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6. Priority setting for adult malnutrition and nutritional screening in healthcare: a James Lind Alliance

Author

Jones, D. J., primary, Baldwin, C., additional, Lal, S., additional, Stanmore, E., additional, Farrer, K., additional, Connolly, E., additional, Weekes, C. E., additional, Anderson, L., additional, Murphy, J., additional, Gillespie, L., additional, Welsh, N., additional, Ogden, M., additional, McDevitt, M., additional, Day, R., additional, Lynne, S., additional, Paulden, P., additional, Gronlund, T., additional, and Burden, S. T., additional

Published
2019
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14. Priority setting for adult malnutrition and nutritional screening in healthcare: a James Lind Alliance.

Author

Jones, D. J., Baldwin, C., Lal, S., Stanmore, E., Farrer, K., Connolly, E., Weekes, C. E., Anderson, L., Murphy, J., Gillespie, L., Welsh, N., Ogden, M., McDevitt, M., Day, R., Lynne, S., Paulden, P., Gronlund, T., and Burden, S. T.

Subjects
MALNUTRITION, ATTITUDE (Psychology), DIETARY supplements, INTERPROFESSIONAL relations, MEDICAL personnel, MEDICAL technology, NUTRITIONAL assessment, PRIORITY (Philosophy), RESEARCH evaluation, SURVEYS, ADULT education workshops, BODY mass index, CAREGIVER attitudes, PATIENTS' attitudes
Abstract

Background: Malnutrition is one the greatest global health challenges of our generation, leading to the increased utilisation of healthcare resources, as well as morbidity and mortality. Research has primarily been driven by industry, academia and clinical working groups and has had little involvement from patients and carers. The project described in the present study aimed to establish a priority setting partnership allowing patients, carers and healthcare professionals an opportunity to influence the research agenda. Methods: A national survey was conducted to gather malnutrition uncertainties and identify key issues (i.e. areas within scope where an evidence‐base is lacking) from those with experience of malnutrition. Uncertainties were analysed according to themes. Similar questions were grouped and summary questions were developed. A second survey was conducted and respondents were asked to choose their 10 most important summary questions. A workshop was conducted to finalise the top 10 research priorities from the most frequently indicated uncertainties on the interim survey. Results: Overall, 1128 uncertainty questions were submitted from 268 people. The interim survey had 71 responses and a list of the top 26 questions was generated for the workshop. There were 26 questions discussed, ranked and agreed by healthcare professionals, carers and patients at the workshop. The top 10 research priorities were then chosen. These included questions on oral nutritional supplements, vulnerable groups, screening, community care, use of body mass index and technology. Conclusions: The top 10 research priorities in malnutrition and nutritional screening have been identified from a robust process involving patients, carers and healthcare professionals. [ABSTRACT FROM AUTHOR]

Published
2020
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19. C/EBP homologous protein contributes to cytokine-induced pro-inflammatory responses and apoptosis in beta-cells.

Author

Allagnat, Florent, Fukaya, Makiko, Nogueira, Tatiane C, Delaroche, Diane, Welsh, N, Marselli, L, Marchetti, Piero, Haefliger, J A, Eizirik, Decio L., Cardozo, Alessandra K, Allagnat, Florent, Fukaya, Makiko, Nogueira, Tatiane C, Delaroche, Diane, Welsh, N, Marselli, L, Marchetti, Piero, Haefliger, J A, Eizirik, Decio L., and Cardozo, Alessandra K

Abstract

Induction of the C/EBP homologous protein (CHOP) is considered a key event for endoplasmic reticulum (ER) stress-mediated apoptosis. Type 1 diabetes (T1D) is characterized by an autoimmune destruction of the pancreatic β-cells. Pro-inflammatory cytokines are early mediators of β-cell death in T1D. Cytokines induce ER stress and CHOP overexpression in β-cells, but the role for CHOP overexpression in cytokine-induced β-cell apoptosis remains controversial. We presently observed that CHOP knockdown (KD) prevents cytokine-mediated degradation of the anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1), thereby decreasing the cleavage of executioner caspases 9 and 3, and apoptosis. Nuclear factor-κB (NF-κB) is a crucial transcription factor regulating β-cell apoptosis and inflammation. CHOP KD resulted in reduced cytokine-induced NF-κB activity and expression of key NF-κB target genes involved in apoptosis and inflammation, including iNOS, FAS, IRF-7, IL-15, CCL5 and CXCL10. This was due to decreased IκB degradation and p65 translocation to the nucleus. The present data suggest that CHOP has a dual role in promoting β-cell death: (1) CHOP directly contributes to cytokine-induced β-cell apoptosis by promoting cytokine-induced mitochondrial pathways of apoptosis; and (2) by supporting the NF-κB activation and subsequent cytokine/chemokine expression, CHOP may contribute to apoptosis and the chemo attraction of mononuclear cells to the islets during insulitis., Journal Article, Research Support, Non-U.S. Gov't, SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2012

