The current and future role of the dietetic support worker.

BACKGROUND: The role of the dietetic support worker (DSW) was developed to provide cost-effective support to dietetic services in the National Health Service (NHS). However, there is little evidence about how the role is perceived or the impact of the introduction of Agenda for Change in 2004 (a guide to pay terms and conditions for NHS staff) on role definition. The present study aimed to gather evidence from DSWs and dietitians on the current role of the DSW to help inform the future development of the role. METHODS: A questionnaire survey was conducted on DSWs and dietitians in 10 trusts in the East of England. Issues included qualifications, experience, training, satisfaction with Agenda for Change, supervision and responsibility. Themes were further explored by semi-structured telephone interviews conducted on a subsample. RESULTS: Eighteen out of 24 DSWs and 62 out of 98 dietitians responded to the questionnaire. The role of the DSW is highly valued by dietitians. Over three-quarters of DSWs and over 90% of dietitians agree that the employment of DSWs improved the working lives of dietitians. Only 50% of DSWs were happy with their Agenda for Change banding, although this did not adversely affect their job satisfaction. Both groups saw the role of the DSW becoming more specialised, despite concerns about access to appropriate training and the lack of a structured career pathway. CONCLUSIONS: This study identified issues relating to the future development of the role of the DSW from the viewpoint of DSWs and dietetic assistants.

Experiences and views of specialist registrars in geriatric medicine on 'do not attempt resuscitation' decisions: a sea of uncertainty?

BACKGROUND: Recent cultural changes place doctors under increasing pressure to work with their patients to reach decisions about end-of-life care. AIM: To survey the experience, practice and opinions of specialist registrars (SPRs) in geriatric medicine regarding 'do not attempt resuscitation' (DNAR) decisions. DESIGN: Postal questionnaire survey. METHODS: A questionnaire was mailed to all members registered as trainees (n = 408) with the British Geriatrics Society in November 2003; a reminder was sent nine weeks later. Responses were analysed using both quantitative and qualitative (thematic) approaches. RESULTS: Response rate was 62% (251/408), of whom 235 were still SpRs. Respondents played a major role in DNAR decision-making in their day-to-day clinical practice. Over a third of respondents did not feel that locally available guidelines were helpful. More than half sometimes disagreed with their consultants' decision, and a fifth were concerned about the possibility of complaints regarding the decisions they made. The majority felt uncomfortable discussing the issue with the patient, and were more likely to discuss the issue with relatives than with patients. DISCUSSION: Further support and training may improve confidence and positive experiences in relation to DNAR decision-making among training-grade doctors in the UK.

Outlet strut fracture of Björk-Shiley convexo concave heart valves: the UK cohort study.

OBJECTIVE: To investigate the risk of outlet strut fracture (OSF) in Björk-Shiley convexo concave (BSCC) valves in relation to patients' clinical and valve characteristics. DESIGN: A cohort of 2977 patients with 3325 valves with a follow up of 18 years. SETTING: 38 cardiac implantation centres in the UK. RESULTS: 56 OSF events were reported with 43 occurring in mitral and 13 in aortic valves. The overall OSF rate was 0.17%/year. No dominant clinical factor of risk was found, but multiple regression analysis identified age, body surface area, valve size, shop order fracture rate, and manufacturing period as risk factors for OSF. A 4% (95% confidence interval (CI) 2% to 6%) decrease in the risk of OSF was observed for each advancing year of age and a fivefold (95% CI 2 to 13) increase in risk for a 0.5 m(2) increase in body surface area. The association between the risk of OSF and valve size was not constant over time. Excess risks among 31 mm and 33 mm sizes (mainly mitral valves) decreased over time while that for 23 mm (almost all aortic valves) increased. The risk of OSF increased by 40% (95% CI 20% to 50%) for a unit increase in the fracture rate of other valves in the same batch. For valves manufactured during 1981 to 1984 the risk of OSF was 4 (95% CI 2 to 12) times greater than for valves manufactured before 1981. CONCLUSIONS: The OSF rates for 60 degrees BSCC valves observed in the UK are the highest among all monitored populations. The changing patterns of mitral and aortic valve OSF rates over time observed in this study have not been identified previously and highlight the need for continued monitoring of patients with the BSCC valve.

Rapid degradation of articular cartilage proteoglycan by neutrophils: comparison with macrophages and synovial fibroblasts.

