121 results on '"Niessen, H. W."'
Search Results
2. The presence of cardiotropic viral genomes is not increased in atrial tissue of atrial fibrillation patients
- Author
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Wu, L., Emmens, R. W., van Wezenbeek, J., Stooker, W., Allaart, C. P., Vonk, A. B. A., van Rossum, A. C., Wolthers, K. C., Niessen, H. W. M., and Krijnen, P. A. J.
- Published
- 2022
- Full Text
- View/download PDF
3. Increased bone morphogenetic protein 10 in precapillary pulmonary hypertension patients
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Llucia-Valldeperas, A, primary, Van Wezenbeek, J, additional, Groeneveldt, J A, additional, Smal, R, additional, Sanchez-Duffhues, G, additional, Becher, C, additional, Handoko, M L, additional, Meijboom, L, additional, Marcus, J T, additional, Symersky, P, additional, Niessen, H W M, additional, Vonk-Noordegraaf, A, additional, Bogaard, H J, additional, Goumans, M J, additional, and De Man, F S, additional
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- 2024
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4. Increased perivascular fibrosis and pro-fibrotic cellular transition in intramyocardial blood vessels in patients with myocardial infarction
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Jiang, Z, primary, Sorrentino, G, additional, Simsek, S, additional, Niessen, H W M, additional, and Krijnen, P A J, additional
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- 2024
- Full Text
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5. The Netherlands Heart Tissue Bank: Strengthening the cardiovascular research infrastructure with an open access Cardiac Tissue Repository
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Henkens, M T H M, van Ast, J F, Te Riele, A S J M, Houweling, A C, Amin, A S, Nijveldt, R, Antoni, M L, Li, X, Wehrens, S M T, von der Thüsen, J H, Damman, K, Ter Horst, E N, Manintveld, O C, Abma-Schouten, R Y, Niessen, H W M, Silljé, H H W, Jukema, J W, Doevendans, P A, Henkens, M T H M, van Ast, J F, Te Riele, A S J M, Houweling, A C, Amin, A S, Nijveldt, R, Antoni, M L, Li, X, Wehrens, S M T, von der Thüsen, J H, Damman, K, Ter Horst, E N, Manintveld, O C, Abma-Schouten, R Y, Niessen, H W M, Silljé, H H W, Jukema, J W, and Doevendans, P A
- Abstract
AIM: Cardiac diseases remain a leading cause of cardiovascular disease (CVD) related hospitalisation and mortality. That is why research to improve our understanding of pathophysiological processes underlying cardiac diseases is of great importance. There is a strong need for healthy and diseased human cardiac tissue and related clinical data to accomplish this, since currently used animal and in vitro disease models do not fully grasp the pathophysiological processes observed in humans. This design paper describes the initiative of the Netherlands Heart Tissue Bank (NHTB) that aims to boost CVD-related research by providing an open-access biobank.METHODS: The NHTB, founded in June 2020, is a non-profit biobank that collects and stores biomaterial (including but not limited to myocardial tissue and blood samples) and clinical data of individuals with and without previously known cardiac diseases. All individuals aged ≥ 18 years living in the Netherlands are eligible for inclusion as a potential future donor. The stored samples and clinical data will be available upon request for cardiovascular researchers.CONCLUSION: To improve the availability of cardiac tissue for cardiovascular research, the NHTB will include extensive (cardiac) biosamples, medical images, and clinical data of donors with and without a previously known cardiac disease. As such, the NHTB will function as a translational bridge to boost a wide range of cardiac disease-related fundamental and translational studies.
- Published
- 2023
6. Fatal neonatal hypertrophic cardiomyopathy caused by compound heterozygous truncating MYBPC3 mutation
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Alsters, S., Wong, L., Peferoen, L., Niessen, H. W. M., Bikker, H., Elting, M. W., and Houweling, A. C.
