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• Conference paper
  Wakeland EK, Goodnow CC, Kuchroo VK, Seed B, Hafler DA, Cookson W, Abbas AK, Behrens TW, Rioux JD, Umetsu D, Foote SJ, Bowcock A, Kere J, Wicker LS, Rao Aet al., 2005,

  Discussion

  , Pages: 212-218, ISSN: 1528-2511
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• Conference paper
  Goldstein DB, Abbas AK, Wijmenga C, Cookson W, Goodnow CC, Rioux JD, Hafler DA, Kere J, Daly MJ, Bowcock A, Behrens TW, Foote SJ, Worthington Jet al., 2005,

  Discussion

  , Pages: 8-13, ISSN: 1528-2511
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• Conference paper
  Wakeland EK, Goodnow CC, Cookson W, Abbas AK, Rioux JD, Foote SJ, Bowcock A, Kere J, Ting Jet al., 2005,

  Discussion

  , Pages: 239-241, ISSN: 1528-2511
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• Conference paper
  Hafler DA, Rao A, Ting J, Rioux JD, Goodnow CC, Abbas AK, Wicker LS, Wakeland EK, Behrens TW, Goldstein DB, Kere J, Cookson W, Seed B, Lindgren C, Bowcock A, Kuchroo VKet al., 2005,

  Discussion

  , Pages: 174-179, ISSN: 1528-2511
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• Journal article
  Hollax EJ, Davies J, Griesenbach U, Burgess J, Alton EW, Armour JAet al., 2005,

  Beta-defensin genomic copy number is not a modifier locus for cystic fibrosis

  , J Negat Results Biomed, Vol: 7
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• Journal article
  Hilliard T, Edwards S, Buchdahl R, Francis J, Rosenthal M, Balfour-Lynn I, Bush A, Davies Jet al., 2005,

  Voriconazole therapy in children with cystic fibrosis.

  , J Cyst Fibros, Vol: 4, Pages: 215-220, ISSN: 1569-1993

  BACKGROUND: There is increasing evidence for the efficacy of the antifungal voriconazole, particularly in immunosuppression. We describe our experience of using voriconazole in children with CF. METHODS: We performed a retrospective case note review of children with CF treated with voriconazole in a single centre over an 18 month period. RESULTS: A total of 21 children aged 5 to 16 years (median 11.3) received voriconazole for between 1 and 50 (22) weeks. Voriconazole was used as monotherapy in 2 children with recurrent allergic bronchopulmonary aspergillosis (ABPA); significant and sustained improvements in clinical and serological parameters for up to 13 months were observed, without recourse to oral steroids. Voriconazole was used in combination with an immunomodulatory agent in a further 11 children with ABPA, with significant improvement in pulmonary function and serology. 8 children without ABPA but who had recurrent Aspergillus fumigatus isolates and increased symptoms also received voriconazole; this group did not improve with treatment. Adverse effects occurred in 7 children (33%: photosensitivity reaction 3, nausea 2, rise in hepatic enzymes 1, hair loss 1). CONCLUSIONS: Voriconazole may be a useful adjunctive therapy for ABPA in CF. Voriconazole monotherapy appears to be an alternative treatment strategy when oral corticosteroids may not be suitable.

  • Abstract
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• Journal article
  Aziz ZA, Wells AU, Desai SR, Ellis SM, Walker AE, MacDonald S, Hansell DMet al., 2005,

  Functional impairment in emphysema: Contribution of airway abnormalities and distribution of parenchymal disease

  , AMERICAN JOURNAL OF ROENTGENOLOGY, Vol: 185, Pages: 1509-1515, ISSN: 0361-803X
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  • Citations: 79
• Journal article
  Safinia L, Datan N, Höhse M, Mantalaris A, Bismarck Aet al., 2005,

  Towards a methodology for the effective surface modification of porous polymer scaffolds

  , BIOMATERIALS, Vol: 26, Pages: 7537-7547, ISSN: 0142-9612
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  • Citations: 82
• Journal article
  Adcock IM, Ito K, Barnes PJ, 2005,

  Histone deacetylation: an important mechanism in inflammatory lung diseases.

  , COPD, Vol: 2, Pages: 445-455, ISSN: 1541-2555

  Inflammatory lung diseases are characterised by increased expression of multiple inflammatory genes that are regulated by proinflammatory transcription factors, such as NF-kappaB. Gene expression is regulated by modifications such as acetylation of core histones through the concerted action of coactivators such as CBP (cAMP-response element binding protein (CREB)-binding protein) which have intrinsic histone acetyltransferase (HAT) activity and are able to recruit other HAT enzymes. Conversely gene repression is mediated via histone deacetylases (HDAC) and other corepressors. In biopsies from asthmatic subjects there is an increase in HAT activity and some reduction in HDAC activity. Both of these changes are partially reversed by corticosteroid therapy. Corticosteroids switch off inflammatory genes in asthma through a combination of a direct inhibition of HAT activity and by the recruitment of HDAC2 to the activated NF-kappaB-stimulated inflammatory gene complex. In chronic obstructive pulmonary disease (COPD), a corticosteroid insensitive disease, there is a reduction in HDAC activity and HDAC2 expression, which may account for the amplified inflammation and resistance to the actions of corticosteroids. The reduction in HDAC2 may be secondary to oxidative and nitrative stress as a result of cigarette smoking and severe inflammation. This may also occur to differing degrees in severe asthma, smoking asthmatic patients and cystic fibrosis. Similar mechanisms may also account for the steroid resistance seen within latent adenovirus infections. The reduction in HDAC activity induced by oxidative stress can be restored by theophylline, acting through specific kinases, which may be able to reverse steroid resistance in COPD and other inflammatory lung diseases. The modulation of HAT/HDAC activity may lead to the development of novel anti-inflammatory approaches to inflammatory lung diseases that are currently difficult to treat.

  • Abstract
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• Journal article
  Saouros S, Edwards-Jones B, Reiss M, Sawmynaden K, Cota E, Simpson P, Dowse TJ, Jäkle U, Ramboarina S, Shivarattan T, Matthews S, Soldati-Favre Det al., 2005,

  A novel galectin-like domain from <i>Toxoplasma gondii</i> micronemal protein 1 assists the folding, assembly, and transport of a cell adhesion complex

  , JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 280, Pages: 38583-38591
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  • Citations: 63

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