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119 results on '"Kuijpers T. W."'

1. An AI‐based imaging flow cytometry approach to study erythrophagocytosis.

Author

Neri, S., Brandsma, E. T., Mul, F. P. J., Kuijpers, T. W., Matlung, H. L., and van Bruggen, R.

Abstract

Erythrophagocytosis is a process consisting of recognition, engulfment and digestion by phagocytes of antibody‐coated or damaged erythrocytes. Understanding the dynamics that are behind erythrophagocytosis is fundamental to comprehend this cellular process under specific circumstances. Several techniques have been used to study phagocytosis. Among these, an interesting approach is the use of Imaging Flow Cytometry (IFC) to distinguish internalization and binding of cells or particles. However, this method requires laborious analysis. Here, we introduce a novel approach to analyze the phagocytosis process by combining Artificial Intelligence (AI) with IFC. Our study demonstrates that this approach is highly suitable to study erythrophagocytosis, categorizing internalized, bound and non‐bound erythrocytes. Validation experiments showed that our pipeline performs with high accuracy and reproducibility. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Management of drug interactions with direct‐acting antivirals in Dutch HIV/hepatitis C virus‐coinfected patients: adequate but not perfect

Author

Smolders, EJ, Smit, C, de Kanter, CTMM, Dofferhoff, ASM, Arends, JE, Brinkman, K, Rijnders, B, van der Valk, M, Reiss, P, Burger, DM, Prins, J. M., Kuijpers, T. W., Scherpbier, H. J., van der Meer, J. T. M., Wit, F. W. M. N., Godfried, M. H., van der Poll, T., Nellen, F. J. B., Geerlings, S. E., van Vugt, M., Pajkrt, D., Wiersinga, W. J., Goorhuis, A., Hovius, J. W., Bijsterveld, M. A. H., van Eden, J., van Hes, A. M. H., Mutschelknauss, M., Nobel, H. E., Pijnappel, F. J. J., Weijsenfeld, A. M., Jurriaans, S., Back, N. K. T., Zaaijer, H. L., Berkhout, B., Cornelissen, M. T. E., Schinkel, C. J., Thomas, X. V., De Ruyter Ziekenhuis, Admiraal, van den Berge, M., Stegeman, A., Baas, S., Hage de Looff, L., Wintermans, B., Veenemans, J., Ziekenhuis, Catharina, Pronk, M. J. H., Ammerlaan, H. S. M., de Munnik, E. S., van Beek, E., Jansz, A. R., Tjhie, J., Wegdam, M. C. A., Deiman, B., Scharnhorst, V., Ziekenhuis, Elisabeth‐TweeSteden, van Kasteren, M. E. E., Brouwer, A. E., van Erve, R., de Kruijf‐van de Wiel, B. A. F. M., Keelan‐Pfaf, S., van der Ven, B., Buiting, A. G. M., Kabel, P. J., Versteeg, D., Kinderziekenhuis, Emma, van der Plas, A., van der Ende, M. E., Bax, H. I., van Gorp, E. C. M., Nouwen, J. L., Schurink, C. A. M., Verbon, A., de Vries‐Sluijs, T. E. M. S., Bassant, N., van Beek, J. E. A., Vriesde, M., van Zonneveld, L. M., van den Berg‐Cameron, H. J., Bruinsma‐Broekman, F. B., de Groot, J., de Zeeuw‐de Man, M., Boucher, C. A. B., Koopmans, M. P. G., van Kampen, J. J. A., Pas, S. D., Driessen, G. J. A., van Rossum, A. M. C., van der Knaap, L. C., Visser, E., Branger, J., Rijkeboer‐Mes, A., Duijf‐van de Ven, C. J. H. M., Schippers, E. F., van Nieuwkoop, C., van IJperen, J. M., Geilings, J., van der Hut, G., Franck, P. F. H., van Eeden, A., Brokking, W., Groot, M., Elsenburg, L. J. M., Damen, M., Kwa, I. S., Groeneveld, P. H. P., Bouwhuis, J. W., van den Berg, J. F., van Hulzen, A. G. W., van der Bliek, G. L., Bor, P. C. J., Bloembergen, P., Wolfhagen, M. J. H. M., Ruijs, G. J. H. M., Kroon, F. P., de Boer, M. G. J., Jolink, H., Vollaard, A. M., Dorama, W., van Holten, N., Claas, E. C. J., Wessels, E., den Hollander, J. G., Pogany, K., Roukens, A., Kastelijns, M., Smit, J. V., Smit, E., Struik‐Kalkman, D., Tearno, C., Bezemer, M., van Niekerk, T., Pontesilli, O., Lowe, S. H., Oude Lashof, A. M. L., Posthouwer, D., Ackens, R. P., Schippers, J., Vergoossen, R., Weijenberg‐Maes, B., van Loo, I. H. M., Havenith, T. R. A., Leyten, E. M. S., Gelinck, L. B. S., van Hartingsveld, A. Y., Meerkerk, C., Wildenbeest, G. S., Mutsaers, J. A. E. M., van Veen, S. Q., Slotervaart, MC, Mulder, J. W., Vrouenraets, S. M. E., Lauw, F. N., van Broekhuizen, M. C., Paap, H., Vlasblom, D. J., Smits, P. H. M., Zuiderzee, MC, Weijer, S., El Moussaoui, R., Bosma, A. S., van Vonderen, M. G. A., van Houte, D. P. F., Kampschreur, L. M., Dijkstra, K., Faber, S., Weel, J., Kootstra, G. J., Delsing, C. E., van der Burg‐van de Plas, M., Heins, H., Lucas, E., Kortmann, W., van Twillert, G., Cohen Stuart, J. W. T., Diederen, B. M. W., Renckens, R., Ruiter‐Pronk, D., van Truijen‐Oud, F. A., van der Reijden, W. A., Jansen, R., van den Berk, G. E. L., Blok, W. L., Frissen, P. H. J., Lettinga, K. D., Schouten, W. E. M., Veenstra, J., Brouwer, C. J., Geerders, G. F., Hoeksema, K., Kleene, M. J., van der Meché, I. B., Spelbrink, M., Sulman, H., Toonen, A. J. M., Wijnands, S., Kwa, D., Witte, E., van Crevel, R., Keuter, M., van der Ven, A. J. A. M., ter Hofstede, H. J. M., Albers, M., Grintjes‐Huisman, K. J. T., Marneef, M., Hairwassers, A., Rahamat‐Langendoen, J., Burger, D., Gisolf, E. H., Hassing, R. J., Claassen, M., ter Beest, G., van Bentum, P. H. M., Langebeek, N., Tiemessen, R., Swanink, C. M. A., van Lelyveld, S. F. L., Soetekouw, R., van der Prijt, L. M. M., van der Swaluw, J., Bermon, N., Herpers, B. L., Veenendaal, D., Verhagen, D. W. M., van Wijk, M., Bierman, W. F. W., Bakker, M., Kleinnijenhuis, J., Kloeze, E., Scholvinck, H., Stienstra, Y., Vermont, C. L., Wilting, K. R., Boonstra, A., de Groot‐de Jonge, H., van der Meulen, P. A., de Weerd, D. A., Niesters, H. G. M., van Leer‐Buter, C. C., Knoester, M., Hoepelman, A. I. M., Barth, R. E., Bruns, A. H. W., Ellerbroek, P. M., Mudrikova, T., Oosterheert, J. J., Schadd, E. M., Wassenberg, M. W. M., van Zoelen, M. A. D., Aarsman, K., van Elst‐Laurijssen, D. H. M., van Oers‐Hazelzet, E. E. B., van Berkel, M., Schuurman, R., Verduyn‐Lunel, F., Wensing, A. M. J., Peters, E. J. G., van Agtmael, M. A., Bomers, M., de Vocht, J., Heitmuller, M., Laan, L. M., Ang, C. W., van Houdt, R., Pettersson, A. M., Vandenbroucke‐Grauls, C. M. J. E., Geelen, S. P. M., Wolfs, T. F. W., Bont, L. J., Nauta, N., Bezemer, D. O., van Sighem, A. I., Boender, T. S., Zaheri, S., Hillebregt, M., de Jong, A., Bergsma, D., de Lang, A., Grivell, S., Jansen, A., Rademaker, M. J., Raethke, M., Meijering, R., Schnörr, S., de Groot, L., van den Akker, M., Bakker, Y., Claessen, E., El Berkaoui, A., Koops, J., Kruijne, E., Lodewijk, C., Munjishvili, L., Peeck, B., Ree, C., Regtop, R., Ruijs, Y., Rutkens, T., van de Sande, L., Schoorl, M., Timmerman, A., Tuijn, E., Veenenberg, L., van der Vliet, S., Wisse, A., Woudstra, T., and Tuk, B.