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- 2019
- Full Text
- View/download PDF
7. First 12-month follow-up of bioresorbable synthetic heart valves implanted in the aortic position in sheep
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Vis, A, primary, De Kort, B J, additional, Szymczyk, W, additional, Van Rijswijk, J W, additional, Dekker, S, additional, Driessen, R, additional, Wijkstra, N, additional, Grundeman, P F, additional, Niessen, H W M, additional, Janssen, H M, additional, Dankers, P Y W, additional, Smits, A I P M, additional, Bouten, C V C, additional, and Kluin, J, additional
- Published
- 2022
- Full Text
- View/download PDF
8. The Netherlands Heart Tissue Bank
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Henkens, M. T. H. M., primary, van Ast, J. F., additional, te Riele, A. S. J. M., additional, Houweling, A. C., additional, Amin, A. S., additional, Nijveldt, R., additional, Antoni, M. L., additional, Li, X., additional, Wehrens, S. M. T., additional, von der Thüsen, J. H., additional, Damman, K., additional, ter Horst, E. N., additional, Manintveld, O. C., additional, Abma-Schouten, R. Y., additional, Niessen, H. W. M., additional, Silljé, H. H. W., additional, Jukema, J. W., additional, and Doevendans, P. A., additional
- Published
- 2022
- Full Text
- View/download PDF
9. The Netherlands Heart Tissue Bank: Strengthening the cardiovascular research infrastructure with an open access Cardiac Tissue Repository
- Author
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Henkens, M T H M, van Ast, J F, Te Riele, A S J M, Houweling, A C, Amin, A S, Nijveldt, R, Antoni, M L, Li, X, Wehrens, S M T, von der Thüsen, J H, Damman, K, Ter Horst, E N, Manintveld, O C, Abma-Schouten, R Y, Niessen, H W M, Silljé, H H W, Jukema, J W, Doevendans, P A, Henkens, M T H M, van Ast, J F, Te Riele, A S J M, Houweling, A C, Amin, A S, Nijveldt, R, Antoni, M L, Li, X, Wehrens, S M T, von der Thüsen, J H, Damman, K, Ter Horst, E N, Manintveld, O C, Abma-Schouten, R Y, Niessen, H W M, Silljé, H H W, Jukema, J W, and Doevendans, P A
- Abstract
AIM: Cardiac diseases remain a leading cause of cardiovascular disease (CVD) related hospitalisation and mortality. That is why research to improve our understanding of pathophysiological processes underlying cardiac diseases is of great importance. There is a strong need for healthy and diseased human cardiac tissue and related clinical data to accomplish this, since currently used animal and in vitro disease models do not fully grasp the pathophysiological processes observed in humans. This design paper describes the initiative of the Netherlands Heart Tissue Bank (NHTB) that aims to boost CVD-related research by providing an open-access biobank.METHODS: The NHTB, founded in June 2020, is a non-profit biobank that collects and stores biomaterial (including but not limited to myocardial tissue and blood samples) and clinical data of individuals with and without previously known cardiac diseases. All individuals aged ≥ 18 years living in the Netherlands are eligible for inclusion as a potential future donor. The stored samples and clinical data will be available upon request for cardiovascular researchers.CONCLUSION: To improve the availability of cardiac tissue for cardiovascular research, the NHTB will include extensive (cardiac) biosamples, medical images, and clinical data of donors with and without a previously known cardiac disease. As such, the NHTB will function as a translational bridge to boost a wide range of cardiac disease-related fundamental and translational studies.
- Published
- 2022
10. The methylglyoxal-derived AGE tetrahydropyrimidine is increased in plasma of individuals with type 1 diabetes mellitus and in atherosclerotic lesions and is associated with sVCAM-1
- Author
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van Eupen, M. G. A., Schram, M. T., Colhoun, H. M., Hanssen, N. M. J., Niessen, H. W. M., Tarnow, L., Parving, H. H., Rossing, P., Stehouwer, C. D. A., and Schalkwijk, C. G.
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- 2013
- Full Text
- View/download PDF
11. The multidrug resistance protein breast cancer resistance protein (BCRP) protects adipose-derived stem cells against ischemic damage
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van Dijk, A., Naaijkens, B. A., Jurgens, W. J. F. M., Oerlemans, R., Scheffer, G. L., Kassies, J., Aznou, J., Brouwer, M., van Rossum, A. C., Schuurhuis, G. J., van Milligen, F. J., and Niessen, H. W. M.
- Published
- 2012
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12. Genetic Diagnosis in Sudden Cardiac Death: The Crucial Role of Multidisciplinary Care
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van der Crabben, S. N., primary, Komdeur, F. L., additional, Nossent, E. J., additional, Deprez, R. H. Lekanne, additional, Broekhuizen, E. A., additional, van der Werf, C., additional, Vermeer, A. M. C., additional, Niessen, H. W. M., additional, and Houweling, A. C., additional
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- 2021
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13. IgM colocalises with complement and C reactive protein in infarcted human myocardium
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Krijnen, P. S. J., Ciurana, C., Cramer, T., Hazes, T., Meijer, C. J. L. M., Visser, C. A., Niessen, H. W. M., and Hack, C. E.
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Myocardial ischemia -- Analysis ,Myocardial ischemia -- Research ,Complement (Immunology) -- Research ,Health - Published
- 2005
14. Apoptosis in myocardial ischaemia and infarction. (Review)
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Krijnen, P. A. J., Nijmeijer, R., Meijer, C. J. L. M., Visser, C. A., Hack, C. E., and Niessen, H. W. M.
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Statistics ,Evaluation ,Physiological aspects ,Myocardial ischemia -- Statistics -- Physiological aspects ,Heart attack -- Statistics -- Physiological aspects ,Myocardium -- Evaluation -- Statistics -- Physiological aspects ,Cell death -- Physiological aspects -- Statistics ,Heart cells -- Physiological aspects -- Statistics ,Heart muscle -- Evaluation -- Statistics -- Physiological aspects - Abstract
Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review [...]
