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3. LIST OF CONTRIBUTORS

Author

Albini, B., primary, Adler, B., additional, Adler, H., additional, Ameratunga, R., additional, Anderson, A.O., additional, Andrews, A.E., additional, Arstila, T.P., additional, Bailey, M., additional, Barnes, H.J., additional, Bazin, H., additional, Bertoni, G., additional, Blacklaws, B., additional, Bos, N.A., additional, Brait, M., additional, Butler, J.E., additional, Cahill, R.N.P., additional, Carter, S.D., additional, Cesbron, J.-Y., additional, Charlemagne, J., additional, Charley, B., additional, Cunningham, C., additional, Cukrowska, B., additional, Daha, M.R., additional, Dammers, P.M., additional, Deenen, G.J., additional, Defresne, M.P., additional, Delhem, N., additional, Demaries, S.L., additional, Desmecht, D., additional, Dijkstra, C.D., additional, Ellis, A.E., additional, Fatzer, R., additional, Felsburg, P.J., additional, Fletcher, O.J., additional, Fluri, A., additional, Foss, D.L., additional, Gianello, P., additional, Giger, U., additional, Goddeeris, B., additional, Govaerts, A., additional, Grant, C.K., additional, Greiner, D.L., additional, Griebel, P.J., additional, Grimholt, U., additional, Groen, H., additional, Hague, B., additional, Haig, D., additional, Hala, K., additional, Hamers, R., additional, Hanken, R.J., additional, Hannant, D., additional, Harbour, D.A., additional, Harlan, J., additional, Hawken, R.J., additional, Hein, W.R., additional, Heinen, E., additional, Helfand, S.C., additional, Hermann, T., additional, Høgåsen, K., additional, Hogenesch, H., additional, Hordvik, I., additional, Horohov, D.W., additional, Howard, C., additional, Hünig, T., additional, Husband, A., additional, Hüttner, S.W., additional, Hylkema, M.N., additional, Ingram, G.A., additional, Ishiguro, N., additional, Jakowlew, S.B., additional, Jeurissen, S.H.M., additional, Joosten, E., additional, Jørgensen, T., additional, Jungi, T.W., additional, Kaplan, M.H., additional, Kaufman, J., additional, Kimpton, W.G., additional, Knight, K.L., additional, Koch, C., additional, Komatsu, M., additional, Koppenheffer, T.L., additional, Krakowka, G.S., additional, Kroese, F.G.M., additional, Landsverk, T., additional, Lanning, D., additional, Latinne, D., additional, Leblond, V., additional, Leutenegger, C., additional, Levy, J.K., additional, Lewin, H., additional, Lie, Ø., additional, Lillehoj, H.S., additional, Llanes, D., additional, Lumsden, J.S., additional, Lunn, D.P., additional, Lunney, J., additional, Lutz, H., additional, MacHugh, N., additional, Maddox, J.F., additional, Mage, R.G., additional, Martin, H.M., additional, McClure, S., additional, McConnell, T.J., additional, McCormack, W.T., additional, McCullagh, P.P., additional, McKeever, D., additional, Mertens, B., additional, Miller, N.W., additional, Modiano, J.F., additional, Morgan, B.P., additional, Morizot, D.C., additional, Moutschen, M.P., additional, Murtaugh, M.P., additional, Muyldermans, S., additional, Naessens, J., additional, Nash, A.D., additional, Nguyen, T.C., additional, Nieuwenhuis, P., additional, Obexer-Ruff, G., additional, Pabst, R., additional, Pastoret, P.P., additional, Pedersen, N.C., additional, Pertile, T.L., additional, Pescovitz, M.D., additional, Peterhans, E., additional, Pilstöm, L., additional, Plachy, J., additional, Press, C. McL., additional, Pu, R., additional, Ramamoorthy, C., additional, Ratcliffe, M.J.H., additional, Rautenschlein, S., additional, Reinacher, M., additional, Ritchey, J.W., additional, Robertsen, B., additional, Rodkey, L.S., additional, Rombout, J.H.W.M., additional, Roth, J., additional, Rothkötter, H.J., additional, Rozing, J., additional, Schat, K.A., additional, Seto, A., additional, Sharar, S., additional, Sharma, J.M., additional, Sinkora, J., additional, Sittisombut, N., additional, Soares, M., additional, Sopp, P., additional, Stokes, C.R., additional, Suter, M., additional, Tabel, H., additional, Tatner, M.F., additional, Tissot, R.G., additional, Tlaskalová-Hogenová, H., additional, Toivanen, P., additional, Tompkins, M.B., additional, Tompkins, W.A.F., additional, Torres-Nagel, N.E., additional, Tournefier, A., additional, Trebichavsky, I., additional, Tucker, E., additional, Urbain, J., additional, Vainio, O., additional, van den Berg, R.H., additional, van den Berg, T.K., additional, van den Broeke, A., additional, van der Meide, P., additional, Vandevelde, M., additional, van Rees, E.P., additional, Vögeli, P., additional, Wagner, J.L., additional, Wakenell, P.S., additional, Watson, D., additional, Weinstein, P.D., additional, Werner, E.R., additional, Westermann, J., additional, Whalen, B.J., additional, Willett, B.J., additional, Winkelstein, J.A., additional, Winn, R., additional, Yamamoto, J.K., additional, Young, A.J., additional, and Zurbriggen, A., additional