OBJECTIVE AND DESIGN: To determine and compare the proteoglycan degradative properties of neutrophils, macrophages and synoviocytes in cultures of articular cartilage. MATERIAL OF SUBJECTS: Bovine articular cartilage was aseptically isolated from metacarpopharyngeal joints. Neutrophils and macrophages were isolated from normal human blood and bovine synovial fibroblasts were isolated from explant cultures before being incubated with the cartilage. TREATMENT: Neutrophils, macrophages or synovial fibroblasts (1 x 10(6)-8 x 10(6)) were incubated with 35SO4 labelled cartilage for 2.5-72 h. METHODS: Cartilage degradation was measured as a loss of 35SO4 into the cartilage medium as a percentage of the total labelled proteoglycan in the cartilage slice. Statistical significances were determined using a 2-tailed unpaired Student's t-test. RESULTS: Neutrophils rapidly degraded articular cartilage. After 2.5 hours of culture, neutrophils degraded cartilage proteoglycan up to 28 times more than either macrophages or synovial fibroblasts. CONCLUSIONS: Neutrophils induce rapid damage to articular cartilage proteoglycan, whereas in comparison, macrophages and synovial fibroblasts degrade articular cartilage proteoglycans poorly. These findings indicate that at least under conditions where the influence of cellular-cellular interactions and soluble mediator action are excluded, adhesion of neutrophils to articular cartilage is sufficient to stimulate rapid and marked cartilage degradation compared to the other two cell types.

Bradykinin increases intracellular calcium levels in a human bronchial epithelial cell line via the B2 receptor subtype.

OBJECTIVE: To determine which types of kinin receptor are present in human bronchial epithelial cells we studied the capability of bradykinin to mobilize intracellular Ca2+ ([Ca2+]i) in a human bronchial epithelial cell line (16HBE cells). MATERIAL: Human bronchial epithelial cell line transformed with an original defective simian virus 40 (SV40). TREATMENT: Bradykinin (0.1 pM to 0.1 microM), des-Arg9 bradykinin (1 microM), des-Arg10) kallidin (1 microM), indomethacin (1 microM), phosphoramidon (1 microM), captopril (1 microM), des-Arg9-[Leu8]bradykinin (1 microM), HOE 140 (DArg-[Hyp3, Thi5, DTic , Oic8]-bradykinin) (1 microM), and NPC 16731 (DArg-[Hyp3, Thi5, DTic7, Tic8]-bradykinin) (1 microM). METHODS: The mobilization of [Ca2+]i was determined by the fura-2 method. Two sample Wilcoxon rank-sum (Mann-Whitney) test was used for statistical calculations. RESULTS: Bradykinin, but not the selective agonists for kinin B1 receptor des-Arg9 bradykinin and des-Arg10 kallidin, increased the mobilization of [Ca2+]i (EC50, 0.079+/-0.009nM) in 16HBE cells in a concentration-dependent manner. Pretreatment with the cyclooxygenase inhibitor indomethacin (1 microM) or the peptidase inhibitors, phosphoramidon (1 microM) or captopril (1 microM), did not affect the response to bradykinin. The kinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin (1 microM), was inactive. HOE 140 and NPC 16731, two selective antagonists of the kinin B2 receptor abolished the response to bradykinin (IC50 of HOE 140 and NPC 16731 were 0.52+/-0.037nM and 1.67 +/- 0.41 nM, respectively). CONCLUSIONS: The present data indicate the presence of kinin B2 receptors in the 16HBE cells.

Elevated nerve growth factor levels in the synovial fluid of patients with inflammatory joint disease.

A novel pH shock extraction procedure was used to measure nerve growth factor (NGF) levels in both normal and inflamed synovial fluids using a sensitive and specific two-site enzyme linked immunosorbant assay. To date no data is available on NGF levels in normal synovial fluids. Synovial fluids were taken from 5 normal volunteers, 12 patients with rheumatoid arthritis and 10 patients with other inflammatory arthropathies. The mean +/- SEM NGF concentration in normal synovial fluids was 95 +/- 33.2 pg/ml (range 39.1-143.1 pg/ml), whereas the mean NGF concentration in the synovial fluids taken from patients with rheumatoid arthritis was 532.5 +/- 123.8 pg/ml (range 152-1686 pg/ml). The mean NGF concentration in patients with other inflammatory arthropathies was also raised (430.6 +/- 90 pg/ml; range 89-1071 pg/ml). The NGF concentrations were significantly higher in the synovial fluids from both inflamed groups (ANOVA p < 0.05) compared to normals. Raised levels of NGF in synovial fluid may contribute directly to joint inflammation via activation of inflammatory cells.