Published
2018
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11. Dysregulated endothelial cell markers in systemic lupus erythematosus: a systematic review and meta-analysis.

Author

Bergkamp, S. C., Wahadat, M. J., Salah, A., Kuijpers, T. W., Smith, V., Tas, S. W., van den Berg, J. M., Kamphuis, S., and Schonenberg-Meinema, D.

Subjects
ENDOTHELIAL cells, FIXED effects model, SYSTEMIC lupus erythematosus, PANEL analysis, BIOMARKERS
Abstract

Objectives: To perform a systematic literature review and meta-analysis on endothelial cell (EC) markers that are involved and dysregulated in systemic lupus erythematosus (SLE) in relation to disease activity, as EC dysregulation plays a major role in the development of premature atherosclerosis in SLE. Methods: Search terms were entered into Embase, MEDLINE, Web of Science, Google Scholar and Cochrane. Inclusion criteria were 1) studies published after 2000 reporting measurements of EC markers in serum and/or plasma of SLE patients (diagnosed according to ACR/SLICC criteria), 2) English language peer reviewed articles, and 3) disease activity measurement. For meta-analysis calculations, the Meta-Essentials tool by Erasmus Research Institute and of Management (ERIM) was used. Only those EC markers, which were 1) reported in at least two articles and 2) reported a correlation coefficient (i.e. Spearman's rank or Pearson's) between the measured levels of the EC marker and disease activity were included. For meta-analyses, a fixed effect model was used. Results: From 2133 hits, 123 eligible articles were selected. The identified SLE-related endothelial markers were involved in EC activation, EC apoptosis, disturbed angiogenesis, defective vascular tone control, immune dysregulation and coagulopathy. Meta-analyses of primarily cross-sectional studies showed significant associations between marker levels and disease activity for the following endothelial markers: Pentraxin-3, Thrombomodulin, VEGF, VCAM-1, ICAM-1, IP-10 and MCP-1. Dysregulated EC markers without associations with disease activity were: Angiopoeitin-2, vWF, P-Selectin, TWEAK and E-Selectin. Conclusions: We provide a complete literature overview for dysregulated EC markers in SLE comprising a wide range of different EC functions. SLE-induced EC marker dysregulation was seen with, but also without, association with disease activity. This study provides some clarity in the eminent complex field of EC markers as biomarkers for SLE. Longitudinal data on EC markers in SLE are now needed to guide us more in unravelling the pathophysiology of premature atherosclerosis and cardiovascular events in SLE patients. [ABSTRACT FROM AUTHOR]

Published
2023
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22. The PedPAD study: boys predominate in the hypogammaglobulinaemia registry of the ESID online database

