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13. Health Care Use and Out-of-pocket Spending by Persons With Dementia Differ Between Europe and the United States

Author

Lenzen, S, Bakx, Pieter, Bom, Judith, van Doorslaer, EKA (Eddy), Lenzen, S, Bakx, Pieter, Bom, Judith, and van Doorslaer, EKA (Eddy)

Abstract

Background: Persons with dementia need much care, but what care is used and how the burden of financing is divided between persons with dementia, caregivers, and public programs may differ between countries. Objective: The objective of this study was to compare how health care use and out-of-pocket (OOP) spending associated with dementia differ between the United States and Europe, with and without controlling for background characteristics. Research Design: We use prospectively collected survey data from the United States-based Health and Retirement Study (n = 48,877) and the Survey of Health, Ageing, and Retirement in Europe (n = 98,971) including all adults over the age of 70 years. Dementia status is imputed using a validated algorithm. After first reporting the observed differences in care use, we analyze how care use is associated with dementia using multivariate regressions, controlling for other health conditions and background characteristics. Results: Persons with dementia in the United States use 50% less formal home care per year than persons living with dementia in Europe [mean (SD) = 236.8 h (1047.4) vs. 463.3 h (1371.2)], but use more nursing home care [75.1 d (131.4) vs. 45.5 d (119.4)). Dementia is associated with higher OOP spending in the United States than Europe [4406 USD (95% confidence interval, 3914-4899) vs. 246 USD (73-418)-2017 price levels]. Conclusions: Health care use and OOP spending differ between Europe and the United States. The far greater reliance on nursing home care in the United States likely causes much higher expenditures for people with dementia and insurance programs alike.

Published
2021

36. What’s so difficult about becoming a health coach in primary care? A process evaluation of an approach to coach patients

Author

Lenzen, S, van Bokhoven, L, Daniels, R, van der Weijden, T, and Beurskens, S

Subjects
health coaching, ddc: 610, education, shared decision making, 610 Medical sciences, Medicine, human activities, nurses
Abstract

Background: Professionals in family medicine are increasingly required to act as coaches to enhance their chronically ill patients’ self-management. We developed an approach aiming to support practice nurses working in family medicine in the Netherlands to coach patients in goal setting and action[for full text, please go to the a.m. URL], 51. Kongress für Allgemeinmedizin und Familienmedizin

Published
2017
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37. TriPer, an optical probe tuned to the endoplasmic reticulum tracks changes in luminal H$_2$O$_2$

Author

Melo, EP, Lopes, C, Gollwitzer, P, Lortz, S, Lenzen, S, Mehmeti, I, Kaminski, Clemens, Ron, David, Avezov, Edward, Kaminski, Clemens [0000-0002-5194-0962], Ron, David [0000-0002-3014-5636], Avezov, Edward [0000-0002-2894-0585], and Apollo - University of Cambridge Repository

Subjects
inorganic chemicals, pancreatic β-cells, Hydrogen-Peroxide, Agricultural and Biological Sciences(all), Biochemistry, Genetics and Molecular Biology(all), Protein, fluorescent protein sensor, Enzyme Gene-Expression, Peroxiredoxin, hydrogen peroxide, Stress, Glutathione, fluorescence lifetime imaging, endoplasmic reticulum, live cell imaging, lcsh:Biology (General), redox, H2O2 probe, Beta-Cell, Poise, glutathione, Disulfide-Bond Formation, lcsh:QH301-705.5, Thiol-Redox
Abstract

