Search Results - (Author, Cooperation:D. S. Postma)
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1A. E. Locke ; B. Kahali ; S. I. Berndt ; A. E. Justice ; T. H. Pers ; F. R. Day ; C. Powell ; S. Vedantam ; M. L. Buchkovich ; J. Yang ; D. C. Croteau-Chonka ; T. Esko ; T. Fall ; T. Ferreira ; S. Gustafsson ; Z. Kutalik ; J. Luan ; R. Magi ; J. C. Randall ; T. W. Winkler ; A. R. Wood ; T. Workalemahu ; J. D. Faul ; J. A. Smith ; J. Hua Zhao ; W. Zhao ; J. Chen ; R. Fehrmann ; A. K. Hedman ; J. Karjalainen ; E. M. Schmidt ; D. Absher ; N. Amin ; D. Anderson ; M. Beekman ; J. L. Bolton ; J. L. Bragg-Gresham ; S. Buyske ; A. Demirkan ; G. Deng ; G. B. Ehret ; B. Feenstra ; M. F. Feitosa ; K. Fischer ; A. Goel ; J. Gong ; A. U. Jackson ; S. Kanoni ; M. E. Kleber ; K. Kristiansson ; U. Lim ; V. Lotay ; M. Mangino ; I. Mateo Leach ; C. Medina-Gomez ; S. E. Medland ; M. A. Nalls ; C. D. Palmer ; D. Pasko ; S. Pechlivanis ; M. J. Peters ; I. Prokopenko ; D. Shungin ; A. Stancakova ; R. J. Strawbridge ; Y. Ju Sung ; T. Tanaka ; A. Teumer ; S. Trompet ; S. W. van der Laan ; J. van Setten ; J. V. Van Vliet-Ostaptchouk ; Z. Wang ; L. Yengo ; W. Zhang ; A. Isaacs ; E. Albrecht ; J. Arnlov ; G. M. Arscott ; A. P. Attwood ; S. Bandinelli ; A. Barrett ; I. N. Bas ; C. Bellis ; A. J. Bennett ; C. Berne ; R. Blagieva ; M. Bluher ; S. Bohringer ; L. L. Bonnycastle ; Y. Bottcher ; H. A. Boyd ; M. Bruinenberg ; I. H. Caspersen ; Y. D. Ida Chen ; R. Clarke ; E. W. Daw ; A. J. de Craen ; G. Delgado ; M. Dimitriou ; A. S. Doney ; N. Eklund ; K. Estrada ; E. Eury ; L. Folkersen ; R. M. Fraser ; M. E. Garcia ; F. Geller ; V. Giedraitis ; B. Gigante ; A. S. Go ; A. Golay ; A. H. Goodall ; S. D. Gordon ; M. Gorski ; H. J. Grabe ; H. Grallert ; T. B. Grammer ; J. Grassler ; H. Gronberg ; C. J. Groves ; G. Gusto ; J. Haessler ; P. Hall ; T. Haller ; G. Hallmans ; C. A. Hartman ; M. Hassinen ; C. Hayward ; N. L. Heard-Costa ; Q. Helmer ; C. Hengstenberg ; O. Holmen ; J. J. Hottenga ; A. L. James ; J. M. Jeff ; A. Johansson ; J. Jolley ; T. Juliusdottir ; L. Kinnunen ; W. Koenig ; M. Koskenvuo ; W. Kratzer ; J. Laitinen ; C. Lamina ; K. Leander ; N. R. Lee ; P. Lichtner ; L. Lind ; J. Lindstrom ; K. Sin Lo ; S. Lobbens ; R. Lorbeer ; Y. Lu ; F. Mach ; P. K. Magnusson ; A. Mahajan ; W. L. McArdle ; S. McLachlan ; C. Menni ; S. Merger ; E. Mihailov ; L. Milani ; A. Moayyeri ; K. L. Monda ; M. A. Morken ; A. Mulas ; G. Muller ; M. Muller-Nurasyid ; A. W. Musk ; R. Nagaraja ; M. M. Nothen ; I. M. Nolte ; S. Pilz ; N. W. Rayner ; F. Renstrom ; R. Rettig ; J. S. Ried ; S. Ripke ; N. R. Robertson ; L. M. Rose ; S. Sanna ; H. Scharnagl ; S. Scholtens ; F. R. Schumacher ; W. R. Scott ; T. Seufferlein ; J. Shi ; A. Vernon Smith ; J. Smolonska ; A. V. Stanton ; V. Steinthorsdottir ; K. Stirrups ; H. M. Stringham ; J. Sundstrom ; M. A. Swertz ; A. J. Swift ; A. C. Syvanen ; S. T. Tan ; B. O. Tayo ; B. Thorand ; G. Thorleifsson ; J. P. Tyrer ; H. W. Uh ; L. Vandenput ; F. C. Verhulst ; S. H. Vermeulen ; N. Verweij ; J. M. Vonk ; L. L. Waite ; H. R. Warren ; D. Waterworth ; M. N. Weedon ; L. R. Wilkens ; C. Willenborg ; T. Wilsgaard ; M. K. Wojczynski ; A. Wong ; A. F. Wright ; Q. Zhang ; E. P. Brennan ; M. Choi ; Z. Dastani ; A. W. Drong ; P. Eriksson ; A. Franco-Cereceda ; J. R. Gadin ; A. G. Gharavi ; M. E. Goddard ; R. E. Handsaker ; J. Huang ; F. Karpe ; S. Kathiresan ; S. Keildson ; K. Kiryluk ; M. Kubo ; J. Y. Lee ; L. Liang ; R. P. Lifton ; B. Ma ; S. A. McCarroll ; A. J. McKnight ; J. L. Min ; M. F. Moffatt ; G. W. Montgomery ; J. M. Murabito ; G. Nicholson ; D. R. Nyholt ; Y. Okada ; J. R. Perry ; R. Dorajoo ; E. Reinmaa ; R. M. Salem ; N. Sandholm ; R. A. Scott ; L. Stolk ; A. Takahashi ; F. M. Van't Hooft ; A. A. Vinkhuyzen ; H. J. Westra ; W. Zheng ; K. T. Zondervan ; A. C. Heath ; D. Arveiler ; S. J. Bakker ; J. Beilby ; R. N. Bergman ; J. Blangero ; P. Bovet ; H. Campbell ; M. J. Caulfield ; G. Cesana ; A. Chakravarti ; D. I. Chasman ; P. S. Chines ; F. S. Collins ; D. C. Crawford ; L. A. Cupples ; D. Cusi ; J. Danesh ; U. de Faire ; H. M. den Ruijter ; A. F. Dominiczak ; R. Erbel ; J. Erdmann ; J. G. Eriksson ; M. Farrall ; S. B. Felix ; E. Ferrannini ; J. Ferrieres ; I. Ford ; N. G. Forouhi ; T. Forrester ; O. H. Franco ; R. T. Gansevoort ; P. V. Gejman ; C. Gieger ; O. Gottesman ; V. Gudnason ; U. Gyllensten ; A. S. Hall ; T. B. Harris ; A. T. Hattersley ; A. A. Hicks ; L. A. Hindorff ; A. D. Hingorani ; A. Hofman ; G. Homuth ; G. K. Hovingh ; S. E. Humphries ; S. C. Hunt ; E. Hypponen ; T. Illig ; K. B. Jacobs ; M. R. Jarvelin ; K. H. Jockel ; B. Johansen ; P. Jousilahti ; J. W. Jukema ; A. M. Jula ; J. Kaprio ; J. J. Kastelein ; S. M. Keinanen-Kiukaanniemi ; L. A. Kiemeney ; P. Knekt ; J. S. Kooner ; C. Kooperberg ; P. Kovacs ; A. T. Kraja ; M. Kumari ; J. Kuusisto ; T. A. Lakka ; C. Langenberg ; L. Le Marchand ; T. Lehtimaki ; V. Lyssenko ; S. Mannisto ; A. Marette ; T. C. Matise ; C. A. McKenzie ; B. McKnight ; F. L. Moll ; A. D. Morris ; A. P. Morris ; J. C. Murray ; M. Nelis ; C. Ohlsson ; A. J. Oldehinkel ; K. K. Ong ; P. A. Madden ; G. Pasterkamp ; J. F. Peden ; A. Peters ; D. S. Postma ; P. P. Pramstaller ; J. F. Price ; L. Qi ; O. T. Raitakari ; T. Rankinen ; D. C. Rao ; T. K. Rice ; P. M. Ridker ; J. D. Rioux ; M. D. Ritchie ; I. Rudan ; V. Salomaa ; N. J. Samani ; J. Saramies ; M. A. Sarzynski ; H. Schunkert ; P. E. Schwarz ; P. Sever ; A. R. Shuldiner ; J. Sinisalo ; R. P. Stolk ; K. Strauch ; A. Tonjes ; D. A. Tregouet ; A. Tremblay ; E. Tremoli ; J. Virtamo ; M. C. Vohl ; U. Volker ; G. Waeber ; G. Willemsen ; J. C. Witteman ; M. C. Zillikens ; L. S. Adair ; P. Amouyel ; F. W. Asselbergs ; T. L. Assimes ; M. Bochud ; B. O. Boehm ; E. Boerwinkle ; S. R. Bornstein ; E. P. Bottinger ; C. Bouchard ; S. Cauchi ; J. C. Chambers ; S. J. Chanock ; R. S. Cooper ; P. I. de Bakker ; G. Dedoussis ; L. Ferrucci ; P. W. Franks ; P. Froguel ; L. C. Groop ; C. A. Haiman ; A. Hamsten ; J. Hui ; D. J. Hunter ; K. Hveem ; R. C. Kaplan ; M. Kivimaki ; D. Kuh ; M. Laakso ; Y. Liu ; N. G. Martin ; W. Marz ; M. Melbye ; A. Metspalu ; S. Moebus ; P. B. Munroe ; I. Njolstad ; B. A. Oostra ; C. N. Palmer ; N. L. Pedersen ; M. Perola ; L. Perusse ; U. Peters ; C. Power ; T. Quertermous ; R. Rauramaa ; F. Rivadeneira ; T. E. Saaristo ; D. Saleheen ; N. Sattar ; E. E. Schadt ; D. Schlessinger ; P. E. Slagboom ; H. Snieder ; T. D. Spector ; U. Thorsteinsdottir ; M. Stumvoll ; J. Tuomilehto ; A. G. Uitterlinden ; M. Uusitupa ; P. van der Harst ; M. Walker ; H. Wallaschofski ; N. J. Wareham ; H. Watkins ; D. R. Weir ; H. E. Wichmann ; J. F. Wilson ; P. Zanen ; I. B. Borecki ; P. Deloukas ; C. S. Fox ; I. M. Heid ; J. R. O'Connell ; D. P. Strachan ; K. Stefansson ; C. M. van Duijn ; G. R. Abecasis ; L. Franke ; T. M. Frayling ; M. I. McCarthy ; P. M. Visscher ; A. Scherag ; C. J. Willer ; M. Boehnke ; K. L. Mohlke ; C. M. Lindgren ; J. S. Beckmann ; I. Barroso ; K. E. North ; E. Ingelsson ; J. N. Hirschhorn ; R. J. Loos ; E. K. Speliotes
Nature Publishing Group (NPG)
Published 2015Staff ViewPublication Date: 2015-02-13Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Adipogenesis/genetics ; Adiposity/genetics ; Age Factors ; *Body Mass Index ; Continental Population Groups/genetics ; Energy Metabolism/genetics ; Europe/ethnology ; Female ; Genetic Predisposition to Disease/genetics ; *Genome-Wide Association Study ; Glutamic Acid/metabolism ; Humans ; Insulin/metabolism/secretion ; Male ; Obesity/*genetics/*metabolism ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Synapses/metabolismPublished by: -
2J. R. Perry ; F. Day ; C. E. Elks ; P. Sulem ; D. J. Thompson ; T. Ferreira ; C. He ; D. I. Chasman ; T. Esko ; G. Thorleifsson ; E. Albrecht ; W. Q. Ang ; T. Corre ; D. L. Cousminer ; B. Feenstra ; N. Franceschini ; A. Ganna ; A. D. Johnson ; S. Kjellqvist ; K. L. Lunetta ; G. McMahon ; I. M. Nolte ; L. Paternoster ; E. Porcu ; A. V. Smith ; L. Stolk ; A. Teumer ; N. Tsernikova ; E. Tikkanen ; S. Ulivi ; E. K. Wagner ; N. Amin ; L. J. Bierut ; E. M. Byrne ; J. J. Hottenga ; D. L. Koller ; M. Mangino ; T. H. Pers ; L. M. Yerges-Armstrong ; J. Hua Zhao ; I. L. Andrulis ; H. Anton-Culver ; F. Atsma ; S. Bandinelli ; M. W. Beckmann ; J. Benitez ; C. Blomqvist ; S. E. Bojesen ; M. K. Bolla ; B. Bonanni ; H. Brauch ; H. Brenner ; J. E. Buring ; J. Chang-Claude ; S. Chanock ; J. Chen ; G. Chenevix-Trench ; J. M. Collee ; F. J. Couch ; D. Couper ; A. D. Coviello ; A. Cox ; K. Czene ; P. D'Adamo A ; G. Davey Smith ; I. De Vivo ; E. W. Demerath ; J. Dennis ; P. Devilee ; A. K. Dieffenbach ; A. M. Dunning ; G. Eiriksdottir ; J. G. Eriksson ; P. A. Fasching ; L. Ferrucci ; D. Flesch-Janys ; H. Flyger ; T. Foroud ; L. Franke ; M. E. Garcia ; M. Garcia-Closas ; F. Geller ; E. E. de Geus ; G. G. Giles ; D. F. Gudbjartsson ; V. Gudnason ; P. Guenel ; S. Guo ; P. Hall ; U. Hamann ; R. Haring ; C. A. Hartman ; A. C. Heath ; A. Hofman ; M. J. Hooning ; J. L. Hopper ; F. B. Hu ; D. J. Hunter ; D. Karasik ; D. P. Kiel ; J. A. Knight ; V. M. Kosma ; Z. Kutalik ; S. Lai ; D. Lambrechts ; A. Lindblom ; R. Magi ; P. K. Magnusson ; A. Mannermaa ; N. G. Martin ; G. Masson ; P. F. McArdle ; W. L. McArdle ; M. Melbye ; K. Michailidou ; E. Mihailov ; L. Milani ; R. L. Milne ; H. Nevanlinna ; P. Neven ; E. A. Nohr ; A. J. Oldehinkel ; B. A. Oostra ; A. Palotie ; M. Peacock ; N. L. Pedersen ; P. Peterlongo ; J. Peto ; P. D. Pharoah ; D. S. Postma ; A. Pouta ; K. Pylkas ; P. Radice ; S. Ring ; F. Rivadeneira ; A. Robino ; L. M. Rose ; A. Rudolph ; V. Salomaa ; S. Sanna ; D. Schlessinger ; M. K. Schmidt ; M. C. Southey ; U. Sovio ; M. J. Stampfer ; D. Stockl ; A. M. Storniolo ; N. J. Timpson ; J. Tyrer ; J. A. Visser ; P. Vollenweider ; H. Volzke ; G. Waeber ; M. Waldenberger ; H. Wallaschofski ; Q. Wang ; G. Willemsen ; R. Winqvist ; B. H. Wolffenbuttel ; M. J. Wright ; D. I. Boomsma ; M. J. Econs ; K. T. Khaw ; R. J. Loos ; M. I. McCarthy ; G. W. Montgomery ; J. P. Rice ; E. A. Streeten ; U. Thorsteinsdottir ; C. M. van Duijn ; B. Z. Alizadeh ; S. Bergmann ; E. Boerwinkle ; H. A. Boyd ; L. Crisponi ; P. Gasparini ; C. Gieger ; T. B. Harris ; E. Ingelsson ; M. R. Jarvelin ; P. Kraft ; D. Lawlor ; A. Metspalu ; C. E. Pennell ; P. M. Ridker ; H. Snieder ; T. I. Sorensen ; T. D. Spector ; D. P. Strachan ; A. G. Uitterlinden ; N. J. Wareham ; E. Widen ; M. Zygmunt ; A. Murray ; D. F. Easton ; K. Stefansson ; J. M. Murabito ; K. K. Ong
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-09-19Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Adolescent ; Age Factors ; *Alleles ; Body Mass Index ; Breast Neoplasms/genetics ; Cardiovascular Diseases/genetics ; Child ; Diabetes Mellitus, Type 2/genetics ; Europe/ethnology ; Female ; Genetic Loci/*genetics ; Genome-Wide Association Study ; Genomic Imprinting/genetics ; Humans ; Hypothalamo-Hypophyseal System/physiology ; Intercellular Signaling Peptides and Proteins/genetics ; Male ; Membrane Proteins/genetics ; Menarche/*genetics ; Obesity/genetics ; Ovary/physiology ; *Parents ; Polymorphism, Single Nucleotide/genetics ; Potassium Channels, Tandem Pore Domain/genetics ; Proteins/genetics ; Quantitative Trait Loci/genetics ; Receptors, GABA-B/metabolism ; Receptors, Retinoic Acid/metabolism ; Ribonucleoproteins/geneticsPublished by: -
3van der Plaat, D. A., de Jong, K., de Vries, M., van Diemen, C. C., Nedeljkovic, I., Amin, N., Kromhout, H., Biobank-based Integrative Omics Study Consortium, Vermeulen, R., Postma, D. S., van Duijn, C. M., Boezen, H. M., Vonk, J. M.