- Published
- 2002
15. Colocalisation of intraplaque C reactive protein, complement, oxidised low density lipoprotein, and macrophages in stable and unstable angina and acute myocardial infarction
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Meuwissen, M, van der Wal, A C, Niessen, H W M, Koch, K T, de Winter, R J, van der Loos, C M, Rittersma, S Z H, Chamuleau, S A J, Tijssen, J G P, Becker, A E, and Piek, J J
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- 2006
16. Amyloid in the cardiovascular system: a review
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Kholová, I and Niessen, H W M
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- 2005
17. Myocardial air collections as a result of infection with a gas producing strain of Escherichia coli
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van der Vliet, H J J, Niessen, H W M, and Perenboom, R M
- Published
- 2004
18. Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction
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Krijnen, P A J, Meischl, C, Hack, C E, Meijer, C J L M, Visser, C A, Roos, D, and Niessen, H W M
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- 2003
19. NADPH oxidase(s): new source(s) of reactive oxygen species in the vascular system?
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Van Heerebeek, L, Meischl, C, Stooker, W, Meijer, C J L M, Niessen, H W M, and Roos, D
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- 2002
20. Localisation of C reactive protein in infarcted tissue sites of multiple organs during sepsis
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Baidoshvili, A, Nijmeijer, R, Lagrand, W K, Hack, C E, and Niessen, H W M
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- 2002
21. Perivenous support reduces early changes in human vein grafts: Studies in whole blood perfused human vein segments
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Stooker, W., Niessen, H. W. M., Baidoshvili, A., Wildevuur, W. R., Van Hinsbergh, V. W. M., Fritz, J., Wildevuur, C. R. H., and Eijsman, L.
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- 2001
22. Apolipoprotein H, a new mediator in the inflammatory changes ensuing in jeopardised human myocardium
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Niessen, H W M, Lagrand, W K, Rensink, H J A M, Meijer, Ch J L M, Aarden, L, and Hack, C E
- Published
- 2000
23. Microorganisms in the aetiology of atherosclerosis
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Morré, S A, Stooker, W, Lagrand, W K, van den Brule, A J C, and Niessen, H W M
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- 2000
24. Hemangioma of the Atherosclerotic Changed Aortic Valve
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van Broekhoven, A., Krijnen, P. A. J., Niessen, H. W. M., and Vonk, A. B. A.
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body regions ,Article Subject ,cardiovascular system ,sense organs ,cardiovascular diseases ,eye diseases - Abstract
The incidence of heart valve hemangioma is very low and is mostly observed in the mitral and tricuspid valve. In 2006, two cases of aortic valve hemangioma were reported for the first time, including one with calcifying aortic valve stenosis. We now present a case of aortic valve hemangioma in a patient suffering from aortic valve insufficiency combined with atherosclerotic thickening.
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- 2019
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25. Atherosclerosis. Pathology of The Vasculature in Live Patients.
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NIESSEN, H W M
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- 1999
26. Hemangioma of the Atherosclerotic Changed the Aortic Valve.
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van Broekhoven, A., Krijnen, P. A. J., Niessen, H. W. M., and Vonk, A. B. A.
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AORTIC valve insufficiency ,AORTIC valve - Abstract
The incidence of heart valve hemangioma is very low and is mostly observed in the mitral and tricuspid valve. In 2006, two cases of aortic valve hemangioma were reported for the first time, including one with calcifying aortic valve stenosis. We now present a case of aortic valve hemangioma in a patient suffering from aortic valve insufficiency combined with atherosclerotic thickening. [ABSTRACT FROM AUTHOR]
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- 2019
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27. Vascular Disease: Molecular Biology and Gene Therapy Protocols. Methods in Molecular Medicine
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NIESSEN, H W M
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Vascular Disease: Molecular Biology and Gene Therapy Protocols. Methods in Molecular Medicine (Book) ,Books -- Book reviews - Abstract
Baker AH, ed. (£72.50.) Humana Press, 1999. ISBN 0 89603 731 2. In this book, an impressive amount of different molecular techniques that can be used in vascular research are [...]
- Published
- 2001
28. Role of plaque inflammation in acute and recurrent coronary syndromes
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Meuwissen, M., van der Wal, A. C., Siebes, M., Koch, K. T., Chamuleau, S. A. J., van der Loos, C. M., Teeling, P., de Winter, R. J., Niessen, H. W. M., Tijssen, J. G. P., Becker, A. E., Piek, J. J., Pathology, Amsterdam Cardiovascular Sciences, Biomedical Engineering and Physics, Cardiology, and Extramural researchers
- Abstract
Inflammation plays an important role in the initiation, development, progression and complications of atherosclerotic vascular disease. Our present knowledge of the elementary role of inflammation for the onset of plaque rupture in atherosclerotic coronary lesions primarily stems from autopsy studies. However, the introduction of directional coronary atherectomy catheters has provided a unique opportunity to directly investigate the role of inflammation in coronary syndromes. In this report we describe the role of coronary plaque inflammation, as determined by immunohistochemistry, on the presentation of coronary syndromes and on the clinical outcome following percutaneous interventions.
