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  • Journal article
    Verdejo R, Lamoriniere S, Cottam B, Bismarck A, Shaffer Met al., 2007,

    Removal of oxidation debris from multi-walled carbon nanotubes

    , CHEMICAL COMMUNICATIONS, Pages: 513-515, ISSN: 1359-7345
  • Book chapter
    Alton EWFW, Davies JC, Geddes DM, 2006,

    Gene therapy for lung diseases

    , Principles of Molecular Medicine, Pages: 259-268

    Gene therapy is under development for a variety of lung disease, both those caused by single gene defects, such as cystic fibrosis and α<inf>1</inf>- antitrypsin deficiency, and multifactorial diseases such as cancer, asthma, lung fibrosis, and ARDS. Both viral and nonviral approaches have been explored, the major limitation to the former being the inability to repeatedly administer, which renders this approach perhaps more applicable to conditions requiring single administration, such as cancer. Progress in development and clinical trials in each of these diseases is reviewed, together with some potential newer approaches for the future. © 2006 Humana Press Inc.
  • Journal article
    Pommet M, Juntaro J, Bismarck A, 2006,

    Natural fibre reinforced cellulose nanocomposites

    , Aiche Annual Meeting Conference Proceedings
  • Conference paper
    Wort SJ, McMaster S, Mitchell JA, Evans TW, Ito M, Ito K, Adcock IMet al., 2006,

    Acetylation of histone H4 at NF-ΚB sites on pre-pro ET-1 promoter is involved in synergistic synthesis of ET-1 in human pulmonary artery smooth muscle cells treated with TNF-α and IFN-γ

    , Winter Meeting of the British-Thoracic-Society/British-Lung-Foundation (BTS/BLF), Publisher: B M J PUBLISHING GROUP, Pages: II19-II19, ISSN: 0040-6376
  • Journal article
    Hoyles RK, Ellis RW, Wellsbury J, Lees B, Newlands P, Goh NSL, Roberts C, Desai S, Herrick AL, McHugh NJ, Foley NM, Pearson SB, Emery P, Veale DJ, Denton CP, Wells AU, Black CM, du Bois RMet al., 2006,

    A multicenter, prospective, randomized, double-blind, placebo-controlled trial of corticosteroids and intravenous cyclophosphamide followed by oral azathioprine for the treatment of pulmonary fibrosis in scleroderma

    , ARTHRITIS AND RHEUMATISM, Vol: 54, Pages: 3962-3970, ISSN: 0004-3591
  • Journal article
    Spratt BG, Staley JT, Fisher MC, 2006,

    Introduction: species and speciation in micro-organisms

    , PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 361, Pages: 1897-1898, ISSN: 0962-8436
  • Journal article
    Caramori G, Ito K, Papi A, Adcock IMet al., 2006,

    Interactions between long-acting β2-agonists and glucocorticoids

    , Drug Discovery Today Therapeutic Strategies, Vol: 3, Pages: 261-268, ISSN: 1740-6773

    Long acting β<inf>2</inf>-agonists and glucocorticoids together control asthma in ∼95% of affected individuals, although symptoms return after treatment is stopped. Treatment of chronic obstructive pulmonary disease (COPD) scarcely influences the natural course of the disease. Neither long-acting β<inf>2</inf>-agonists (LABAs) nor glucocorticoids alone significantly influence the course of COPD. Recent evidence suggests that a combination of the two therapies is more promising: It can decrease the exacerbation rates in severe COPD and may also decrease mortality. © 2006 Elsevier Ltd. All rights reserved.
  • Journal article
    Morello S, Ito K, Yamamura S, Lee KY, Jazrawi E, Desouza P, Barnes P, Cicala C, Adcock IMet al., 2006,

    IL-1 beta and TNF-alpha regulation of the adenosine receptor (A2A) expression: differential requirement for NF-kappa B binding to the proximal promoter.

