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3. Structure–function correlation of retinal photoreceptors in PRPH2‐associated central areolar choroidal dystrophy patients assessed by high‐resolution scanning laser imaging and microperimetry.

Author

Mulders, Timo, van der Zanden, Ludo, Klevering, B. Jeroen, Hoyng, Carel, and Theelen, Thomas

Subjects
PHOTORECEPTORS, DYSTROPHY, RETINAL imaging, LASERS, RETINA
Abstract

Purpose: High Magnification Module (HMM™, Heidelberg Engineering, Heidelberg, Germany) imaging is a novel technique, designed to visualize the retina at a cellular level. To assess the potential of HMM™‐based metrics as endpoints for future trials, we evaluated correlations between structural HMM™ cone metrics, spectral‐domain OCT (SD‐OCT, Heidelberg Engineering, Heidelberg, Germany) and retinal sensitivity on microperimetry (MP, MAIA, CenterVue, Padova, Italy) in healthy subjects and p.(Arg142Trp) PRPH2‐associated Central Areolar Choroidal Dystrophy (CACD) patients. Methods: We projected a default 10° MP grid on composite HMM™ images and performed automated cone density (CD), intercell distance (ICD) and nearest neighbour distance (NND) analysis at stimuli located at 3° and 5° retinal eccentricity. We manually measured intrasubject outer retinal thickness on SD‐OCT in absolute and relative scotomas, located outside of focal atrophy. Results: We included 15 CACD patients and five healthy subjects. We found moderate‐to‐strong correlations of HMM™ metrics and MP sensitivity at 3° eccentricity from the fovea. We found the outer retina at the locations of absolute scotomas to be statistically significant thinner (p = 0.000003, one‐sample t‐test), as the outer retinal thickness at locations of relative scotomas. Interestingly, HMM™ metrics of these areas did not differ significantly. Conclusions: We found significant correlations between structural photoreceptors metrics on HMM™ imaging and retinal sensitivity on MP in healthy subjects and CACD patients. A multimodal approach, combining SD‐OCT, MP and HMM™ imaging, allows for detailed mapping of retinal photoreceptor integrity and restitution potential, important data that could serve as biomarkers in future clinical trials. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Gait Adaptability and the Effect of Ocular Disorders on Visually Guided Walking in Parkinson's Disease.

Author

Borm, Carlijn D.J.M., De Graaf, Debbie, Bloem, Bastiaan R., Theelen, Thomas, Hoyng, Carel, de Vries, Nienke, and Weerdesteyn, Vivian

Subjects
PARKINSON'S disease, GAIT in humans, GAIT disorders, VISION disorders, RESPONSE inhibition
Abstract

Gait disorders are a disabling feature of Parkinson's disease (PD). To avoid falls, people with PD should be able to adequately adapt their gait. This requires correct response inhibition and integration of visual information. In this small pilot study, we investigated PD-related impairments in gait adaptability and the influence of ocular disorders thereon. Compared with controls, persons with PD were less able to adapt their gait in unexpected situations (U = 21.5, p = 0.013), with only a small influence of ocular disorders on precision stepping (U = 6, p = 0.012 in the ML-direction and in the AP-direction, (U = 20, p = 0.456). This shows that people with PD have more difficulty with precision stepping than healthy controls and experience more problems with adapting their gait. We found only a small impact of ocular disorders on successfully execute precision stepping. The ability to adapt gait, particularly in challenging environmental conditions or with impaired vision, may provide a useful assessment and training option for fall prevention in PD. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Cardiac Troponin T and I Release After a 30-km Run

Author

Klinkenberg, Lieke J.J., Luyten, Peter, van der Linden, Noreen, Urgel, Kim, Snijders, Daniëlle P.C., Knackstedt, Christian, Dennert, Robert, Kietselaer, Bastiaan L.J.H., Mingels, Alma M.A., Cardinaels, Eline P.M., Peeters, Frederique E.C.M., van Suijlen, Jeroen D.E., ten Kate, Joop, Marsch, Elke, Theelen, Thomas L., Sluimer, Judith C., Wouters, Kristiaan, Bekers, Otto, Bekkers, Sebastiaan C.A.M., van Loon, Luc J.C., van Dieijen-Visser, Marja P., and Meex, Steven J.R.

Published
2016
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22. Natural History of Facioscapulohumeral Dystrophy in Children

Author

Dijkstra, Jildou N., Goselink, Rianne J.M., van Alfen, Nens, de Groot, Imelda J.M., Pelsma, Maaike, van der Stoep, Nienke, Theelen, Thomas, van Engelen, Baziel G.M., Voermans, Nicol C., and Erasmus, Corrie E.