- Published
- 2004
29. C-reactive protein as a pro-inflammatory mediator in cardiovascular disease by its ability to activate complement: additional proof and hypothetical mechanisms
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Lagrand, W. K., Nijmeijer, R., Niessen, H. W. M., Visser, C. A., Hermens, W. T., Hack, C. E., Intensive Care Medicine, Other departments, and Landsteiner Laboratory
- Published
- 2002
30. Decreased smooth muscle cell/extracellular matrix ratio of media of femoral artery in patients with atherosclerosis and hyperhomocysteinemia
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Vermeulen, E G, Niessen, H W, Bogels, M, Stehouwer, C D, Rauwerda, J A, van Hinsbergh, V W, Surgery, Pathology, Cardio-thoracic surgery, ACS - Heart failure & arrhythmias, AGEM - Digestive immunity, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, CCA - Target Discovery & Preclinial Therapy Development, AII - Inflammatory diseases, and Physiology
- Abstract
The aim of this study was to determine whether the morphology of the muscular femoral artery in patients with atherosclerosis and hyperhomocysteinemia differs from that of atherosclerotic vessels from patients with normal homocysteine levels. Whole-vessel biopsies of the superficial femoral artery were taken from patients with symptomatic atherosclerotic disease with and without hyperhomocysteinemia and from patients without atherosclerosis from traumatic amputations. The morphology of these specimens was studied qualitatively by light and electron microscopy and quantitatively by light microscopy in combination with a video overlay system. Atherosclerotic lesions in patients with hyperhomocysteinemia were morphologically similar to those in patients with normal homocysteine levels, except for a significantly decreased smooth muscle cell/extracellular matrix ratio of the media in hyperhomocysteinemic patients (P=0.02 versus normohomocysteinemic atherosclerotic group and P=0.001 versus group without a history of cardiovascular disease). Hyperhomocysteinemia is associated with a significant decrease of the smooth muscle cell/extracellular matrix ratio of the media of muscular femoral arteries without significant changes in medial thickness. Further investigations should concentrate on the cause of this newly discovered phenomenon and its impact on vascular compliance.
- Published
- 2001
31. C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon?
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Lagrand, W. K., Visser, C. A., Hermens, W. T., Niessen, H. W., Verheugt, F. W., Wolbink, G. J., Hack, C. E., and Other departments
- Abstract
BACKGROUND: Circulating levels of C-reactive protein (CRP) may constitute an independent risk factor for cardiovascular disease. How CRP as a risk factor is involved in cardiovascular disease is still unclear. METHODS AND RESULTS: By reviewing available studies, we discuss explanations for the associations between CRP and cardiovascular disease. CRP levels within the upper quartile/quintile of the normal range constitute an increased risk for cardiovascular events, both in apparently healthy persons and in persons with preexisting angina pectoris. High CRP responses after acute myocardial infarction indicate an unfavorable outcome, even after correction for other risk factors. This link between CRP and cardiovascular disease has been considered to reflect the response of the body to the inflammatory reactions in the atherosclerotic (coronary) vessels and adjacent myocardium. However, because CRP localizes in infarcted myocardium (with colocalization of activated complement), we hypothesize that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis. CONCLUSIONS: CRP constitutes an independent cardiovascular risk factor. Unraveling the molecular background of this association may provide new directions for prevention of cardiovascular events
- Published
- 1999
32. Monocyte subset accumulation in the human heart following acute myocardial infarction and the role of the spleen as monocyte reservoir
- Author
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van der Laan, A. M., primary, ter Horst, E. N., additional, Delewi, R., additional, Begieneman, M. P. V., additional, Krijnen, P. A. J., additional, Hirsch, A., additional, Lavaei, M., additional, Nahrendorf, M., additional, Horrevoets, A. J., additional, Niessen, H. W. M., additional, and Piek, J. J., additional
- Published
- 2013
- Full Text
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33. The GLP-1 analogue liraglutide decreases the pro-inflammatory status of the heart in diabetes
- Author
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Emmens, R. W., primary, Baylan, U., additional, Naaijkens, B., additional, Schalkwijk, C. G., additional, Niessen, H. W. M., additional, Krijnen, P. A. J., additional, and Simsek, S., additional
- Published
- 2013
- Full Text
- View/download PDF
