, MIB/MS analysis identified MEK and IKKα as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML. These results demonstrate the utility of MIB/MS as a tool to identify dysregulated kinases and to interrogate kinome dynamics as cells respond to targeted kinase inhibition.

The metastasis-associated tyrosine phosphatase PRL-3/PTP4A is upregulated in numerous cancers, but the mechanisms modulating PRL-3 activity other than its expression levels have not been investigated. Here we report evidence for both Src-dependent tyrosine phosphorylation of PRL-3 and Src-mediated regulation of PRL-3 biological activities. We used structural mutants, pharmacological inhibitors and siRNA to demonstrate Src-dependent phosphorylation of endogenous PRL-3 in SW480 colon cancer cells. We also demonstrated that PRL-3 was not tyrosine phosphorylated in SYF mouse embryo fibroblasts deficient in Src, Yes and Fyn unless Src was re-expressed. Further, we show that platelet-derived growth factor (PDGF) can stimulate PRL-3 phosphorylation in a Src-dependent manner. Finally, we show that PRL-3-induced cell motility, Matrigel invasion and activation of the cytoskeleton-regulating small GTPase RhoC were abrogated in the presence of the phosphodeficient PRL-3 mutant Y53F, or by use of a Src inhibitor. Thus, PRL-3 requires the activity of a Src kinase, likely Src itself, to promote these cancer-associated phenotypes. Our data establish a model for the regulation of PRL-3 by Src that supports the possibility of their coordinate roles in signaling pathways promoting invasion and metastasis, and supports simultaneous use of novel molecularly targeted therapeutics directed at these proteins.

Kes1, and other oxysterol-binding protein superfamily members, are involved in membrane and lipid trafficking through trans-Golgi network (TGN) and endosomal systems. We demonstrate that Kes1 represents a sterol-regulated antagonist of TGN/endosomal phosphatidylinositol-4-phosphate signaling. This regulation modulates TOR activation by amino acids and dampens gene expression driven by Gcn4, the primary transcriptional activator of the general amino acid control regulon. Kes1-mediated repression of Gcn4 transcription factor activity is characterized by nonproductive Gcn4 binding to its target sequences, involves TGN/endosome-derived sphingolipid signaling, and requires activity of the cyclin-dependent kinase 8 (CDK8) module of the enigmatic "large Mediator" complex. These data describe a pathway by which Kes1 integrates lipid metabolism with TORC1 signaling and nitrogen sensing., (Copyright © 2012 Elsevier Inc. All rights reserved.)

The goal of this study was to examine metabolic differences between a novel chronic myelogenous leukemic (CML) cell line, MyL, and a sub-clone, MyL-R, which displays enhanced resistance to the targeted Bcr-Abl tyrosine kinase inhibitor imatinib. (1)H nuclear magnetic resonance (NMR) spectroscopy was carried out on cell extracts and conditioned media from each cell type. Both principal component analysis (PCA) and specific metabolite identification and quantification were used to examine metabolic differences between the cell types. MyL cells showed enhanced glucose removal from the media compared to MyL-R cells with significant differences in production rates of the glycolytic end-products, lactate and alanine. Interestingly, the total intracellular creatine pool (creatine + phosphocreatine) was significantly elevated in MyL-R compared to MyL cells. We further demonstrated that the MyL-R cells converted the creatine to phosphocreatine using non-invasive monitoring of perfused alginate-encapsulated MyL-R and MyL cells by in vivo (31)P NMR spectroscopy and subsequent HPLC analysis of extracts. Our data demonstrated a clear difference in the metabolite profiles of drug-resistant and sensitive cells, with the biggest difference being an elevation of creatine metabolites in the imatinib-resistant MyL-R cells.