The substance P fragment SP-(7-11) increases prostaglandin E2, intracellular Ca2+ and collagenase production in bovine articular chondrocytes.

Substance P (SP) is found in increased concentrations in inflamed joints and is believed to play a role in joint pathology. Culture of bovine articular chondrocytes with SP or with the related mammalian tachykinins neurokinin A or B (NKA or NKB) produced no effect on prostaglandin E2 (PGE2) or collagenase production. However, the C-terminal fragment of SP, SP-(7-11), increased PGE2 and collagenase production at concentrations greater than 1 microM. The N-terminal fragments SP-(1-4) and SP-(1-6) had no effect on PGE2 or collagenase production. In addition, SP-(7-11), but not intact SP, SP-(1-4), SP-(1-6), SP-(8-11) or SP-(9-11), nor the tachykinins NKA and NKB, caused an increase in the intracellular calcium concentration as measured by the fluorescent dye Fura-2. The maximal change in intra-cellular calcium induced by 10 microM SP-(7-11) was 140 +/- 30 nM. We postulate that cleavage of SP by neutral endopeptidases which are present in the synovial fluid and which yield SP-(7-11) may be of biological importance in chondrocyte-mediated cartilage pathology.

A metabolite of substance P, SP7-11 is involved in the pathogenesis of inflammatory joint disease.

The possibility that neuropeptides, in particular members of the tachykinin family are involved in inflammatory joint disease is widely disputed. Both clinical and experimental observations indicate that the tachykinin substance P (SP) may be involved in the pathogenesis of arthritis. We have studied the effects of tachykinins and the metabolites of SP on chondrocyte function. We have shown that the C-terminal pentapeptide sequence; H-Phe-Phe-Gly-Leu-Met-NH2 is biologically active in bovine chondrocyte cultures. The production of SP7-11 is limited by hydrolysis of the intact peptide by neutral endopeptidase (E.C. 3.4.24.11). The regulation of this enzyme would modulate the activity of substance P on articular cartilage chondrocytes.

Failure of tachykinins including substance P and its fragments to influence proteoglycan and protein synthesis in bovine chondrocytes in vitro.

Adult bovine articular chondrocytes were exposed to substance P, neurokinins A and B or substance P fragments, SP1-4, SP1-6 and SP7-11 in vitro. Proteoglycan synthesis was assessed by measuring proteoglycans which were released into the culture medium or incorporated into the cell layer. The intact tachykinins or substance P fragments had no direct effect on proteoglycan synthesis. Nor was total protein production affected. Gel chromatography, under dissociative conditions, revealed that sulphated proteoglycans detected in the medium or cell layer following treatment of chondrocytes with substance P, contained proteoglycans of similar molecular weight to those produced by cells exposed only to diluent controls. Therefore, we conclude that the acceleration of arthritis by substance P does not appear to be mediated through an effect on chondrocyte synthetic function.

Muscle and bone in paraplegic patients, and the effect of functional electrical stimulation.

1. Four paraplegic men volunteered for an exercise programme in which their paralysed quadriceps muscles were stimulated by means of computer-regulated electrical impulses applied through external electrodes. The first exercise regimen consisted of leg raising against a graded load, and during the second regimen exercise took the form of cycling on a modified bicycle ergometer. Each subject exercised five times weekly for 10 weeks during the first regimen and 32 weeks during the second regimen. 2. Whole-body protein turnover determined by L-[1-13C]leucine during feeding remained constant during both exercise regimens, when expressed either in terms of body weight or fat-free mass derived from measurements of total body potassium. 3. Quadriceps muscle protein synthetic rate increased during the study, from 0.0712 to 0.0985%/h (P less than 0.05), as did quadriceps muscle area assessed by computed tomography. 4. Bone mineral content for lumbar vertebrae was normal in all four patients, but for the femoral mid-shaft bone mineral content averaged only 66% of normal for three of the patients. Trabecular bone density in the distal tibia ranged from normal to 2% of normal for the men with the shortest and longest periods of disability, respectively. No changes in bone mineral content or bone density occurred during the exercise period.