34. Directing stem cells to the infarcted heart using targeted microbubbles: development of a new molecular therapeutic technique
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Naaijkens, B., primary, Bogaards, S. J. P., additional, Krijnen, P. A. J., additional, Kamp, O., additional, Musters, R. J. P., additional, Kokhuis, T. J. A., additional, De Jong, N., additional, Niessen, H. W. M., additional, Van Dijk, A., additional, and Juffermans, L. J. M., additional
- Published
- 2013
- Full Text
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35. Poster session 3
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Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. L., additional, Pinho, M., additional, Pinho, S., additional, Sena, C., additional, Seica, R., additional, Leite-Moreira, A., additional, Dabroi, F., additional, Schiaffino, S., additional, Kiseleva, E., additional, Krukov, N., additional, Nikitin, O., additional, Ardatova, L., additional, Mourouzis, I., additional, Pantos, C., additional, Kokkinos, A. D., additional, Cokkinos, D. V., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M. A., additional, Pellegrino, M., additional, Calabriso, N., additional, Gastaldelli, A., additional, Storelli, C., additional, De Caterina, R., additional, Lindner, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschope, C., additional, Westermann, D., additional, Everaert, B. R., additional, Nijenhuis, V. J., additional, Reith, F. C. M., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, Vrints, C. 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36. Poster session 2
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Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. 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M., additional, Madonna, R., additional, Delli Pizzi, S., additional, Di Donato, L., additional, Mariotti, A., additional, Di Carlo, L., additional, D'ugo, E., additional, Teberino, M. A., additional, Merla, A., additional, T, A., additional, De Caterina, R., additional, Kolker, L., additional, Ali, N. N., additional, Maclellan, K., additional, Moore, M., additional, Wheeler, J., additional, Harding, S. E., additional, Fleck, R. A., additional, Rowlinson, J. M., additional, Kraenkel, N., additional, Ascione, R., additional, Madeddu, P., additional, O'sullivan, J. F., additional, Leblond, A. L., additional, Kelly, G., additional, Kumar, A. H. S., additional, Metharom, P., additional, Buneker, C. K., additional, Alizadeh-Vikali, N., additional, Hynes, B. G., additional, O'connor, R., additional, Caplice, N. M., additional, Noseda, M., additional, De Smith, A. J., additional, Leja, T., additional, Rao, P. H., additional, Al-Beidh, F., additional, Abreu Pavia, M. S., additional, Blakemore, A. I., additional, Schneider, M. D., additional, Stathopoulou, K., additional, Cuello, F., additional, Ehler, E., additional, Haworth, R. S., additional, Avkiran, M., additional, Morawietz, H., additional, Eickholt, C., additional, Langbein, H., additional, Brux, M., additional, Goettsch, C., additional, Goettsch, W., additional, Arsov, A., additional, Brunssen, C., additional, Mazilu, L., additional, Parepa, I. R., additional, Suceveanu, A. I., additional, Suceveanu, A. P., additional, De Man, F. S., additional, Guignabert, C., additional, Tu, L., additional, Handoko, M. L., additional, Schalij, I., additional, Fadel, E., additional, Postmus, P. 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F., additional, Villar, A. V., additional, Perez-Moreno, A., additional, Gilabert, R., additional, and Ros, E., additional
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- 2012
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37. Fluoride prevents degranulation of the azurophilic and specific granules in electropermeabilized neutrophils
- Author
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Niessen, H W, Kessels, G C, Verhoeven, A J, Pathology, Cardio-thoracic surgery, ACS - Heart failure & arrhythmias, AGEM - Digestive immunity, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, CCA - Target Discovery & Preclinial Therapy Development, and AII - Inflammatory diseases
- Abstract
The effect of AlF4- on the degranulation process in human neutrophils was investigated. In intact neutrophils, AlF4- induced degranulation, whereas in electropermeabilized neutrophils AlF4- did not stimulate degranulation. In electropermeabilized neutrophils, fluoride ions proved to be inhibitory for the degranulation induced by addition of Ca2+ and/or GTP-gamma-S. Another phosphatase inhibitor, okadaic acid, inhibited degranulation induced by Ca2+ or by GTP-gamma-S but not degranulation induced by the combination of Ca2+ plus GTP-gamma-S. It is concluded that under suboptimal conditions of stimulation with Ca2+ or GTP-gamma-S, protein dephosphorylation plays an important role in the degranulation response in human neutrophils.