Subjects
musculoskeletal diseases, congenital, hereditary, and neonatal diseases and abnormalities, Quality of Life, Superficial Back Muscles, Humans, Prospective Studies, Child, Muscular Dystrophy, Facioscapulohumeral, Research Article, Follow-Up Studies
Abstract

Background and Objectives Data on the natural history of facioscapulohumeral dystrophy (FSHD) in childhood are limited and critical for improved patient care and clinical trial readiness. Our objective was to describe the disease course of FSHD in children. Methods We performed a nationwide, single-center, prospective cohort study of FSHD in childhood assessing muscle functioning, imaging, and quality of life over 2 years of follow-up. Results We included 20 children with genetically confirmed FSHD who were 2 to 17 years of age. Overall, symptoms were slowly progressive, and the mean FSHD clinical score increased from 2.1 to 2.8 (p = 0.003). The rate of progression was highly variable. At baseline, 16 of 20 symptomatic children had facial weakness; after 2 years, facial weakness was observed in 19 of 20 children. Muscle strength did not change between baseline and follow-up. The most frequently and most severely affected muscles were the trapezius and deltoid. The functional exercise capacity, measured with the 6-minute walk test, improved. Systemic features were infrequent and nonprogressive. Weakness-associated complications such as lumbar hyperlordosis and dysarthria were common, and their prevalence increased during follow-up. Pain and fatigue were frequent complaints in children, and their prevalence also increased during follow-up. Muscle ultrasonography revealed a progressive increase in echogenicity. Discussion FSHD in childhood has a slowly progressive but variable course over 2 years of follow-up. The most promising outcome measures to detect progression were the FSHD clinical score and muscle ultrasonography. Despite this disease progression, an improvement on functional capacity may still occur as the child grows up. Pain, fatigue, and a decreased quality of life were common symptoms and need to be addressed in the management of childhood FSHD. Our data can be used to counsel patients and as baseline measures for treatment trials in childhood FSHD.

Published
2021

33. Whole-Body Prolyl Hydroxylase Domain (PHD) 3 Deficiency Increased Plasma Lipids and Hematocrit Without Impacting Plaque Size in Low-Density Lipoprotein Receptor Knockout Mice

Author

Demandt, Jasper A. F., primary, van Kuijk, Kim, additional, Theelen, Thomas L., additional, Marsch, Elke, additional, Heffron, Sean P., additional, Fisher, Edward A., additional, Carmeliet, Peter, additional, Biessen, Erik A. L., additional, and Sluimer, Judith C., additional

Published
2021
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34. A Switch from Cell-Associated to Soluble PDGF-B Protects against Atherosclerosis, despite Driving Extramedullary Hematopoiesis

Author

Tillie, Renee J. H. A., Theelen, Thomas L., van Kuijk, Kim, Temmerman, Lieve, de Bruijn, Jenny, Gijbels, Marion, Betsholtz, Christer, Biessen, Erik A. L., Sluimer, Judith C., Tillie, Renee J. H. A., Theelen, Thomas L., van Kuijk, Kim, Temmerman, Lieve, de Bruijn, Jenny, Gijbels, Marion, Betsholtz, Christer, Biessen, Erik A. L., and Sluimer, Judith C.

Abstract

Platelet-derived growth factor B (PDGF-B) is a mitogenic, migratory and survival factor. Cell-associated PDGF-B recruits stabilizing pericytes towards blood vessels through retention in extracellular matrix. We hypothesized that the genetic ablation of cell-associated PDGF-B by retention motif deletion would reduce the local availability of PDGF-B, resulting in microvascular pericyte loss, microvascular permeability and exacerbated atherosclerosis. Therefore, Ldlr(-/-)Pdgfb(ret)(/ret) mice were fed a high cholesterol diet. Although plaque size was increased in the aortic root of Pdgfb(ret)(/ret) mice, microvessel density and intraplaque hemorrhage were unexpectedly unaffected. Plaque macrophage content was reduced, which is likely attributable to increased apoptosis, as judged by increased TUNEL+ cells in Pdgfb(ret)(/ret) plaques (2.1-fold) and increased Pdgfb(ret)(/ret) macrophage apoptosis upon 7-ketocholesterol or oxidized LDL incubation in vitro. Moreover, Pdgfb(ret)(/ret) plaque collagen content increased independent of mesenchymal cell density. The decreased macrophage matrix metalloproteinase activity could partly explain Pdgfb(ret)(/ret) collagen content. In addition to the beneficial vascular effects, we observed reduced body weight gain related to smaller fat deposition in Pdgfb(ret)(/ret) liver and adipose tissue. While dampening plaque inflammation, Pdgfb(ret)(/ret) paradoxically induced systemic leukocytosis. The increased incorporation of 5-ethynyl-2 '-deoxyuridine indicated increased extramedullary hematopoiesis and the increased proliferation of circulating leukocytes. We concluded that Pdgfb(ret)(/ret) confers vascular and metabolic effects, which appeared to be protective against diet-induced cardiovascular burden. These effects were unrelated to arterial mesenchymal cell content or adventitial microvessel density and leakage. In contrast, the deletion drives splenic hematopoiesis and subsequent leukocytosis in hypercholesterolemia.