22. Clinical effectiveness

Author

McGhee, D. J. M., primary, Royle, P. L., additional, Counsell, C. E., additional, Abbas, A., additional, Sethi, P., additional, Manku, L., additional, Narayan, A., additional, Clegg, K., additional, Bardai, A., additional, Brown, S. H. M., additional, Hafeez, U., additional, Abdelhafiz, A. H., additional, McGovern, A., additional, Breckenridge, A., additional, Seenan, P., additional, Samani, A., additional, Das, S., additional, Khan, S., additional, Puffett, A. J., additional, Morgan, J., additional, Ross, G., additional, Cantlay, A., additional, Khan, N., additional, Bhalla, A., additional, Sweeting, M., additional, Nimmo, C. A. M. D., additional, Fleet, J., additional, Igbedioh, C., additional, Harari, D., additional, Downey, C. L., additional, Handforth, C., additional, Stothard, C., additional, Cracknell, A., additional, Barnes, C., additional, Shaw, L., additional, Bainbridge, L., additional, Crabtree, L., additional, Clark, T., additional, Root, S., additional, Aitken, E., additional, Haroon, K., additional, Sudlow, M., additional, Hanley, K., additional, Welsh, S., additional, Hill, E., additional, Falconer, A., additional, Miller, H., additional, Martin, B., additional, Tidy, E., additional, Pendlebury, S., additional, Thompson, S., additional, Burnett, E., additional, Taylor, H., additional, Lonan, J., additional, Adler, B., additional, McCallion, J., additional, Sykes, E., additional, Bancroft, R., additional, Tullo, E. S., additional, Young, T. J., additional, Clift, E., additional, Flavin, B., additional, Roberts, H. C., additional, Sayer, A. A., additional, Belludi, G., additional, Aithal, S., additional, Verma, A., additional, Singh, I., additional, Barne, M., additional, Wilkinson, I., additional, Sakoane, R., additional, Singh, N., additional, Cottee, M., additional, Irani, T. S., additional, Martinovic, O., additional, Abdulla, A. J. J., additional, Riglin, J., additional, Husk, J., additional, Lowe, D., additional, Treml, J., additional, Vasilakis, J. N., additional, Buttery, A., additional, Reid, J., additional, Healy, P., additional, Grant-Casey, J., additional, Pendry, K., additional, Richards, J., additional, Singh, A., additional, Jarrett, D., additional, Hewitt, J., additional, Slevin, J., additional, Barwell, G., additional, Youde, J., additional, Kennedy, C., additional, Romero-Ortuno, R., additional, O'Shea, D., additional, Robinson, D., additional, Kenny, R. A., additional, O'Connell, J., additional, Topp, J. D., additional, Warburton, K., additional, Simpson, L., additional, Bryce, K., additional, Suntharalingam, S., additional, Grosser, K., additional, D'Silva, A., additional, Southern, L., additional, Bielawski, C., additional, Cook, L., additional, Sutton, G. M., additional, Flanagan, L., additional, Storr, A., additional, Charlton, L., additional, Kerr, S., additional, Robinson, L., additional, Shaw, F., additional, Finch, L. K., additional, Weerasuriya, N., additional, Walker, M., additional, Sahota, O., additional, Logan, P., additional, Brown, F., additional, Rossiter, F., additional, Baxter, M., additional, Mucci, E., additional, Brown, A., additional, Jackson, S. H. D., additional, de Savary, N., additional, Hasan, S., additional, Jones, H., additional, Birrell, J., additional, Hockley, J., additional, Hensey, N., additional, Meiring, R., additional, Athavale, N., additional, Simms, J., additional, Brown, S., additional, West, A., additional, Diem, P., additional, Davies, R., additional, Kings, R., additional, Coleman, H., additional, Stevens, D., additional, Campbell, C., additional, Hope, S., additional, Morris, A., additional, Ong, T., additional, Harwood, R., additional, Dasgupta, D., additional, Mitchell, S., additional, Dimmock, V., additional, Collin, F., additional, Wood, E., additional, Green, V., additional, Hendrickse-Welsh, N., additional, Eccles, J., additional, Beezer, J., additional, Garside, M., additional, and Baxter, J., additional

Published
2013
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25. The NOTCH pathway contributes to cell fate decision in myelopoiesis

Author

Bugeon, L., primary, Taylor, H. B., additional, Progatzky, F., additional, Lin, M. I., additional, Ellis, C. D., additional, Welsh, N., additional, Smith, E., additional, Vargesson, N., additional, Gray, C., additional, Renshaw, S. A., additional, Chico, T. J. A., additional, Zon, L. I., additional, Lamb, J., additional, and Dallman, M. J., additional

Published
2011
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33. Liposome-mediated transfer of IL-1 receptor antagonist gene to dispersed islet cells does not prevent recurrence of disease in syngeneically transplanted NOD mice

Author

Saldeen, J, Sandler, S, Bendtzen, K, Welsh, N, Saldeen, J, Sandler, S, Bendtzen, K, and Welsh, N

Abstract

IL-1beta is cytotoxic to pancreatic beta-cells in vitro but its role in the vicinity of beta-cells in vivo is unknown. We explored whether liposome-mediated transfer of the interleukin 1 receptor antagonist (IL-1ra) gene to islet cells might prevent recurrence of disease in syngeneically transplanted non-obese diabetic (NOD) mice. NOD mouse islet cells were transfected using liposome-mediated gene transfer with a human IL-1ra cDNA construct and transplanted two days later to prediabetic NOD mice. Graft infiltration and destruction were monitored three, five and eight days posttransplantation by histology and determination of insulin and cytokine content. IL-1ra gene transfer resulted in transient expression of IL-1ra protein in islet cells in vitro as assessed by ELISA and of IL-1ra mRNA in transplanted islets as revealed by RT-PCR. However, both control and IL-1ra transfected NOD grafts exhibited massive infiltration and loss of insulin-positive cells, paralleled by a decreased insulin content. Increased IL-1ra expression did not clearly affect other cytokine profiles (IL-1beta, IFN-gamma, IL-2), except for an increase of IL-10 on day eight. In conclusion, liposome-mediated IL-1ra gene transfer to mouse islet cells results in transient expression of IL-1ra which is, however, insufficient to confer resistance to destruction of grafted insulin-producing cells in the NOD mouse.

Published
2000

48. Evidence of a negative feedback system regulating the total beta-cell volume in nondiabetic rats that received pancreas transplants

Author

Wahlberg, Jeanette, Korsgren, O., Welsh, N., Jansson, L., Wahlberg, Jeanette, Korsgren, O., Welsh, N., and Jansson, L.

Abstract

BACKGROUND: The aim of the present study was to investigate the long-term regulation of pancreatic beta-cell volume after pancreas transplantation into adult rats. METHODS: A syngeneic pancreaticoduodenal transplantation was made in normoglycemic Wistar-Furth rats. By this means, the recipients doubled their pancreatic islet volume. Nine months after transplantation, the total beta-cell volume was measured in serial pancreatic sections immunostained for insulin from both the native and transplanted pancreata, and in the native pancreas of age-matched Wistar-Furth rats that did not receive transplants. RESULTS: No changes in the volume of individual beta-cells were seen. A 50% decrease in total beta-cell volume was observed in both the native and transplanted pancreas when compared with that of age-matched controls. However, the combined beta-cell volumes of the native and transplanted pancreas in the rats that received transplants were similar to those of the native pancreas in control animals. No signs of increased apoptosis in any of the glands could be seen during the first postoperative week or after 9 months. CONCLUSIONS: These findings provide evidence of a negative feedback system, which regulates the total beta-cell volume to the levels seen in age-matched rats that did not receive transplants. The underlying mechanisms for the decreased beta-cell volume are unknown, but may involve a diminished replicatory rate of the beta-cells.

Published
1998
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