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- 1994
38. Pulmonary embolism causes endomyocarditis in the human heart
- Author
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Begieneman, M P V, primary, van de Goot, F R W, additional, van der Bilt, I A C, additional, Noordegraaf, A V., additional, Spreeuwenberg, M D, additional, Paulus, W J, additional, van Hinsbergh, V W M, additional, Visser, F C, additional, and Niessen, H W M, additional
- Published
- 2007
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39. The effect of monohydroxyethylrutoside on doxorubicin-induced cardiotoxicity in patients treated for metastatic cancer in a phase II study
- Author
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Bruynzeel, A M E, primary, Niessen, H W M, additional, Bronzwaer, J G F, additional, van der Hoeven, J J M, additional, Berkhof, J, additional, Bast, A, additional, van der Vijgh, W J F, additional, and van Groeningen, C J, additional
- Published
- 2007
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40. Anti-inflammatory agents and monoHER protect against DOX-induced cardiotoxicity and accumulation of CML in mice
- Author
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Bruynzeel, A M E, primary, Abou El Hassan, M A, additional, Schalkwijk, C, additional, Berkhof, J, additional, Bast, A, additional, Niessen, H W M, additional, and van der Vijgh, W J F, additional
- Published
- 2007
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41. Clusterin: a protective mediator for ischemic cardiomyocytes?
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Krijnen, P. A. J., primary, Cillessen, S. A. G. M., additional, Manoe, R., additional, Muller, A., additional, Visser, C. A., additional, Meijer, C. J. L. M., additional, Musters, R. J. P., additional, Hack, C. E., additional, Aarden, L. A., additional, and Niessen, H. W. M., additional
- Published
- 2005
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42. Type II secretory phospholipase A2binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death
- Author
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Nijmeijer, R., primary, Willemsen, M., additional, Meijer, C. J. L. M., additional, Visser, C. A., additional, Verheijen, R. H., additional, Gottlieb, R. A., additional, Hack, C. E., additional, and Niessen, H. W. M., additional
- Published
- 2003
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43. C‐reactive protein and cardiovascular disease: linked by complement?
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Lagrand, W. K., primary, Visser, C. A., additional, Hack, C. E., additional, Niessen, H. W. M., additional, and Nijmeijer, R., additional
- Published
- 2000
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44. Role for complement as an intermediate between C-reactive protein and intercellular adhesion molecule-1 expression?
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Lagrand, W K, Niessen, H W, Nijmeijer, R, and Hack, C E
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- 2001
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45. Reduction of vascular leakage by imatinib is associated with preserved microcirculatory perfusion and reduced renal injury markers in a rat model of cardiopulmonary bypass.
- Author
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Koning, N. J., de Lange, F., van Meurs, M., Jongman, R. M., Ahmed, Y., Schwarte, L. A., van Nieuw Amerongen, G. P., Vonk, A. B. A., Niessen, H. W., Baufreton, C., and Boer, C.
- Subjects
- *
IMATINIB , *CARDIOPULMONARY bypass , *MICROCIRCULATION disorders - Abstract
Background: Cardiopulmonary bypass during cardiac surgery leads to impaired microcirculatory perfusion. We hypothesized that vascular leakage is an important contributor to microcirculatory dysfunction. Imatinib, a tyrosine kinase inhibitor, has been shown to reduce vascular leakage in septic mice. We investigated whether prevention of vascular leakage using imatinib preserves microcirculatory perfusion and reduces organ injury markers in a rat model of cardiopulmonary bypass.Methods: Male Wistar rats underwent cardiopulmonary bypass after treatment with imatinib or vehicle (n=8 per group). Cremaster muscle microcirculatory perfusion and quadriceps microvascular oxygen saturation were measured using intravital microscopy and reflectance spectroscopy. Evans Blue extravasation was determined in separate experiments. Organ injury markers were determined in plasma, intestine, kidney, and lungs.Results: The onset of cardiopulmonary bypass decreased the number of perfused microvessels by 40% in the control group [9.4 (8.6-10.6) to 5.7 (4.8-6.2) per microscope field; P<0.001 vs baseline], whereas this reduction was not seen in the imatinib group. In the control group, the number of perfused capillaries remained low throughout the experiment, whilst perfusion remained normal after imatinib administration. Microvascular oxygen saturation was less impaired after imatinib treatment compared with controls. Imatinib reduced vascular leakage and decreased fluid resuscitation compared with control [3 (3-6) vs 12 ml (7-16); P=0.024]. Plasma neutrophil-gelatinase-associated-lipocalin concentrations were reduced by imatinib.Conclusions: Prevention of endothelial barrier dysfunction using imatinib preserved microcirculatory perfusion and oxygenation during and after cardiopulmonary bypass. Moreover, imatinib-induced protection of endothelial barrier integrity reduced fluid-resuscitation requirements and attenuated renal and pulmonary injury markers. [ABSTRACT FROM AUTHOR]- Published
- 2018
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- View/download PDF
46. Development of a new therapeutic technique to direct stem cells to the infarcted heart using targeted microbubbles: StemBells.
- Author
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Woudstra L, Krijnen PA, Bogaards SJ, Meinster E, Emmens RW, Kokhuis TJ, Bollen IA, Baltzer H, Baart SM, Parbhudayal R, Helder MN, van Hinsbergh VW, Musters RJ, de Jong N, Kamp O, Niessen HW, van Dijk A, and Juffermans LJ
- Subjects
- Adipose Tissue cytology, Adipose Tissue metabolism, Administration, Intravenous, Animals, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Cell Survival, Cells, Cultured, Disease Models, Animal, Echocardiography, Heart diagnostic imaging, Heart physiopathology, Humans, Macrophages metabolism, Macrophages pathology, Male, Myocardial Infarction metabolism, Myocardial Infarction pathology, Pilot Projects, Rats, Rats, Wistar, Sonication, Stem Cells cytology, Stem Cells metabolism, Microbubbles, Myocardial Infarction therapy, Stem Cell Transplantation methods
- Abstract
Successful stem cell therapy after acute myocardial infarction (AMI) is hindered by lack of engraftment of sufficient stem cells at the site of injury. We designed a novel technique to overcome this problem by assembling stem cell-microbubble complexes, named 'StemBells'. StemBells were assembled through binding of dual-targeted microbubbles (~3μm) to adipose-derived stem cells (ASCs) via a CD90 antibody. StemBells were targeted to the infarct area via an ICAM-1 antibody on the microbubbles. StemBells were characterized microscopically and by flow cytometry. The effect of ultrasound on directing StemBells towards the vessel wall was demonstrated in an in vitro flow model. In a rat AMI-reperfusion model, StemBells or ASCs were injected one week post-infarction. A pilot study demonstrated feasibility of intravenous StemBell injection, resulting in localization in ICAM-1-positive infarct area three hours post-injection. In a functional study five weeks after injection of StemBells cardiac function was significantly improved compared with controls, as monitored by 2D-echocardiography. This functional improvement neither coincided with a reduction in infarct size as determined by histochemical analysis, nor with a change in anti- and pro-inflammatory macrophages. In conclusion, the StemBell technique is a novel and feasible method, able to improve cardiac function post-AMI in rats., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
47. Adipose tissue-derived stromal cells acquire endothelial-like features upon reprogramming with SOX18.
- Author
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Fontijn RD, Favre J, Naaijkens BA, Meinster E, Paauw NJ, Ragghoe SL, Nauta TD, van den Broek MA, Weijers EM, Niessen HW, Koolwijk P, and Horrevoets AJ
- Subjects
- Cell Differentiation, Cell Movement drug effects, Cells, Cultured, Cellular Reprogramming, Chemotaxis drug effects, Endothelial Cells cytology, Genetic Vectors genetics, Genetic Vectors metabolism, Human Umbilical Vein Endothelial Cells, Humans, Matrix Metalloproteinase 7 metabolism, Microtubules chemistry, Microtubules metabolism, SOXF Transcription Factors genetics, Shear Strength, Stromal Cells cytology, Vascular Endothelial Growth Factor A pharmacology, Adipose Tissue cytology, Endothelial Cells metabolism, SOXF Transcription Factors metabolism, Stromal Cells metabolism
- Abstract
Adipose tissue-derived stromal cells (ASC) form a rich source of autologous cells for use in regenerative medicine. In vitro induction of an endothelial phenotype may improve performance of ASCs in cardiovascular repair. Here, we report on an in vitro strategy using direct reprogramming of ASCs by means of ectopic expression of the endothelial-specific transcription factor SRY (sex determining region Y)-box18 (SOX18). SOX18 induces ASCs to express a set of genes involved in vascular patterning: MMP7, KDR, EFNB2, SEMA3G and CXCR4. Accordingly, SOX18 transduced ASCs reorganize under conditions of shear stress, display VEGF-induced chemotaxis and form tubular structures in 3D matrices in an MMP7-dependent manner. These in vitro findings provide insight into molecular and cellular processes downstream of SOX18 and show that reprogramming using SOX18 is sufficient to induce several endothelial-like features in ASCs., (Copyright © 2014. Published by Elsevier B.V.)
- Published
- 2014
- Full Text
- View/download PDF
48. Reduction of infarct size by intravenous injection of uncultured adipose derived stromal cells in a rat model is dependent on the time point of application.