Wrch-1 is an atypical Rho family small GTPase with roles in migration, epithelial cell morphogenesis, osteoclastogenesis, and oncogenic transformation. Here, we observed rapid relocalization of Wrch-1 from the plasma membrane upon serum stimulation. Studies revealed a requirement for serum-stimulated tyrosine phosphorylation of Wrch-1 at residue Y254 within its C-terminal membrane targeting domain, mediated by the nonreceptor tyrosine kinase Src. Genetic or pharmacological loss of Src kinase activity blocked both phosphorylation and relocalization of Wrch-1. Functionally, Y254 was required for proper Wrch-1 modulation of cystogenesis in three-dimensional culture, and the phospho-deficient mutant, Y254F, was enhanced in Wrch-1-mediated anchorage-independent growth. Mechanistically, C-terminal tyrosine phosphorylation and subsequent relocalization of Wrch-1 downregulated its ability to interact with and activate its effectors by decreasing active Wrch-1-GTP, perhaps by altering proximity to a GEF or GAP. Phospho-deficient Wrch-1(Y254F) remained at the plasma membrane and GTP bound and continued to recruit and activate its effector PAK, even upon serum stimulation. In contrast, a phospho-mimetic mutant, Y254E, was constitutively endosomally localized and GDP bound and failed to recruit PAK unless mutated to be constitutively active/GAP insensitive. C-terminal tyrosine phosphorylation thus represents a new paradigm in posttranslational control of small GTPase localization, activation, and biological function.

The purpose of this study was to combine a three-dimensional NMR-compatible bioreactor with hyperpolarized (13)C NMR spectroscopy in order to probe cellular metabolism in real time. JM1 (immortalized rat hepatoma) cells were cultured in a three-dimensional NMR-compatible fluidized bioreactor. (31)P spectra were acquired before and after each injection of hyperpolarized [1-(13)C] pyruvate and subsequent (13)C spectroscopy at 11.7 T. (1)H and two-dimensional (1)H-(1)H-total correlation spectroscopy spectra were acquired from extracts of cells grown in uniformly labeled (13)C-glucose, on a 16.4 T, to determine (13)C fractional enrichment and distribution of (13)C label. JM1 cells were found to have a high rate of aerobic glycolysis in both two-dimensional culture and in the bioreactor, with 85% of the (13)C label from uniformly labeled (13)C-glucose being present as either lactate or alanine after 23 h. Flux measurements of pyruvate through lactate dehydrogenase and alanine aminotransferase in the bioreactor system were 12.18 +/- 0.49 nmols/sec/10(8) cells and 2.39 +/- 0.30 nmols/sec/10(8) cells, respectively, were reproducible in the same bioreactor, and were not significantly different over the course of 2 days. Although this preliminary study involved immortalized cells, this combination of technologies can be extended to the real-time metabolic exploration of primary benign and cancerous cells and tissues prior to and after therapy.

The Rnd proteins (Rnd1, Rnd2 and Rnd3/RhoE) form a distinct branch of the Rho family of small GTPases. Altered Rnd3 expression causes changes in cytoskeletal organization and cell cycle progression. Rnd3 functions to decrease RhoA activity, but how Rnd3 itself is regulated to cause these changes is still under investigation. Unlike other Rho family proteins, Rnd3 is regulated not by GTP/GDP cycling, but at the level of expression and by post-translational modifications such as prenylation and phosphorylation. We show in the present study that, upon PKC (protein kinase C) agonist stimulation, Rnd3 undergoes an electrophoretic mobility shift and its subcellular localization becomes enriched at internal membranes. These changes are blocked by inhibition of conventional PKC isoforms and do not occur in PKCalpha-null cells or to a non-phosphorylatable mutant of Rnd3. We further show that PKCalpha directly phosphorylates Rnd3 in an in vitro kinase assay. Additionally, we provide evidence that the phosphorylation status of Rnd3 has a direct effect on its ability to block signalling from the Rho-ROCK (Rho-kinase) pathway. These results identify an additional mechanism of regulation and provide clarification of how Rnd3 modulates Rho signalling to alter cytoskeletal organization.

Thiazolidinediones (TZDs) are synthetic ligands for the peroxisome proliferator-activated receptor gamma (PPARgamma) but also elicit PPARgamma-independent effects, most notably activation of mitogen-activated protein kinases (MAPKs). Ciglitazone rapidly activates extracellular signal-regulated kinase (Erk) MAPK, an event requiring c-Src kinase-dependent epidermal growth factor receptor (EGFR) transactivation, whereas troglitazone only weakly activates Erk and does not induce EGFR transactivation; the mechanism underlying this difference remains unclear. In this study, both ciglitazone and troglitazone increased Src activation. Similar effects were observed with Delta2-derivatives of each TZD, compounds that bind PPARgamma but do not lead to its activation, further indicating a PPARgamma-independent mechanism. Neither EGFR kinase nor Pyk2 inhibition prevented Src activation; however, inhibition of Src kinase activity prevented Pyk2 activation. Intracellular calcium chelation blocks TZD-induced Pyk2 activation; here, Src activation by both TZDs and ciglitazone-induced EGFR transactivation were prevented by calcium chelation. Accordingly, both TZDs increased calcium concentrations from intracellular stores; however, only ciglitazone produced a secondary calcium influx in the presence of extracellular calcium. Removal of extracellular calcium or inhibition of capacitative calcium entry by 2-APB prevented ciglitazone-induced EGFR transactivation and Erk activation but did not affect upstream kinase signaling pathways. These results demonstrate that upstream kinases (i.e., Src and Pyk2) are required but not sufficient for EGFR transactivation by TZDs. Moreover, influx of extracellular calcium through capacitative calcium entry may be an unrecognized component that provides a mechanism for the differential induction of EGFR transactivation by these compounds.

Peroxisome proliferator-activated receptors (PPARs) are a subfamily of nuclear hormone receptors that function as ligand-activated transcription factors to regulate lipid metabolism and homeostasis. In addition to their ability to promote gene transcription in a PPAR-dependent manner, ligands for this receptor family have recently been shown to induce mitogen-activated protein kinase (MAPK) phosphorylation. It is noteworthy that the transcriptional changes induced by PPAR ligands can be separated into distinct PPAR- and MAPK-dependent signaling pathways, suggesting that MAPKs alone mediate some of the effects of PPAR agonists in a nongenomic manner. This review will highlight recent studies that elucidate the nongenomic mechanisms of PPAR ligand-induced MAPK phosphorylation. The potential relevance of MAPK signaling in PPAR biology is also discussed.

Research and development work in health and social care are increasingly required to involve users at all stages of the research process yet there is scant empirical evidence to support the justification of this laudable aim. Evidence does suggest that at present efforts to achieve this are primarily tokenistic and that more work is needed, both to examine what user involvement in research activity actually means, and how this can best be supported. This paper sets out to describe developments to support involvement of older people through work at the Royal Bank of Scotland Centre for the Older Person's Agenda and to identify a number of challenges that this has raised for researchers. These challenges have arisen out of a number of assumptions that underpin the process of user involvement. The paper discusses some of the benefits of working in partnership with older people and identifies strategic issues for consideration in order to promote future partnership working.

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that function as ligand-activated transcription factors regulating lipid metabolism and homeostasis. In addition to their ability to regulate PPAR-mediated gene transcription, PPARalpha and gamma ligands have recently been shown to induce activation of mitogen-activated protein kinases (MAPKs), which in turn phosphorylate PPARs, thereby affecting transcriptional activity. However, the mechanism for PPAR ligand-dependent MAPK activation is unclear. In the current study, we demonstrate that various PPARalpha (nafenopin) and gamma (ciglitazone and troglitazone) agonists rapidly induced extracellular signal-regulated kinase (Erk) and/or p38 phosphorylation in rat liver epithelial cells (GN4). The selective epidermal growth factor receptor (EGFR) kinase inhibitors, PD153035 and ZD1839 (Iressa), abolished PPARalpha and gamma agonist-dependent Erk activation. Consistent with this, PPAR agonists increased tyrosine autophosphorylation of the EGFR as well as phosphorylation at a putative Src-specific site, Tyr845. Experiments with the Src inhibitor, PP2, and the antioxidant N-acetyl-L-cysteine revealed critical roles for Src and reactive oxygen species as upstream mediators of EGFR transactivation in response to PPAR ligands. Moreover, PPARalpha and gamma ligands increased Src autophosphorylation as well as kinase activity. EGFR phosphorylation, in turn, led to Ras-dependent Erk activation. In contrast, p38 activation by PPARalpha and gamma ligands occurred independently of Src, oxidative stress, the EGFR, and Ras. Interestingly, PPARalpha and gamma agonists caused rapid activation of proline-rich tyrosine kinase or Pyk2; Pyk2 as well as p38 phosphorylation was reduced by intracellular Ca2+ chelation without an observable effect on EGFR and Erk activation, suggesting a possible role for Pyk2 as an upstream activator of p38. In summary, PPARalpha and gamma ligands activate two distinct signaling cascades in GN4 cells leading to MAPK activation.