    , J Immunol, Vol: 177, Pages: 7173-7183, ISSN: 0022-1767

    Adenosine is a potent endogenous regulator of airway inflammation that acts through specific receptor subtypes that can either cause constriction (A1R, A2BR, and A3R) or relaxation (A2AR) of the airways. We therefore examined the effects of key inflammatory mediators on the expression of the A2AR in a lung epithelial cell line (A549). IL-1beta and TNF-alpha increased the expression of the A2AR gene at the mRNA and protein levels. In contrast, LPS had no effect on A2AR gene expression. IL-1beta and TNF-alpha rapidly activated p50 and p65, but not C-Rel, RelB, or p52, and both IL-1beta- and TNF-alpha-stimulated A2AR expression was inhibited by the IkappaB kinase 2 inhibitor AS602868 in a concentration-dependent manner. Using chromatin immunoprecipitation assays, we demonstrate that IL-1beta can enhance p65 association with putative kappaB binding sites in the A2AR promoter in a temporal manner. In contrast, TNF-alpha failed to enhance p65 binding to these putative sites. Functionally, the two most 5' kappaB sites were important for IL-1beta-, but not TNF-alpha-, induced A2AR promoter reporter gene activity. Finally, neither TNF-alpha nor Il-1beta had any effect on A2AR mRNA transcript degradation. These results directly implicate a major role for NF-kappaB in the regulation of A2AR gene transcription by IL-1beta and TNF-alpha but suggest that the effects of TNF-alpha on A2AR gene transcription are not mediated through the proximal promoter.
  • Journal article
    Morello S, Ito K, Yamamura S, Lee KY, Jazrawi E, DeSouza P, Barnes P, Cicala C, Adcock IMet al., 2006,

    IL-1β and TNF-α regulation of the adenosine receptor (A 2A) expression: Differential requirement for NF-κB binding to the proximal promoter

    , Journal of Immunology, Vol: 177, Pages: 7173-7183, ISSN: 0022-1767

    Adenosine is a potent endogenous regulator of airway inflammation that acts through specific receptor subtypes that can either cause constriction (A <inf>1</inf>R, A<inf>2B</inf>R, and A<inf>3</inf>R) or relaxation (A <inf>2A</inf>R) of the airways. We therefore examined the effects of key inflammatory mediators on the expression of the A<inf>2A</inf>R in a lung epithelial cell line (A549). IL-1β and TNF-α increased the expression of the A<inf>2A</inf>R gene at the mRNA and protein levels. In contrast, LPS had no effect on A<inf>2A</inf>R gene expression. IL-1β and TNF-α rapidly activated p50 and p65, but not C-Rel, RelB, or p52, and both IL-1β- and TNF-α-stimulated A<inf>2A</inf>R expression was inhibited by the IκB kinase 2 inhibitor AS602868 in a concentration-dependent manner. Using chromatin immunoprecipitation assays, we demonstrate that IL-1β can enhance p65 association with putative κB binding sites in the A <inf>2A</inf>R promoter in a temporal manner. In contrast, TNF-α failed to enhance p65 binding to these putative sites. Functionally, the two most 5′ κB sites were important for IL-1β-, but not TNF-α-, induced A<inf>2A</inf>R promoter reporter gene activity. Finally, neither TNF-α nor Il-1β had any effect on A<inf>2A</inf>R mRNA transcript degradation. These results directly implicate a major role for NF-κB in the regulation of A<inf>2A</inf>R gene transcription by IL-1β and TNF-α but suggest that the effects of TNF-α on A<inf>2A</inf>R gene transcription are not mediated through the proximal promoter. Copyright © 2006 by The American Association of Immunologists, Inc.
  • Journal article
    Morozov IY, Negrete-Urtasun S, Tilburn J, Jansen CA, Caddick MX, Arst HNet al., 2006,

    Nonsense-mediated mRNA decay mutation in <i>Aspergillus nidulans</i>

    , EUKARYOTIC CELL, Vol: 5, Pages: 1838-1846, ISSN: 1535-9778

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