- Author
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van Dijk A, Naaijkens BA, Jurgens WJ, Nalliah K, Sairras S, van der Pijl RJ, Vo K, Vonk AB, van Rossum AC, Paulus WJ, van Milligen FJ, and Niessen HW
- Subjects
- Animals, Biomarkers metabolism, Blood Vessels pathology, Cell Count, Cell Differentiation, Cells, Cultured, Disease Models, Animal, Heart Function Tests, Injections, Intravenous, Macrophages pathology, Male, Myocardial Infarction physiopathology, Myocytes, Cardiac pathology, Rats, Rats, Wistar, Stromal Cells cytology, Stromal Cells transplantation, Thromboembolism etiology, Thromboembolism pathology, Time Factors, Adipose Tissue cytology, Myocardial Infarction pathology, Myocardial Infarction therapy, Stem Cell Transplantation adverse effects, Stem Cells cytology
- Abstract
Stem cell therapy is a promising tool to improve outcome after acute myocardial infarction (AMI), but needs to be optimized since results from clinical applications remain ambiguous. A potent source of stem cells is the stromal vascular fraction of adipose tissue (SVF), which contains high numbers of adipose derived stem cells (ASC). We hypothesized that: 1) intravenous injection can be used to apply stem cells to the heart. 2) Uncultured SVF cells are easier and safer when cultured ASCs. 3) Transplantation after the acute inflammation period of AMI is favorable over early injection. For this, AMI was induced in rats by 40min of coronary occlusion. One or seven days after AMI, rats were intravenously injected with vehicle, 5×10(6) uncultured rat SVF cells or 1×10(6) rat ASCs. Rats were analyzed 35 days after AMI. Intravenous delivery of both fresh SVF cells and cultured ASCs 7 days after AMI significantly reduced infarct size compared to vehicle. Similar numbers of stem cells were found in the heart, after treatment with fresh SVF cells and cultured ASCs. Importantly, no adverse effects were found after injection of SVF cells. Using cultured ASCs, however, 3 animals had shortness of breath, and one animal died during injection. In contrast to application at 7 days post AMI, injection of SVF cells 1 day post AMI resulted in a small but non-significant infarct reduction (p=0.35). Taken together, intravenous injection of uncultured SVF cells subsequent to the acute inflammation period, is a promising stem cell therapy for AMI., (Copyright © 2011 Elsevier B.V. All rights reserved.)
- Published
- 2011
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49. N(epsilon)-(carboxymethyl)lysine depositions in intramyocardial blood vessels in human and rat acute myocardial infarction: a predictor or reflection of infarction?
- Author
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Baidoshvili A, Krijnen PA, Kupreishvili K, Ciurana C, Bleeker W, Nijmeijer R, Visser CA, Visser FC, Meijer CJ, Stooker W, Eijsman L, van Hinsbergh VW, Hack CE, Niessen HW, and Schalkwijk CG
- Subjects
- Aged, Animals, E-Selectin metabolism, Endothelial Cells metabolism, Female, Humans, Immunohistochemistry, Lysine biosynthesis, Lysine metabolism, Male, Middle Aged, Myocardial Infarction etiology, Myocardial Reperfusion, Myocarditis metabolism, Oxidative Stress, Peroxidase metabolism, Prognosis, Rats, Risk Factors, Time Factors, Coronary Vessels metabolism, Lysine analogs & derivatives, Myocardial Infarction metabolism
- Abstract
Objective: Advanced glycation end products (AGEs), such as N(epsilon)-(carboxymethyl)lysine (CML), are implicated in vascular disease. We previously reported increased CML accumulation in small intramyocardial blood vessels in diabetes patients. Diabetes patients have an increased risk for acute myocardial infarction (AMI). Here, we examined a putative relationship between CML and AMI., Methods and Results: Heart tissue was stained for CML, myeloperoxidase, and E-selectin in AMI patients (n=26), myocarditis patients (n=17), and control patients (n=15). In AMI patients, CML depositions were 3-fold increased compared with controls in the small intramyocardial blood vessels and predominantly colocalized with activated endothelium (E-selectin-positive) both in infarction and noninfarction areas. A trend of increased CML positivity of the intima of epicardial coronary arteries did not reach significance in AMI patients. In the rat heart AMI model, CML depositions were undetectable after 24 hours of reperfusion, but became clearly visible after 5 days of reperfusion. In line with an inflammatory contribution, human myocarditis was also accompanied by accumulation of CML on the endothelium of intramyocardial blood vessels., Conclusions: CML, present predominantly on activated endothelium in small intramyocardial blood vessels in patients with AMI, might reflect an increased risk for AMI rather than being a result of AMI.
- Published
- 2006
- Full Text
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50. Role of plaque inflammation in acute and recurrent coronary syndromes.
- Author
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Meuwissen M, van der Wal AC, Siebes M, Koch KT, Chamuleau SA, van der Loos CM, Teeling P, de Winter RJ, Niessen HW, Tijssen JG, Becker AE, and Piek JJ
- Abstract
Inflammation plays an important role in the initiation, development, progression and complications of atherosclerotic vascular disease. Our present knowledge of the elementary role of inflammation for the onset of plaque rupture in atherosclerotic coronary lesions primarily stems from autopsy studies. However, the introduction of directional coronary atherectomy catheters has provided a unique opportunity to directly investigate the role of inflammation in coronary syndromes. In this report we describe the role of coronary plaque inflammation, as determined by immunohistochemistry, on the presentation of coronary syndromes and on the clinical outcome following percutaneous interventions.
- Published
- 2004
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