Published
1998
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8. Of flies, mice and men: a systematic approach to understanding the early life origins of chronic lung disease

Author

Krauss-Etschmann, S., Bush, A., Bellusci, S., Brusselle, G.G., Dahlén, S.E., Dehmel, S., Eickelberg, O., Gibson, G., Hylkema, M.N., Knaus, P., Königshoff, M., Lloyd, C.M., Macciarini, P., Mailleux, A., Marsland, B.J., Postma, D.S., Roberts, G., Samakovlis, C., Stocks, J., Vandesompele, J., Wjst, M., and Holloway, J.

Subjects
respiratory tract diseases
Abstract

Despite intensive research efforts, the aetiology of the majority of chronic lung diseases (CLD) in both, children and adults, remains elusive. Current therapeutic options are limited, providing only symptomatic relief, rather than treating the underlying condition, or preventing its development in the first place. Thus, there is a strong and unmet clinical need for the development of both, novel effective therapies and preventative strategies for CLD. Many studies suggest that modifications of prenatal and/or early postnatal lung development will have important implications for future lung function and risk of CLD throughout life. This view represents a fundamental change of current pathophysiological concepts and treatment paradigms, and holds the potential to develop novel preventative and/or therapeutic strategies. However, for the successful development of such approaches, key questions, such as a clear understanding of underlying mechanisms of impaired lung development, the identification and validation of relevant preclinical models to facilitate translational research, and the development of concepts for correction of aberrant development, all need to be solved. Accordingly, a European Science Foundation Exploratory Workshop was held where clinical, translational and basic research scientists from different disciplines met to discuss potential mechanisms of developmental origins of CLD, and to identify major knowledge gaps in order to delineate a roadmap for future integrative research.

Published
2013

10. Maternal smoking during pregnancy decreases Wnt signalling in neonatal mice

Author

Blacquiere, M.J., Timens, W., van den Berg, A., Geerlings, M., Postma, D.S., and Hylkema, M.N.

Subjects
Smoking in pregnancy -- Research, Wnt proteins -- Physiological aspects, Wnt proteins -- Genetic aspects, Wnt proteins -- Research, Asthma -- Risk factors, Asthma -- Development and progression, Asthma -- Research, Health
Published
2010

15. Specificity on monoclonal anti-nucleosome auto-antibodies derived from lupus mice

Author

Kramers, C., Stemmer, C., Monestier, M., Bruggen, M.C.J. van, Rijke-Schilder, G.P.M., Hylkema, M.N., Smeenk, R.J.T., Muller, S.H., Berden, J.H.M., Kramers, C., Stemmer, C., Monestier, M., Bruggen, M.C.J. van, Rijke-Schilder, G.P.M., Hylkema, M.N., Smeenk, R.J.T., Muller, S.H., and Berden, J.H.M.