BMJ Publishing Group
Published 2018Staff ViewPublication Date: 2018-05-18Publisher: BMJ Publishing GroupPrint ISSN: 1351-0711Electronic ISSN: 1470-7926Topics: MedicineKeywords: Open accessPublished by: -
4Meijer, G. G. ; Postma, D. S. ; Van Der Heide, S. ; Koéuter, G. H. ; Van Aalderen, W. M. C.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1398-9995Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
5Kerkhof, M. ; Postma, D. S. ; Schouten, J. P. ; De Monchy, J. G. R.
Oxford, UK : Munksgaard International Publishers
Published 2003Staff ViewISSN: 1398-9995Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background: Most previous epidemiological studies on the relationship between allergy and bronchial hyperresponsiveness (BHR) have made no distinction between sensitization to indoor and outdoor allergens. We studied the relationship between specific sensitization to allergen and BHR and further assessed whether this was different in young adults and older subjects.Methods: Specific IgE to indoor allergens (house dust mite and cat) and outdoor allergens (timothy grass and birch) were measured using the CAP System. BHR was defined as PD20 ≤ 2 mg methacholine. Multiple logistic regression analysis was performed to study independent relationships between BHR and specific IgE to indoor and outdoor allergens in 1018 young adults (20–44 years) and 909 older subjects (45–70 years).Results: In the older age group specific IgE to indoor allergens was associated with BHR at a lower level (class 2) than in young adults (class ≥ 3). Young adults with multiple sensitization had the highest risk of BHR. Subjects who were exclusively sensitized to pollen did not show increased BHR in both age groups. Total IgE had, independently of sensitization, only a significant dose–response relationship with BHR in the oldest age group.Conclusions: The association between sensitization and BHR is dependent on the nature of the allergen and the level of specific IgE. Furthermore, this study shows for the first time that total IgE is associated with BHR at older ages, independently of sensitization.Type of Medium: Electronic ResourceURL: -
6Meijer, G. G. ; Heide, S. ; Postma, D. S. ; Reus, D. M. ; Koeter, G. H. ; Aalderen, W. M. C.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1399-3038Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Aim - To determine whether house dust mite (HDM) exposure in living rooms and bedrooms is higher in asthmatic children than in those of age and sex matched healthy children, living in the same area. Methods - Types of floor-coverings were recorded and dust samples were collected by vacuum cleaning the total area of living rooms and bedrooms; Der p I and Der p II per gram fine dust concentrations were assessed. Twenty-five asthmatic children (RAST HDM 〉= class 3, age 6–12 years) and 25 healthy children participated in the study. Results - The frequency of cleaning and prevalence of smooth floor-coverings in bedrooms of asthmatic children were significantly higher. There were no differences in living rooms in this respect. The amount of fine dust/m2 floor space was significantly lower in bedrooms of asthmatic children. Concentrations of HDM were low and no differences in Der p I and Der p II concentrations were observed between the two groups (asthmatic children: Der p I living room: 1.1 (0.04 - 59.4 μg/ g), bedroom: 0.5 (below detection - 19.3 μg/g); nonasthmatic children: Der p I living room: 1.4 (below detection - 27.5 μg/g), bedroom: 0.9 (below detection - 68.8 ug/g. Smooth floor coverings contained significantly less fine dust, Der p I, and Der p II than carpeted floors. Conclusions - Low HDM concentrations are a general finding in Dutch dwellings in the present generation of children.We observed a higher cleaning frequency, and more smooth floor coverings in bedrooms of asthmatic children than of healthy children, yet HDM concentrations were not significantly different. The latter can be explained by the observation that only 40% of the asthmatic children had smooth floor coverings in their bedrooms. Smooth floor coverings contain less fine dust and lower concentrations of Der p I and Der p II than carpeted floors.Type of Medium: Electronic ResourceURL: -
7Staff View
ISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
8Staff View
ISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
9PANHUYSEN, C. I. M. ; BLEECKER, E. R. ; KOÉTER, G. H. ; MEYERS, D. A. ; POSTMA, D. S.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
10Melgert, B. N. ; Postma, D. S. ; Kuipers, I. ; Geerlings, M. ; Luinge, M. A. ; Strate, B. W. A. ; Kerstjens, H. A. M. ; Timens, W. ; Hylkema, M. N.