Author

Schatorjé, E. J. H., Gathmann, B., van Hout, R. W. N. M., de Vries, E., Alsina, L, Baumann, U, Belohradsky, B H, Bienemann, K, Boardman, B, Borte, M, Bredius, R G, Brodszki, N, Caracseghi, F, Ciznar, P, de Vries, E, Driessen, G J, Dückers, G, Duppenthaler, A, Farmaki, E, Galal, N, Gennery, A, Gonzalez-Granado, L I, Hlavackova, E, Hoernes, M, Kilic, S S, Krüger, R, Kuijpers, T W, Kütükcüler, N, Llobet, P, Marques, L, van Montfrans, J M, Papadopoulou-Alataki, E, Paschenko, O, Pasic, S, Pietrogrande, M C, Pignata, C, Reda, S M, Reisli, I, Roesler, J, Santos, J L, Schölvinck, E H, Schulze, Ilka, Seidel, M G, Shcherbina, A, Sundin, M, Szaflarska, A, Velbri, S, Warnatz, K, and Warris, A

Published
2014
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48. Dissecting Kawasaki disease: a state-of-the-art review.

Author

Dietz, S., Stijn, D., Burgner, D., Levin, M., Kuipers, I., Hutten, B., Kuijpers, T., Dietz, S M, van Stijn, D, Kuipers, I M, Hutten, B A, and Kuijpers, T W

Subjects
MUCOCUTANEOUS lymph node syndrome, VASCULITIS, LYMPHADENITIS, IMMUNOGLOBULINS, ECHOCARDIOGRAPHY
Abstract

Kawasaki disease (KD) is a pediatric vasculitis with coronary artery aneurysms (CAA) as its main complication. The diagnosis is based on the presence of persistent fever and clinical features including exanthema, lymphadenopathy, conjunctival injection, and changes to the mucosae and extremities. Although the etiology remains unknown, the current consensus is that it is likely caused by an (infectious) trigger initiating an abnormal immune response in genetically predisposed children. Treatment consists of high dose intravenous immunoglobulin (IVIG) and is directed at preventing the development of CAA. Unfortunately, 10-20% of all patients fail to respond to IVIG and these children need additional anti-inflammatory treatment. Coronary artery lesions are diagnosed by echocardiography in the acute and subacute phases. Both absolute arterial diameters and z-scores, adjusted for height and weight, are used as criteria for CAA. Close monitoring of CAA is important as ischemic symptoms or myocardial infarction due to thrombosis or stenosis can occur. These complications are most likely to arise in the largest, so-called giant CAA. Apart from the presence of CAA, it is unclear whether KD causes an increased cardiovascular risk due to the vasculitis itself.Conclusion: Many aspects of KD remain unknown, although there is growing knowledge on the etiology, treatment, and development and classification of CAA. Since children with previous KD are entering adulthood, long-term follow-up is increasingly important. What is known: • Kawasaki disease (KD) is a pediatric vasculitis with coronary artery damage as its main complication. • Although KD approaches its 50th birthday since its first description, many aspects of the disease remain poorly understood. What is new: • In recent years, multiple genetic candidate pathways involved in KD have been identified, with recently promising information about the ITPKC pathway. • As increasing numbers of KD patients are reaching adulthood, increasing information is available about the long-term consequences of coronary artery damage and broader cardiovascular risk. [ABSTRACT FROM AUTHOR]

Published
2017
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49. A comparison of three treatment strategies in recent onset non-systemic Juvenile Idiopathic Arthritis: initial 3-months results of the BeSt for Kids-study.

Author

Hissink Muller, P. C. E., Brinkman, D. M. C., Schonenberg, D., Koopman-Keemink, Y., Brederije, I. C. J., Bekkering, W. P., Kuijpers, T. W., van Rossum, M. A. J., van Suijlekom-Smit, L. W. A., van den Berg, J. M., Allaart, C. F., and Cate, R. ten

Subjects
JUVENILE idiopathic arthritis, PREDNISONE, ETANERCEPT, COMBINATION drug therapy, ANTIRHEUMATIC agents, THERAPEUTICS
Abstract

Background: Combination therapy with prednisone or etanercept may induce earlier and/or more improvement in disease activity in Disease Modifying Anti Rheumatic Drug (DMARD) naïve non-systemic Juvenile Idiopathic Arthritis (JIA) patients. Here we present three months clinical outcome of initial treatments of the BeSt-for-Kids study. Methods: Included patients were randomized to either: 1. initial DMARD-monotherapy (sulfasalazine (SSZ) or methotrexate (MTX)), 2. Initial MTX / prednisolone-bridging, 3. Initial combination MTX/etanercept. Percentage inactive disease, adjusted (a) ACR Pedi30, 50 and 70 and JADAS after 6 and 12 weeks of treatment (intention to treat analysis) and side effects are reported. Results: 94 patients (67% girls, 32 (arm 1), 32 (arm 2) and 30 (arm 3) with median (InterQuartileRange) age of 9.1 (4.7-12.9) years were included. 38% were ANA positive, 10 had oligo-articular disease, 68 polyarticular JIA and 16 psoriatic arthritis. Baseline median (IQR) ACRpedi-scores: VAS physician 49 (40-58) mm, VAS patient 54 (37-70) mm, ESR 6.5 (2-14.8)mm/hr, active joint count 8 (5-12), limited joint count 3 (1-5), CHAQ score 0.88 (0.63-1.5). In arm 1, 17 started with MTX, 15 with SSZ. After 3 months, aACR Pedi 50 was reached by 10/32 (31%), 12/32(38%) and 16/30 (53%) (p = 0.19) and aACR Pedi 70 was reached by 8/32 (25%), 6/32(19%) and 14/30(47%) in arms 1-3 (p = 0.04). Toxicity was similar. Few serious adverse events were reported. Conclusion: After 3 months of treatment in a randomized trial, patients with recent-onset JIA achieved significantly more clinical improvement (aACRPedi70) on initial combination therapy with MTX / etanercept than on initial MTX or SSZ monotherapy. [ABSTRACT FROM AUTHOR]

Published
2017
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50. Characterization of buffy coat-derived granulocytes for clinical use: a comparison with granulocyte colony-stimulating factor/dexamethasone-pretreated donor-derived products.

Author

Geer, A., Gazendam, R. P., Tool, A. T. J., Hamme, J. L., Korte, D., Berg, T. K., Zeerleder, S. S., and Kuijpers, T. W.

Subjects
BUFFY coat, GRANULOCYTES, DEXAMETHASONE, HEMAPHERESIS, GRANULOCYTE colony stimulating factor receptor
Abstract

Background and objectives Buffy coat-derived granulocytes have been described as an alternative to the apheresis product from donors pretreated with dexamethasone and granulocyte colony-stimulating factor (G-CSF). The latter is - dependent on the local and national settings - obtained following a demanding and time-consuming procedure, which is undesirable in critically ill septic patients. In contrast, buffy coat-derived products have a large volume and are often heavily contaminated with red cells and platelets. We developed a new pooled buffy coat-derived product with high purity and small volume, and performed a comprehensive functional characterization of these granulocytes. Materials and methods We pooled ten buffy coats following the production of platelet concentrates. Saline 0·9% was added to decrease the viscosity and the product was split into plasma, red cells and a 'super' buffy coat. Functional data of the granulocytes were compared to those obtained with granulocytes from healthy controls and G-CSF/dexamethasone-pretreated donors. Results Buffy coat-derived granulocytes showed adhesion, chemotaxis, reactive oxygen species production, degranulation, NETosis and in vitro killing of Staphylococcus aureus, Escherichia coli and Aspergillus species comparable to control and G-CSF/dexamethasone-derived granulocytes. Candida killing was superior compared to G-CSF/dexamethasone-derived granulocytes. Immunophenotyping was normal; especially no signs of activation in the buffy coat-derived granulocytes were seen. Viability was reduced. Buffy coats are readily available in the regular blood production process and would take away the concerns around the apheresis product. Conclusion The product described appears a promising alternative for transfusion purposes. [ABSTRACT FROM AUTHOR]

Published
2017
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