Zn(2+) is a ubiquitous ambient air contaminant that is found as a constituent of airborne particulate matter (PM). Previous studies have associated Zn(2+) levels in PM with health effects in exposed populations and have shown proinflammatory properties of Zn(2+) exposure in vivo and in vitro. In the present study, we studied the mechanisms of epidermal growth factor receptor (EGFR) dimerization, phosphorylation, and kinase activity in A431 cells treated with Zn(2+). EGF, but not Zn(2+), induced dimerization of EGFR in A431 cells and membrane extracts. Like EGF, Zn(2+) induced phosphorylation of EGFR at tyrosines 845, 1068, and 1173. However, unlike EGF, Zn(2+) failed to induce detectable dimerization of EGFR. The EGFR kinase inhibitor PD153035 ablated all phosphorylation induced by EGF but none caused by Zn(2+). PD153035 abolished EGF-induced phosphorylation of the EGFR substrate Cbl, but had no effect on levels of phospho-Cbl caused by Zn(2+). Inhibition of EGFR kinase activity did, however, blunt Zn(2+)-induced phosphorylation of ERK. Exposure to Zn(2+), but not EGF, induced phosphorylation of the activating site of c-Src (tyrosine 416), and Zn(2+)-induced phosphorylation of EGFR at tyrosines 845 and 1068 was blocked by the c-Src kinase activity inhibitor PP2. In summary, Zn(2+) ions induce EGFR phosphorylation in a manner dependent on c-Src but not on EGFR dimerization or EGFR kinase activation, suggesting that Zn(2+) induces EGFR transactivation by c-Src.

Nicotine influences energy metabolism, yet mechanisms remain unclear. Since the liver is one of the largest organs and performs many metabolic functions, the goal of this study was to determine whether nicotine would affect respiration and other metabolic functions in the isolated perfused liver. Infusion of 85 microM nicotine caused a rapid 10% increase in oxygen uptake over basal values of 105 +/- 5 micromol/g/h in perfused livers from fed rats, and an increase of 27% was observed with 850 microM nicotine. Concomitantly, rates of glycolysis of 105 +/- 8 micromol/g/h were decreased to 52 +/- 9 micromol/g/h with nicotine, whereas ketone body production was unaffected. Nicotine had no effect on oxygen uptake in glycogen-depleted livers from 24-h fasted rats. Furthermore, addition of glucose to perfused livers from fasted rats partially restored the stimulatory effect of nicotine. Infusion of atractyloside, potassium cyanide, or glucagon blocked the nicotine-induced increase in respiration. Intracellular calcium was increased in isolated hepatocytes by nicotine, a phenomenon prevented by incubation of cells with d-tubocurarine, a nicotinic acetylcholine receptor antagonist. Respiration was also increased approximately 30% in hepatocytes isolated from fed rats by nicotine, whereas hepatocytes isolated from fasted rats showed little response. In the presence of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), an inhibitor of cyclic AMP-dependent protein kinase A, nicotine failed to stimulate respiration. These data support the hypothesis that inhibition of glycolysis by nicotine increases oxygen uptake due to an ADP-dependent increase in mitochondrial respiration.

The aim of this study was to examine current practices within the Lothian Health Board area in relation to reporting of occupationally induced musculoskeletal injuries, training in moving and handling, and use of mechanical aids. A sample of 5,184 nurses working throughout the health board was given a questionnaire containing both open and closed questions. The results showed a significant proportion of nurses had time off work due to musculoskeletal injury and that this was related to grade and specialty. There was also a significant proportion of the respondents who did not report injuries and/or who experienced pain/discomfort, but did not take time off work. Present moving and handling training appears to be inadequate and too infrequent for the needs of staff. These findings emphasise the need for a review of both accident reporting systems and training, in particular in the use of mechanical aids.

This paper presents an overview of research into the role of paid non-professional nursing helpers. This term refers to auxiliaries, ward clerks, healthcare assistants and support workers. The focus of the review is on work carried out on attitudes of qualified staff to the role of the helper, role descriptions and the role of the helper in different organizational modes of work. Some of the research reviewed in relation to the role description and attitudes to the helper date back to 1978. However, the emphasis of the paper is on research published in the past 3 years. The research is reviewed against the background of two theoretical frameworks, both of which are perceived to be useful in analysing the division of labour between the nurse, the patient and the helper.