Oxford, UK : Blackwell Science Ltd
Published 2005Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background In humans the prevalence of asthma is higher among females than among males after puberty. The reason for this phenomenon is not clear.Objective We tested the hypothesis that female mice are more susceptible to the development of allergic asthma than male mice and studied allergic immune responses in the lung.Methods We compared allergic airway inflammation, i.e. methacholine (MCh) responsiveness, serum IgE, and cytokines, and the number of the different leucocytes in lungs of male and female BALB/c mice, twice-sensitized to ovalbumin (OVA) and subsequently challenged with OVA (OVA-mice) or phosphate-buffered saline (PBS-mice) aerosols on days 24–26, 30, and 31.Results OVA challenge significantly increased MCh responsiveness, numbers of eosinophils, CD4+ T cells, CD4+/CD25+ T cells, B cells, and levels of Thelper (Th)2 cytokines, total, and OVA-specific IgE. There was, however, also an effect of gender, with female mice responding to OVA challenges with higher numbers of eosinophils, CD4+ T cells, B cells, and levels of IL-4, IL-13, IFN-γ, total, and OVA-specific IgE than male mice. In contrast, female PBS-mice had significantly lower percentages of regulatory CD4+/CD25+ T cells than males (females 4.2±0.2% vs. males 5.3±0.1% of CD4+ T cells, P〈0.05).Conclusion Female mice develop a more pronounced type of allergic airway inflammation than male mice after OVA challenge. The reduced percentage of regulatory T cells in the lungs of female PBS-mice may indicate that the level of these cells in the lung during the sensitization phase is important for the development and/or progression of an allergic immune response after multiple OVA challenges.Type of Medium: Electronic ResourceURL: -
11Heijink, I. H. ; Van Den Berge, M. ; Vellenga, E. ; De Monchy, J. G. R. ; Postma, D. S. ; Kauffman, H. F.
Oxford, UK : Blackwell Science Ltd
Published 2004Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background Airway inflammation in asthma is orchestrated by recruitment of T helper (Th)2 lymphocytes to the lung and subsequent production of Th2-like cytokines upon allergen challenge.Objective To examine whether allergen-induced dysfunction of the β2-adrenergic receptor (β2-AR) contributes to the enhanced T(h2) cell activity in asthma.Methods β2-adrenergic regulation of cytokine mRNA expression was studied in α-CD3/α-CD28-activated peripheral blood lymphocytes from seven asthma patients before and 6 h after allergen challenge, in conjunction with the effects of β2-agonist fenoterol on T cell chemotaxis and signalling pathways.Results A complete loss of β2-AR control over expression of the Th2 cytokines IL-4, IL-5 and IL-13, but not of the Th1 cytokine IFN-γ, was observed after allergen challenge. Furthermore, we found impaired β2-AR regulation of T cell migration as well as signal transduction pathways, i.e. the phosphorylation of cyclic adenosine monophosphate-responsive element binding protein and the inhibition of the mitogen-activated protein kinase pathway. The loss of β2-AR control was associated with increased β-adrenergic receptor kinase expression, which might be involved in β2-AR desensitization. In addition, we demonstrate for the first time that T cells exposed to the chemokine thymus and activation-regulated chemokine show hyporesponsiveness to fenoterol.Conclusion Our results suggest that allergen-induced loss of β2-AR control, possibly mediated by chemokine release, plays an important role in enhanced Th2-like activity in asthma.Type of Medium: Electronic ResourceURL: -
12De Meer, G. ; Postma, D. S. ; Janssen, N. A. H. ; De Jongste, J. C. ; Brunekreef, B.
Oxford, UK : Blackwell Science Ltd
Published 2004Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background In adult asthma, bronchial hyper-responsiveness (BHR) to indirect stimuli reflects eosinophilic activation more closely than BHR to stimuli that directly cause smooth muscle contraction.Aim To assess the relationship between BHR to the indirect stimulus hypertonic saline (HS), blood eosinophil numbers, and serum eosinophilic cationic protein (ECP) in children with and without current wheeze.Methods A cross-sectional survey among 8–13-year-old schoolchildren, using the International Study of Asthma and Allergic disease in Childhood questionnaire, bronchial challenge with HS, skin prick tests, serum IgE, blood eosinophil counts and ECP (in a subset). Based upon the presence of current wheeze (WHE) and BHR, we defined three case groups (WHE+BHR+, WHE−BHR+, WHE+BHR−) and the reference group (WHE−BHR−). By regression analyses, each case group was compared with the reference group for differences in atopic sensitization, blood eosinophil counts and serum ECP.Results Complete data were obtained for 470 children. BHR was present in 103 children (22%), 66 being asymptomatic and 37 symptomatic. Children of all three case groups were more often atopic. Sensitization to indoor allergens particularly occurred in children with BHR, irrespective of symptoms (P〈0.05).Children with WHE+BHR+ had highest values for blood eosinophils and serum ECP (P〈0.05). Children with WHE−BHR+ had less severe responsiveness. In atopic children with WHE−BHR+, serum ECP was higher than in children with WHE-BHR-(P〈0.05).Conclusions BHR to HS is associated with blood markers of eosinophilic activation, particularly in atopic children.Type of Medium: Electronic ResourceURL: -
13Kerkhof, M. ; Koopman, L. P. ; Van Strien, R. T. ; Wijga, A. ; Smit, H. A. ; Aalberse, R. C. ; Neijens, H. J. ; Brunekreef, B. ; Postma, D. S. ; Gerritsen, J.