Published
2021
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35. Natural History of Facioscapulohumeral Dystrophy in Children A 2-Year Follow-up

Author

Dijkstra, Jildou N., Goselink, Rianne J. M., van Alfen, Nens, de Groot, Imelda J. M., Pelsma, Maaike, van der Stoep, Nienke, Theelen, Thomas, van Engelen, Baziel G. M., Voermans, Nicol C., Erasmus, Corrie E., Dijkstra, Jildou N., Goselink, Rianne J. M., van Alfen, Nens, de Groot, Imelda J. M., Pelsma, Maaike, van der Stoep, Nienke, Theelen, Thomas, van Engelen, Baziel G. M., Voermans, Nicol C., and Erasmus, Corrie E.

Abstract

Background and Objectives Data on the natural history of facioscapulohumeral dystrophy (FSHD) in childhood are limited and critical for improved patient care and clinical trial readiness. Our objective was to describe the disease course of FSHD in children. Methods We performed a nationwide, single-center, prospective cohort study of FSHD in childhood assessing muscle functioning, imaging, and quality of life over 2 years of follow-up. Results We included 20 children with genetically confirmed FSHD who were 2 to 17 years of age. Overall, symptoms were slowly progressive, and the mean FSHD clinical score increased from 2.1 to 2.8 (p = 0.003). The rate of progression was highly variable. At baseline, 16 of 20 symptomatic children had facial weakness; after 2 years, facial weakness was observed in 19 of 20 children. Muscle strength did not change between baseline and follow-up. The most frequently and most severely affected muscles were the trapezius and deltoid. The functional exercise capacity, measured with the 6-minute walk test, improved. Systemic features were infrequent and nonprogressive. Weakness-associated complications such as lumbar hyperlordosis and dysarthria were common, and their prevalence increased during follow-up. Pain and fatigue were frequent complaints in children, and their prevalence also increased during follow-up. Muscle ultrasonography revealed a progressive increase in echogenicity. Discussion FSHD in childhood has a slowly progressive but variable course over 2 years of follow-up. The most promising outcome measures to detect progression were the FSHD clinical score and muscle ultrasonography. Despite this disease progression, an improvement on functional capacity may still occur as the child grows up. Pain, fatigue, and a decreased quality of life were common symptoms and need to be addressed in the management of childhood FSHD. Our data can be used to counsel patients and as baseline measures for treatment trials in childhood FSHD., Funding Agencies|charitable foundation Prinses Beatrix Spierfonds/Spieren voor Spieren [W.OR14.22]

Published
2021
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36. Author Correction: Ablation of CD8α+ dendritic cell mediated cross-presentation does not impact atherosclerosis in hyperlipidemic mice (Scientific Reports, (2015), 5, 1, (15414), 10.1038/srep15414)

Author

Legein, Bart, Janssen, Edith M., Theelen, Thomas L., Gijbels, Marion J., Walraven, Joep, Klarquist, Jared S., Hennies, Cassandra M., Wouters, Kristiaan, Seijkens, Tom T. P., Wijnands, Erwin, Sluimer, Judith C., Lutgens, Esther, Zenke, Martin, Hildner, Kai, Biessen, Erik A. L., Temmerman, Lieve, Medical Biochemistry, and ACS - Atherosclerosis & ischemic syndromes

Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

42. Deficiency of myeloid PHD proteins aggravates atherogenesis via macrophage apoptosis and paracrine fibrotic signalling

Author

van Kuijk, Kim, primary, Demandt, Jasper A F, additional, Perales-Patón, Javier, additional, Theelen, Thomas L, additional, Kuppe, Christoph, additional, Marsch, Elke, additional, de Bruijn, Jenny, additional, Jin, Han, additional, Gijbels, Marion J, additional, Matic, Ljubica, additional, Mees, Barend M E, additional, Reutelingsperger, Chris P M, additional, Hedin, Ulf, additional, Biessen, Erik A L, additional, Carmeliet, Peter, additional, Baker, Andrew H, additional, Kramann, Rafael K, additional, Schurgers, Leon J, additional, Saez-Rodriguez, Julio, additional, and Sluimer, Judith C, additional

Published
2021
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44. In vivo photoreceptor imaging by non-adaptive optics confocal scanning laser ophthalmoscopy

Author

Theelen, Thomas, Dhooge, P.P.A., Mulders, T.W.F., and Hoyng, C.B.