Abstract

Item does not contain fulltext

Published
1996

17. In vivo ANA is a fixation artifact : nucleosome-complexed antinucleosome autoantibodies bind to the cell surface and are internalized

Author

Kramers, K., Bruggen, M.C.J. van, Rijke-Schilder, G.P.M., Dijkman, H.B.P.M., Hylkema, M.N., Croes, H.J.E., Fransen, J.A.M., Assmann, K.J.M., Tax, W.J.M., Smeenk, R.J.T., Berden, J.H.M., Kramers, K., Bruggen, M.C.J. van, Rijke-Schilder, G.P.M., Dijkman, H.B.P.M., Hylkema, M.N., Croes, H.J.E., Fransen, J.A.M., Assmann, K.J.M., Tax, W.J.M., Smeenk, R.J.T., and Berden, J.H.M.

Abstract

Contains fulltext : 24092___.PDF (publisher's version ) (Open Access)

Published
1996

24. Airway eosinophilia in remission and progression of asthma: Accumulation with a fast decline of FEV1.

Author

Broekema, M., Volbeda, F., Timens, W., Dijkstra, A., Lee, N.A., Lee, J.J., Lodewijk, M.E., Postma, D.S., Hylkema, M.N., and ten Hacken, N.H.T.

Abstract

Summary: Background: As it is unknown whether complete asthma remission or progression of asthma is associated with airway inflammation and remodeling, we assessed these characteristics in bronchial biopsies of relevant subsets of asthma patients. Methods: Sputum and bronchial biopsies were obtained from asthma patients in remission (PC20 histamine>32mg/ml, PC20 AMP>320mg/ml) and from those with either a slow FEV1 decline (<30ml/year) or fast decline (>30ml/year). Inflammatory cells and mediators were determined in sputum, inflammatory cells and aspects of airway remodeling in bronchial biopsies. Results: Asthmatics in remission and asthma patients with a slow FEV1 decline had a similar extent of airway inflammation and remodeling in sputum and bronchial biopsies. Asthma patients with a fast FEV1 decline had high sputum eosinophil numbers. Moreover, FEV1 decline (ml/year) correlated with sputum eosinophil numbers (Rs=0.51, p=0.003) and ECP levels (Rs=0.57, p=0.001). Airway remodeling, i.e. basement membrane thickness, correlated with sputum eosinophils (Rs=0.69, p<0.001), sputum ECP (Rs=0.46, p=0.018) and airway wall eosinophil numbers (Rs=0.49, p=0.002). Conclusions: Asthma, even when in remission, is accompanied by airway inflammation and remodeling. Data suggest that eosinophils are important in a subset of asthma patients by association to accelerated FEV1 decline and change of basement membrane thickness. [ABSTRACT FROM AUTHOR]

Published
2010
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27. Novel treatment options for bronchopulmonary dysplasia

Author

Chen, X., Chen X., Walther, F.J., Wagenaar, G.T.M., Hiemstra, P.S., Kramer, B.W., Hylkema, M.N., Leiden University, and Chen X.

Subjects
Inflammation, Second hit, respiratory system, Bronchopulmonary dysplasia, Fibrosis, Right ventricular hypertrophy, respiratory tract diseases, Pulmonary hypertension
Abstract

Bronchopulmonary dysplasia is the most common complication when premature birth occurs at less than 28 weeks gestational age. The general aim of this thesis is to explore the therapeutic potential of interventions in signaling pathways, involved in lung development and oxidative stress-induced lung injury, to prevent or attenuate BPD in a neonatal rat model, in which experimental BPD is induced by exposure to hyperoxia. The therapeutic potential of the targeting compounds of signaling pathways was investigated by studying their beneficial effects on contributing factors to severe experimental BPD pathology, including aberrant alveolar and vascular development, inflammation, fibrosis, coagulation, vascular remodeling, pulmonary arterial hypertension and right ventricular hypertrophy. We found ⑴angiotensin II type 2 receptor ligand PD123319 attenuates hyperoxia-induced lung and heart injury at a low dose in newborn rats; ⑵ Metformin attenuates hyperoxia-induced lung injury in neonatal rats by reducing the inflammatory response; ⑶ Deficiency or inhibition of lysophosphatidic acid receptor 1 protects against hyperoxia-induced lung injury in neonatal rats; ⑷Adult lysophosphatidic acid receptor 1-deficient rats with hyperoxia-induced neonatal chronic lung disease are protected against lipopolysaccharide-induced acute lung injury; ⑸ Bone morphogenetic protein 9 protects against neonatal hyperoxia-induced impairment of alveolarization and pulmonary inflammation.

Published
2017

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