Oxford, UK : Blackwell Science Ltd
Published 2003Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background It has been suggested that the period immediately after birth is a sensitive period for the development of atopic disease.Objective We investigated whether birth characteristics and environmental factors are associated with the development of atopic dermatitis in the first year of life.Methods Seventy-six children with and 228 without atopic dermatitis, all children of mothers with respiratory allergy or asthma (PIAMA birth cohort study) were included in the study. Atopic dermatitis was defined as a positive history of an itchy skin condition with at least two of the following characteristics: visible dermatitis, history of outer arms/leg involvement, or general dry skin. Multiple logistic regression analysis was performed to study the independent effects of various risk factors.Results A birth weight 〈inlineGraphic alt="geqslant R: gt-or-equal, slanted" extraInfo="nonStandardEntity" href="urn:x-wiley:09547894:CEA1751:ges" location="ges.gif"/〉4000 g compared to 3000–4000 g was a significant risk factor for atopic dermatitis (odds ratio (OR)=2.4; 95% CI: 1.1–5.1) as was day care attendance (OR=2.9; 95% CI: 1.5–5.9). Exclusive breastfeeding in the first 3 months was negatively associated with atopic dermatitis (OR=0.6; 95% CI: 0.3–1.2), especially with visible dermatitis (OR=0.4; 95% CI: 0.2–1.0). Gender, gestational age, the presence of siblings or pets, and parental smoking were not significantly associated with atopic dermatitis.Conclusion This study shows that a high birth weight and day care attendance increase the risk of atopic dermatitis in the first year of life, while exclusive breastfeeding is a protective factor when dermatitis is found on inspection.Type of Medium: Electronic ResourceURL: -
14Visser, M. J. ; Brand, P. L. P. ; Boezen, H. M. ; Van Aalderen, W. M. C. ; Kauffman, H. F. ; Postma, D. S.
Oxford, UK : Blackwell Science, Ltd
Published 2002Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background During the baseline period of a clinical trial comparing different dosage schedules of inhaled steroids, asthmatic children (aged 6–10 years) were expected to meet the inclusion criterion of airways hyper-responsiveness (PD20 methacholine 〈 80 µg) after withdrawal of inhaled corticosteroids for 2–8 weeks. However, many children failed to do so.Objective It has been shown that young wheezing children may outgrow their symptoms. We investigated if differences between children with and without airways hyper-responsiveness after withdrawal of inhaled corticosteroids were compatible with differences between transient and persistent wheezers found in other studies.Methods Seventy-eight children entered the study, of which 41 developed airways hyper- responsiveness after withdrawal of inhaled corticosteroids, and 37 did not. These two groups of children were compared with respect to differences in demographic, clinical, and immunological features (IL-4, IL-5, IL-10, and IFN-γ produced by Con A stimulated peripheral mononuclear cells (PBMCs) and serum IL-4, IL-5 and soluble intercellular adhesion molecule-1 (sICAM-1)).Results Hyper-responsive children had more atopic features (positive RAST, high IgE, eczema), lower levels of FEV1 and lower concentrations of sICAM-1 than non-hyper-responsive children. Apart from a borderline significantly higher IL-4 production in the hyper-responsive group, other immunologic parameters were comparable. Multivariate logistic regression analysis showed that high serum IgE, low FEV1, and low sICAM-1 levels were independently associated with the presence of airways hyper-responsiveness after stopping inhaled corticosteroids. Atopy was associated with higher concentrations of IL-4 in the hyper-responsive group.Conclusion After withdrawal of inhaled corticosteroids many children previously diagnosed with asthma did not develop airways hyper-responsiveness. We conclude that hyper-responsive children share features with persistent wheezers as found in previous studies, whereas the non-hyper- responsive children may represent transient wheezers.Type of Medium: Electronic ResourceURL: -
15Visser, M. J. ; Postma, D. S. ; Brand, P. L. P. ; Arends, L. R. ; Duiverman, E. J. ; Kauffman, H. F.