Subjects
genetic structures, ddc: 610, sense organs, 610 Medical sciences, Medicine, eye diseases
Abstract

Purpose: Retinal photoreceptor (PR) imaging has been proven to be possible by adaptive optics (AO) systems. Here, we aim to show the mosaic of human PRs in vivo by a non-AO system. Methods: Healthy subjects and patients with macular disease were examined by a Heidelberg Engineering Spectralis™[for full text, please go to the a.m. URL], 7th International Symposium on AMD: Age-related Macular Degeneration - Understanding Pathogenetic Mechanisms of Disease

Published
2020
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45. Mutations in the peripherin/RDS gene are an important cause of multifocal pattern dystrophy simulating STGD1/fundus flavimaculatus

Author

Boon, Camiel J.F., van Schooneveld, Mary J., den Hollander, Anneke I., van Lith-Verhoeven, Janneke J.C., Zonneveld-Vrieling, Marijke N., Theelen, Thomas, Cremers, Frans P.M., Hoyng, Carel B., and Klevering, B. Jeroen

Subjects
Retinal degeneration -- Genetic aspects, Retinal degeneration -- Research, Genetic research -- Reports, Gene mutations -- Research, Intermediate filament proteins -- Genetic aspects, Intermediate filament proteins -- Research, Health
Published
2007

48. Deficiency of myeloid PHD proteins aggravates atherogenesis via macrophage apoptosis and paracrine fibrotic signalling.

Author

Kuijk, Kim van, Demandt, Jasper A F, Perales-Patón, Javier, Theelen, Thomas L, Kuppe, Christoph, Marsch, Elke, Bruijn, Jenny de, Jin, Han, Gijbels, Marion J, Matic, Ljubica, Mees, Barend M E, Reutelingsperger, Chris P M, Hedin, Ulf, Biessen, Erik A L, Carmeliet, Peter, Baker, Andrew H, Kramann, Rafael K, Schurgers, Leon J, Saez-Rodriguez, Julio, and Sluimer, Judith C

Subjects
MACROPHAGES, HIGH cholesterol diet, BONE marrow transplantation, ATHEROSCLEROTIC plaque, HYPOXIA-inducible factors
Abstract

Aims Atherosclerotic plaque hypoxia is detrimental for macrophage function. Prolyl hydroxylases (PHDs) initiate cellular hypoxic responses, possibly influencing macrophage function in plaque hypoxia. Thus, we aimed to elucidate the role of myeloid PHDs in atherosclerosis. Methods and results Myeloid-specific PHD knockout (PHDko) mice were obtained via bone marrow transplantation (PHD1ko, PHD3ko) or conditional knockdown through lysozyme M-driven Cre recombinase (PHD2cko). Mice were fed high cholesterol diet for 6–12 weeks to induce atherosclerosis. Aortic root plaque size was significantly augmented 2.6-fold in PHD2cko, and 1.4-fold in PHD3ko compared to controls but was unchanged in PHD1ko mice. Macrophage apoptosis was promoted in PHD2cko and PHD3ko mice in vitro and in vivo , via the hypoxia-inducible factor (HIF) 1α/BNIP3 axis. Bulk and single-cell RNA data of PHD2cko bone marrow-derived macrophages (BMDMs) and plaque macrophages, respectively, showed enhanced HIF1α/BNIP3 signalling, which was validated in vitro by siRNA silencing. Human plaque BNIP3 mRNA was positively associated with plaque necrotic core size, suggesting similar pro-apoptotic effects in human. Furthermore, PHD2cko plaques displayed enhanced fibrosis, while macrophage collagen breakdown by matrix metalloproteinases, collagen production, and proliferation were unaltered. Instead, PHD2cko BMDMs enhanced fibroblast collagen secretion in a paracrine manner. In silico analysis of macrophage-fibroblast communication predicted SPP1 (osteopontin) signalling as regulator, which was corroborated by enhanced plaque SPP1 protein in vivo. Increased SPP1 mRNA expression upon PHD2cko was preferentially observed in foamy plaque macrophages expressing 'triggering receptor expressed on myeloid cells-2' (TREM2hi) evidenced by single-cell RNA, but not in neutrophils. This confirmed enhanced fibrotic signalling by PHD2cko macrophages to fibroblasts, in vitro as well as in vivo. Conclusion Myeloid PHD2cko and PHD3ko enhanced atherosclerotic plaque growth and macrophage apoptosis, while PHD2cko macrophages further activated collagen secretion by fibroblasts in vitro , likely via paracrine SPP1 signalling through TREM2hi macrophages. [ABSTRACT FROM AUTHOR]

Published
2022
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