$\textbf{Background:}$ The fate of hydrogen peroxide (H$_2$O$_2$) in the endoplasmic reticulum (ER) has been inferred indirectly from the activity of ER-localized thiol oxidases and peroxiredoxins, in vitro, and the consequences of their genetic manipulation, in vivo. Over the years hints have suggested that glutathione, puzzlingly abundant in the ER lumen, might have a role in reducing the heavy burden of H$_2$O$_2$ produced by the luminal enzymatic machinery for disulfide bond formation. However, limitations in existing organelle-targeted H$_2$O$_2$ probes have rendered them inert in the thiol-oxidizing ER, precluding experimental follow-up of glutathione’s role in ER H$_2$O$_2$ metabolism. $\textbf{Results:}$ Here we report on the development of TriPer, a vital optical probe sensitive to changes in the concentration of H$_2$O$_2$ in the thiol-oxidizing environment of the ER. Consistent with the hypothesized contribution of oxidative protein folding to H$_2$O$_2$ production, ER-localized TriPer detected an increase in the luminal H$_2$O$_2$ signal upon induction of pro-insulin (a disulfide-bonded protein of pancreatic β-cells), which was attenuated by the ectopic expression of catalase in the ER lumen. Interfering with glutathione production in the cytosol by buthionine sulfoximine (BSO) or enhancing its localized destruction by expression of the glutathione-degrading enzyme ChaC1 in the lumen of the ER further enhanced the luminal H$_2$O$_2$ signal and eroded β-cell viability. $\textbf{Conclusions:}$ A tri-cysteine system with a single peroxidatic thiol enables H$_2$O$_2$ detection in oxidizing milieux such as that of the ER. Tracking ER H$_2$O$_2$ in live pancreatic β-cells points to a role for glutathione in H$_2$O$_2$ turnover., This work is supported by grants from the Wellcome Trust (Wellcome 200848/Z/16/Z, WT: UNS18966), Fundação para a Ciência e Tecnologia, Portugal (PTDC/QUI/BIQ/119677/2010 and UID/BIM/04773/2013-CBMR), European Commission (EU FP7 Beta-Bat No: 277713), EPSRC (1503478), MRC (MR/K015850/1), and a Wellcome Trust Strategic Award for core facilities to the Cambridge Institute for Medical Research (Wellcome 100140). DR is a Wellcome Trust Principal Research Fellow.

Published
2017

39. Pancreas Pathology of Latent Autoimmune Diabetes in Adults (LADA) in Patients and in a LADA Rat Model Compared With Type 1 Diabetes.

Author

Jörns, Anne, Wedekind, Dirk, Jähne, Joachim, Lenzen, Sigurd, Jörns A J, Anne, Wedekind D W, Dirk, Jähne J J, Joachim, and Lenzen S L, Sigurd

Abstract

Approximately 10% of patients with type 2 diabetes suffer from latent autoimmune diabetes in adults (LADA). This study provides a systematic assessment of the pathology of the endocrine pancreas of patients with LADA and for comparison in a first rat model mimicking the characteristics of patients with LADA. Islets in human and rat pancreases were analyzed by immunohistochemistry for immune cell infiltrate composition, by in situ RT-PCR and quantitative real-time PCR of laser microdissected islets for gene expression of proinflammatory cytokines, the proliferation marker proliferating cell nuclear antigen (PCNA), the anti-inflammatory cytokine interleukin (IL) 10, and the apoptosis markers caspase 3 and TUNEL as well as insulin. Human and rat LADA pancreases showed differences in areas of the pancreas with respect to immune cell infiltration and a changed ratio between the number of macrophages and CD8 T cells toward macrophages in the islet infiltrate. Gene expression analyses revealed a changed ratio due to an increase of IL-1β and a decrease of tumor necrosis factor-α. IL-10, PCNA, and insulin expression were increased in the LADA situation, whereas caspase 3 gene expression was reduced. The analyses into the underlying pathology in human as well as rat LADA pancreases provided identical results, allowing the conclusion that LADA is a milder form of autoimmune diabetes in patients of an advanced age. [ABSTRACT FROM AUTHOR]

Published
2020
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41. Systems biology of the IMIDIA biobank from organ donors and pancreatectomised patients defines a novel transcriptomic signature of islets from individuals with type 2 diabetes