Oxford, UK : Blackwell Science, Ltd
Published 2002Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background Asthma is characterized by eosinophilic airways inflammation with elevated levels of IL-4, IL-5 and sICAM-1, and reduced levels of IL-10 and IFN-γ. Inhaled corticosteroids powerfully reduce airways inflammation.Objective To investigate if eosinophil counts, serum eosinophilic cationic protein (ECP) and sICAM-1 levels, as well as serum and production of cytokines (IL-4, IL-5, IL-10, IFN-γ) by peripheral blood monocytes (PBMCs) are useful markers to monitor therapy with inhaled fluticasone propionate (FP) in asthmatic children.Methods In a double-blind, 1-year study, 55 asthmatic children (aged 6–10 years) stopped inhaled corticosteroids for a mean period of 24 days and were randomized to receive either FP 200 µg/day (constant dose group), or a starting dose of FP 1000 µg/day with two monthly reductions to 500, 200 and 100 µg/day (stepdown group). Hyper-responsiveness, symptom scores and blood sampling were performed at 2-month intervals.Results Symptoms and hyper-responsiveness improved significantly in both treatment groups after reintroduction of FP. Eosinophil counts decreased significantly more during the first 2 months of FP in the stepdown group than in the constant dose group (P = 0.03). We found a trend towards a dose-dependent response in changes of eosinophil counts and serum ECP levels during treatment. Serum IL-4 and IL-5 levels were undetectable in the majority of children. No significant effect of the dose of FP on the release of IL-4, IL-5, IL-10 or IFN-γ by Con A stimulated PBMCs was found. sICAM-1 levels did not significantly differ at any time point between the two groups.Conclusion Serum ECP as well as peripheral blood eosinophils, cytokine production by PBMCs and sICAM-1 levels are insensitive markers in titrating and monitoring therapy with inhaled corticosteroids over a wide dose range in childhood asthma.Type of Medium: Electronic ResourceURL: -
16Rijssenbeek-Nouwens, L. H. M. ; Oosting, A. J. ; De Monchy, J. G. R. ; Bregman, I. ; Postma, D. S. ; De Bruin-Weller, M. S.
Oxford, UK : Blackwell Science, Ltd
Published 2002Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background Anti-allergic mattress encasing may provide clinical benefit in asthmatic patients. However, the effect of mattress encasings on allergen-specific parameters, such as bronchial reactions to house dust mite (HDM) challenge, is not clear.Objective To investigate the effect of anti-allergic mattress encasings on allergen sensitivity in patients with moderate to severe asthma.Methods Twenty-seven patients with asthma and HDM allergy were studied in a double-blind, placebo-controlled study. Concentrations of Dermatophagoides pteronyssinus (Der p 1) were measured in mattress dust before and after 1 year of treatment; bronchial histamine challenge, bronchial challenge with HDM and intradermal skin challenges with HDM were performed. The number of eosinophils in peripheral blood was assessed.Results In the active group, but not in the placebo group, there was a significant reduction in Der p 1 concentration in the dust collected from the mattresses after 1 year of treatment compared to before. There was a significant difference between the groups with respect to HDM-induced early-reaction (ER) in the airways and the number of blood eosinophils, which reflected an increase in ER and eosinophils in the placebo group without significant change in the active group. No significant improvement in PC20 histamine, late-reaction (LR) and skin tests was found in either groups.Conclusion Our data suggest that encasings protect against a further increase in allergen sensitivity in asthmatic patients, so their use should be recommended.Type of Medium: Electronic ResourceURL: -
17MEYERS, D. A. ; XU, J. ; POSTMA, D. S. ; LEVITT, R. C. ; BLEECKER, E. R.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
18Staff View
ISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
19Spoelstra, F. M. ; Postma, D. S. ; Kauffman, H. F.
Oxford, UK : Blackwell Science, Ltd
Published 2001Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineType of Medium: Electronic ResourceURL: -
20Howard, T. D. ; Wiesch, D. G. ; Koppelman, G. H. ; Postma, D. S. ; Meyers, D. A. ; Bleecker, E. R.
Oxford BSL : Blackwell Science Ltd
Published 1999Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Allergy and asthma are closely related complex diseases caused by a combination of both genetic and environmental influences. Two common genetic approaches, candidate gene studies and genome-wide screens, have been used to localize and evaluate potential genetic factors that confer susceptibility or modify the phenotype of these diseases. Four genome screens suggest multiple chromosomal locations likely to contain asthma and allergy genes and many potential candidate genes exist in these regions. These screens were performed in six different populations and identified many common susceptibility regions as well as novel regions for each population. Ideally, these genes may point towards key biological pathways that will eventually serve as targets for therapeutic agents.Type of Medium: Electronic ResourceURL: