Evaluation of adherence to a nutrition-screening programme over a 5-year period.

BACKGROUND: Nutrition screening using the Malnutrition Universal Screening Tool (MUST) was implemented for adult patients in 2006. The aim of this study was to assess adherence to the screening programme over a 5-year period after a targeted approach to training ward staff. SUBJECTS/METHODS: Following the implementation of MUST on 32 wards, regular audits were carried out. Data on completion rates at ward level were collected by nutrition link nurses and submitted electronically for collation. RESULTS: Data on MUST were collected on a total of 17 876 patients during this period. Mean percentage of patients screened with a moderate or high risk of malnutrition was 19% in those screened within 24 h after admission and 28% in those screened at 7 days. Twenty percent of patients had an uncompleted MUST score at 24 h after admission and 15% were uncompleted after 7 inpatient days. After implementation, half the hospital population were being screened on admission. However, a number of wards were neither reporting the data nor completing the screening process. Following targeted training on wards, screening rates improved in 2009 and the number of patients screened improved as ward engagement increased. CONCLUSION: Audit has been fundamental in the implementation of MUST and has allowed training, additional time and educational resources to be allocated to specific wards to facilitate improvements in screening. Lead nurse support and monitoring has improved adherence rates and facilitated an increase in the identification of patients at moderate and high risk of malnutrition.

Improving adherence to a care plan generated from the Malnutrition Universal Screening Tool.

BACKGROUND/OBJECTIVES: Recommendations state that all hospital patients should be screened for malnutrition and for each level of risk, a suitable care plan should be available. This study investigates current practice at ward level regarding adherence to a care plan generated from a nutrition screening tool, and then aims to improve basic nutritional support actions by modifying a care plan and finally evaluates change in practice. SUBJECTS/METHODS: Pro formas were completed on nutrition care plans of 100 patients. Subsequently, 7 focus groups were conducted, which included 30 ward staff and 6 dietitians. Care plans were re-designed using information from focus groups, followed by a second set of pro formas on the care plans of 103 patients. RESULTS: Themes regarding barriers and facilitators for completion of care plans were derived from the focus groups including: 'duplication', 'time pressures', 'leadership support', 'operational issues', 'document style' and 'training'. Pro formas before and after re-design showed that nutritional support actions increased from 13 (9%) to 98 (52%) for patients at moderate or severe risk of malnutrition (P=0.033). CONCLUSIONS: Focus groups allowed engagement with ward staff to explore how care plans were used, which assisted in re-designing the care plan, while the pro formas identified limitations of initial procedures and then evaluated change. Subsequently, basic nutritional support actions that resulted from screening improved. The suitability of care plans to facilitate basic nutritional support and documentation was enhanced. However, improvements are still required, emphasising the necessity for continued training and a strategic approach to the delivery of basic nutritional care.

The potential for short rotation energy forestry on restored landfill caps.

This review examines the potential for producing biomass on restored landfills using willow and poplar species in short rotation energy forestry. In southern England, the potential production may be about 20 t ha(-1) of dry stem wood annually. However, actual yields are likely to be constrained by detrimental soil conditions, including shallow depth, compaction, low water holding capacity and poor nutritional status. These factors will affect plant growth by causing drought, waterlogging, poor soil aeration and nutritional deficiencies. Practical solutions to these problems include the correct placement and handling of the agricultural cap material, soil amelioration using tillage and the addition of organic matter (such as sewage sludge), irrigation (possibly using landfill leachate), the installation of drainage and the application of inorganic fertilizers. The correct choice of species and clone, along with good site management are also essential if economically viable yields are to be obtained. Further investigations are required to determine the actual yields that can be obtained on landfill sites using a range of management inputs.

Role of mitochondrial DNA mutations in disease and aging.

Since Harman in 1972 first proposed a role in the process of aging for the mitochondrial genome, a wealth of evidence has been accumulated to support this theory. We discuss the hereditary mitochondrial DNA disorders, which we believe may give insight into both normal aging and neurodegenerative conditions. We then review the evidence for the role of mitochondrial DNA mutations in both aging and age-related disorders and also discuss new approaches for investigating the mitochondrial genome at a single cell level, by observing the activity of the mitochondrial enzyme cytochrome c oxidase.

Analysis of mitochondrial DNA mutations : deletions.

Although the precise mechanisms of the aging process remain poorly understood, a plausible theory for cellular dysfunction and deterioration during aging involves mitochondria (1, 2). The major function of mitochondria is to generate energy for cellular processes in the form of ATP by oxidative phosphorylation. Mitochondria contain their own DNA (mtDNA), a small 16.5 kb circular molecule that encodes 13 essential polypeptides of the mitochondrial respiratory chain, as well as 2 rRNAs and 22 tRNAs required for intramitochondrial protein synthesis (3). The mitochondrial respiratory chain is a series of five, multisubunit protein complexes located within the inner mitochondrial membrane. The first four of these (complexes I-IV) reoxidize reduced cofactors (NADH and FADH(2)) generated by the oxidation of foodstuffs, thereby generating an electrochemical gradient across the inner mitochondrial membrane which is harnessed by the fifth complex, the ATP synthetase, to drive the formation of ATP.

Role of mitochondrial DNA mutations in human aging: implications for the central nervous system and muscle.

It has been proposed that one mechanism for nerve and muscle dysfunction with age involves the mitochondria. Mitochondria contain the only DNA outside the nucleus in mammalian cells. Mitochondrial DNA (mtDNA) has a high mutation rate, and low levels of pathogenic mutations have been found in tissues from elderly subjects. However, the role of these mutations in the aging process is uncertain unless a mechanism can be identified that would lead to a biochemical defect. In muscle tissue from normal elderly subjects we show that there are muscle fibers with very low activity of cytochrome c oxidase, suggestive of a mtDNA defect. In these cytochrome c oxidase-deficient fibers we have found very high levels of mutant mtDNA. In addition, different mtDNA mutations are present in different fibers, which explains why there is a low overall incidence of an individual mutation in tissues from elderly subjects. These studies show a direct age-related correlation between a biochemical and genetic defect in normal human tissues and that mtDNA abnormalities are involved in the aging process in human muscle.

Mitochondrial involvement in the ageing process. Facts and controversies.

Mitochondria are believed to be involved in human ageing. Whilst it is clear that various mitochondrial DNA mutations do accumulate in human tissues with age, whether or not they interfere with respiratory chain function is uncertain. We question the results of previous studies which have measured respiratory chain function in human skeletal muscle with age. Whilst cytochrome c oxidase deficient fibres are a real finding in skeletal muscle, the contribution of mitochondrial DNA mutations to human ageing is still controversial. Our results show for mitochondria to be involved in ageing then it must be through a more subtle mechanism than a global decline in respiratory chain function.

A new mtDNA mutation showing accumulation with time and restriction to skeletal muscle.

We have identified a new mutation in mtDNA, involving tRNALeu(CUN) in a patient manifesting an isolated skeletal myopathy. This heteroplasmic A-->G transition at position 12320 affects the T psi C loop at a conserved site and was not found in 120 controls. Analysis of cultured fibroblasts, white blood cells/platelets, and skeletal muscle showed that only skeletal muscle contained the mutation and that only this tissue demonstrated a biochemical defect of respiratory-chain activity. In a series of four muscle-biopsy specimens taken over a 12-year period, there was a gradual increase, from 70% to 90%, in the overall level of mutation, as well as a marked clinical deterioration. Single-fiber PCR confirmed that the proportion of mutant mtDNA was highest in cytochrome c oxidase-negative fibers. This study, which reports a mutation involving tRNALeu(CUN), demonstrates clearly that mtDNA point mutations can accumulate over time and may be restricted in their tissue distribution. Furthermore, clinical deterioration seemed to follow the increase in the level of mutation, although, interestingly, the appearance of fibers deficient in respiratory-chain activity showed a lag period.

Effects of physical activity and age on mitochondrial function.

It has been proposed that ageing results from the accumulation of mitochondrial DNA mutations with age which interfere with respiratory chain ATP production. Insufficient ATP production impairs cell function, and tissue dysfunction ensues, leading to morbidity, decline and eventually death. Supporting this theory, mitochondrial DNA mutations accumulate with age and respiratory chain function declines dramatically in human skeletal muscle. However, the extent of decline in respiratory chain function is greater (50%) than anticipated from the low levels of mitochondrial DNA mutations (< 1%) observed in aged muscle. We hypothesized that an age-related reduction in physical activity could be an important factor in this decline and thus studied the influence of chronological age on muscle mitochondria in subjects matched for levels of physical activity. In this carefully selected group, there was little correlation between oxidative metabolism and age. However, several parameters of respiratory chain function did correlate with markers of physical activity (activity score and handgrip strength). Our results suggest that reduced physical activity is a major contribution to the decline in mitochondrial oxidations during ageing. Physical activity ameliorates and may even mask mitochondrial 'ageing' in muscle.

Normal respiratory chain function in patients with low-tension glaucoma.

OBJECTIVE: To test the hypothesis that low-tension glaucoma has a pathogenesis similar to Leber's hereditary optic neuropathy and results from a defect in the mitochondrial respiratory chain. METHODS: Mitochondrial fractions were prepared from skeletal muscle samples collected from eight subjects with low-tension glaucoma. Their oxidative metabolism was compared with that of age- and sex-matched controls. Skeletal muscle DNA prepared from the subjects with glaucoma was also screened for the 3,460, 11,778, and 14,484 mitochondrial DNA mutations that are associated with Leber's hereditary optic neuropathy. RESULTS: No subject with low-tension glaucoma had a defect in respiratory chain activity or one of three mitochondrial DNA mutations that are commonly associated with Leber's hereditary optic neuropathy. CONCLUSION: Although these results do not exclude the possibility that low-tension glaucoma is caused by an organ-specific defect of mitochondrial function, we have excluded a systemic defect of the mitochondrial respiratory chain.

Reduced awareness of hypoglycaemia in the elderly despite an intact counter-regulatory response.

We investigated awareness of hypoglycaemia and its counter-regulatory hormone response in six young (ages 24-49, mean 30 years) and seven elderly (ages 65-80, mean 72 years) healthy non-diabetic subjects. A hyperinsulinaemic glucose clamp was used to control blood glucose level on two separate occasions. During the hypoglycaemic study, blood glucose was lowered in a stepwise manner to plateaus of 3.5, 3.0 and 2.5 mmol/l. A symptom score, visual reaction time test and digit symbol substitution test was completed pre-study, and at the end of each plateau. Pulse rate, blood pressure and counter-regulatory hormone measurements were taken every 15-30 min. The euglycaemic study was identical except that blood glucose remained at the fasting level. During hypoglycaemia, the elderly group had lower symptom scores than the young group (total relative score at glucose 2.5 mmol/l, mean +/- SEM: elderly -1 +/- 2.5, young 23 +/- 6.7, p < 0.01) and fewer individual symptoms despite a similar counter-regulatory hormone response. There was no difference in deterioration of the visual reaction times or digit symbol substitution scores during hypoglycaemia between the age groups. Unlike the young group, the elderly subjects had no tachycardia in response to hypoglycaemia. Their reduced awareness of hypoglycaemia may be due to an impaired end-organ response to counter-regulatory hormones, resulting in fewer symptoms.

General practitioner referrals to a clinical child psychologist.

An analysis of the problems that are referred by general practitioners to a clinical child psychologist working in the community is presented. To illustrate some of the principles of assessment and management an example from each of three main categories--behaviour problems, emotional disturbances, and disorders of function--is given.