Author

Solimena, Michele, Schulte, A., Marselli, L., Ehehalt, F., Richter, D., Kleeberg, M., Mziaut, H., Knoch, K., Parnis, J., Bugliani, M., Siddiq, A., Jörns, A., Burdet, F., Liechti, R., Suleiman, M., Margerie, D., Syed, F., Distler, M., Grützmann, R., Petretto, E., Moreno-Moral, A., Wegbrod, C., Sönmez, A., Pfriem, K., Friedrich, A., Meinel, J., Wollheim, C., Baretton, G., Scharfmann, R., Nogoceke, E., Bonifacio, E., Sturm, D., Meyer-Puttlitz, B., Boggi, U., Saeger, H., Filipponi, F., Lesche, M., Meda, P., Dahl, A., Wigger, L., Xenarios, I., Falchi, M., Thorens, B., Weitz, J., Bokvist, K., Lenzen, S., Rutter, G., Froguel, P., von Bülow, M., Ibberson, M., Marchetti, P., Solimena, Michele, Schulte, A., Marselli, L., Ehehalt, F., Richter, D., Kleeberg, M., Mziaut, H., Knoch, K., Parnis, J., Bugliani, M., Siddiq, A., Jörns, A., Burdet, F., Liechti, R., Suleiman, M., Margerie, D., Syed, F., Distler, M., Grützmann, R., Petretto, E., Moreno-Moral, A., Wegbrod, C., Sönmez, A., Pfriem, K., Friedrich, A., Meinel, J., Wollheim, C., Baretton, G., Scharfmann, R., Nogoceke, E., Bonifacio, E., Sturm, D., Meyer-Puttlitz, B., Boggi, U., Saeger, H., Filipponi, F., Lesche, M., Meda, P., Dahl, A., Wigger, L., Xenarios, I., Falchi, M., Thorens, B., Weitz, J., Bokvist, K., Lenzen, S., Rutter, G., Froguel, P., von Bülow, M., Ibberson, M., and Marchetti, P.

Abstract

© 2017, The Author(s). Aims/hypothesis: Pancreatic islet beta cell failure causes type 2 diabetes in humans. To identify transcriptomic changes in type 2 diabetic islets, the Innovative Medicines Initiative for Diabetes: Improving beta-cell function and identification of diagnostic biomarkers for treatment monitoring in Diabetes (IMIDIA) consortium (www.imidia.org) established a comprehensive, unique multicentre biobank of human islets and pancreas tissues from organ donors and metabolically phenotyped pancreatectomised patients (PPP). Methods: Affymetrix microarrays were used to assess the islet transcriptome of islets isolated either by enzymatic digestion from 103 organ donors (OD), including 84 non-diabetic and 19 type 2 diabetic individuals, or by laser capture microdissection (LCM) from surgical specimens of 103 PPP, including 32 non-diabetic, 36 with type 2 diabetes, 15 with impaired glucose tolerance (IGT) and 20 with recent-onset diabetes (<1 year), conceivably secondary to the pancreatic disorder leading to surgery (type 3c diabetes). Bioinformatics tools were used to (1) compare the islet transcriptome of type 2 diabetic vs non-diabetic OD and PPP as well as vs IGT and type 3c diabetes within the PPP group; and (2) identify transcription factors driving gene co-expression modules correlated with insulin secretion ex vivo and glucose tolerance in vivo. Selected genes of interest were validated for their expression and function in beta cells. Results: Comparative transcriptomic analysis identified 19 genes differentially expressed (false discovery rate =0.05, fold change =1.5) in type 2 diabetic vs non-diabetic islets from OD and PPP. Nine out of these 19 dysregulated genes were not previously reported to be dysregulated in type 2 diabetic islets. Signature genes included TMEM37, which inhibited Ca2+-influx and insulin secretion in beta cells, and ARG2 and PPP1R1A, which promoted insulin secretion. Systems biology approaches identified HNF1A, PDX1 and RE

Published
2018

42. Sequencing of candidate genes selected by beta cell experts in monogenic diabetes of unknown aetiology

Author

Edghill, E. L., Minton, J. A. L., Groves, C. J., Flanagan, S. E., Patch, A. -M, Rubio-Cabezas, O., Shepherd, M., Lenzen, S., Mark McCarthy, Ellard, S., and Hattersley, A. T.

Subjects
Diabetes Mellitus, Type 2, Genetics, Insulin-Secreting Cells
Abstract

Context Approximately 39% of cases with permanent neonatal diabetes (PNDM) and about 11% with maturity onset diabetes of the young (MODY) have an unknown genetic aetiology. Many of the known genes causing MODY and PNDM were identified as being critical for beta cell function before their identification as a cause of monogenic diabetes. Objective We used nominations from the EU beta cell consortium EURODIA project partners to guide gene candidacy. Subjects Seventeen cases with permanent neonatal diabetes and 8 cases with maturity onset diabetes of the young. Main outcome measures The beta cell experts within the EURODIA consortium were asked to nominate 3 "gold", 3 "silver" and 4 "bronze" genes based on biological or genetic grounds. We sequenced twelve candidate genes from the list based on evidence for candidacy. Results Sequencing ISL1, LMX1A, MAFA, NGN3, NKX2.2, NKX6.1, PAX4, PAX6, SOX2, SREBF1, SYT9 and UCP2 did not identify any pathogenic mutations. Conclusion Further work is needed to identify novel causes of permanent neonatal diabetes and maturity onset diabetes of the young utilising genetic approaches as well as further candidate genes. Image: Peninsula Medical School logo. Exeter, United Kingdom., JOP. Journal of the Pancreas, Vol 11, N° 1 (2010): January - P. 1-94

Published
2016

43. Gene Therapy of Diabetes Mellitus — Aims, Methods and Future Prospects

Author

Tiedge M and Lenzen S

Subjects
business.industry, Genetically engineered, Endocrinology, Diabetes and Metabolism, Genetic enhancement, Gene Transfer Techniques, Gene Expression, Gene transfer, Genetic Therapy, General Medicine, Bioinformatics, medicine.disease, Genetically modified organism, Endocrinology, Diabetes mellitus, Insulin Secretion, Diabetes Mellitus, Internal Medicine, Animals, Humans, Insulin, Medicine, business
Abstract

Progress in pancreatic islet research and molecular biology techniques has opened the perspective for gene therapy of diabetes mellitus. This review will focus on the prerequisites for the generation of genetically engineered insulin-producing cells and current methods of gene transfer. A short account of the genetically modified insulin-secreting cell lines generated so far is also given. Although still experimental each of these new insulin-secreting cell lines is a step forward on the way to gene therapy of human diabetes.

Published
2009
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47. Influence of age and cognitive performance on resting-state brain networks of older adults in a population-based cohort

Author

Jockwitz, C., Caspers, S., Lux, S., Eickhoff, S.B., Jütten, K., Lenzen, S., Moebus, S., Pundt, N., Reid, A.T., Hoffstaedter, F., Jöckel, K.H., Erbel, R., Cichon, S., Nöthen, M.M., Shah, N.J., Zilles, K., Amunts, K., Jockwitz, C., Caspers, S., Lux, S., Eickhoff, S.B., Jütten, K., Lenzen, S., Moebus, S., Pundt, N., Reid, A.T., Hoffstaedter, F., Jöckel, K.H., Erbel, R., Cichon, S., Nöthen, M.M., Shah, N.J., Zilles, K., and Amunts, K.

Abstract

Contains fulltext : 167029.pdf (publisher's version ) (Closed access), Aging leads to global changes in brain structure and cognitive performance, with reorganization of functional brain networks. Importantly, these age-related changes show higher inter-individual variability in older subjects. To particularly address this variability is a challenge for studies on lifetime trajectories from early to late adulthood. The present study therefore had a dedicated focus on late adulthood to characterize the functional connectivity in resting-state networks (RSFC) in relation to age and cognitive performance in 711 older adults (55-85 years) from the 1000BRAINS project. The executive, left and right frontoparietal resting-state (RS) networks showed age-related increases in RSFC. However, older adults did not show changes in RSFC in the default mode network (DMN). Furthermore, lower performance in working memory was associated with higher RSFC in the left frontoparietal RS network. The results suggest age-related compensatory increases in RSFC which might help to maintain cognitive performance. Nevertheless, the negative correlation between RSFC and working memory performance hints at limited cognitive reserve capacity in lower performing older adults. Consequently, the current results provide evidence for a functional reorganization of the brain until late adulthood that might additionally explain parts of the variability of cognitive abilities in older adults.

Published
2017

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