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Journal articleDesai SR, Ryan SM, Colby TV, 2003,
Smoking-related interstitial lung diseases: Histopathological and imaging perspectives
, CLINICAL RADIOLOGY, Vol: 58, Pages: 259-268, ISSN: 0009-9260- Author Web Link
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- Citations: 37
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Journal articleMoffatt MF, Faux JA, Lester S, et al., 2003,
Atopy, respiratory function and HLA-DR in aboriginal Australians
, HUMAN MOLECULAR GENETICS, Vol: 12, Pages: 625-630, ISSN: 0964-6906- Author Web Link
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- Citations: 24
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Journal articleMoffatt MF, Faux JA, Lester S, et al., 2003,
Atopy, respiratory function and HLA-DR in aboriginal Australians
, Human Molecular Genetics, Vol: 12, Pages: 625-630, ISSN: 0964-6906The Class II genes of the MHC represent a major locus with quantified effects on atopic (allergic) phenotypes in many studies of westernized Caucasians. Although asthma is considered a disease of western societies, typical components of the asthma phenotype, such as elevations of the IgE, are seen with parasitic infestation. We have therefore investigated the effects of the HLA-DRB1 locus on asthma and its intermediate phenotypes in Aboriginal people from the Kimberly region of Australia who were suffering from endemic hookworm infection. Recognizable correlates of allergic asthma were present in the subjects, including skin test positivity to house dust mite (HDM), specific IgE responses to HDM, and the total serum IgE. HLA-DRB1 alleles did not predict the presence of asthma, but multi-allelic tests of association showed the locus accounted for ∼33% of the variance of the total serum IgE concentration and 17% of the variance of the specific IgE titres to HDM. Genetic admixture was excluded as a cause of the results. These effects of the MHC on IgE levels were an order of magnitude greater than that seen in Caucasians, consistent with the hypothesis that the genetic predisposition to allergic disease may be driven by adaptation to helminth infection. The results further suggest that parasitism per se is not protective against asthma.
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Journal articleInoue K, Ozaki S, Ito K, et al., 2003,
<i>Runx3</i> is essential for the target-specific axon pathfinding of <i>trkC</i>-expressing dorsal root ganglion neurons
, BLOOD CELLS MOLECULES AND DISEASES, Vol: 30, Pages: 157-160, ISSN: 1079-9796- Author Web Link
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- Citations: 28
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Journal articleMangoni AA, Desai SR, Shaikh H, et al., 2003,
An unusual case of pneumonia
, INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Vol: 57, Pages: 153-154, ISSN: 1368-5031 -
Journal articleHorsefield R, Yankovskaya V, Törnroth S, et al., 2003,
Using rational screening and electron microscopy to optimize the crystallization of succinate:ubiquinone oxidoreductase from <i>Escherichia coli</i>
, ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY, Vol: 59, Pages: 600-602, ISSN: 0907-4449- Author Web Link
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- Citations: 10
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Journal articleVincent O, Rainbow L, Tilburn J, et al., 2003,
YPXL/I is a protein interaction motif recognized by <i>Aspergillus</i> PalA and its human homologue, AIP1/Alix
, MOLECULAR AND CELLULAR BIOLOGY, Vol: 23, Pages: 1647-1655, ISSN: 0270-7306- Author Web Link
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- Citations: 135
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Journal articleKagoshima M, Ito K, Cosio B, et al., 2003,
Glucocorticoid suppression of nuclear factor-κB:: a role for histone modifications
, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 31, Pages: 60-65, ISSN: 0300-5127- Author Web Link
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- Citations: 47
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Journal articleYankovskaya V, Horsefield R, Törnroth S, et al., 2003,
Architecture of succinate dehydrogenase and reactive oxygen species generation
, SCIENCE, Vol: 299, Pages: 700-704, ISSN: 0036-8075- Author Web Link
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- Citations: 697
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Conference paperKagoshima M, Ito K, Cosio B, et al., 2003,
Glucocorticoid suppression of nuclear factor-κB: A role for histone modifications
, Pages: 60-65, ISSN: 0300-5127Corticosteroids are by far the most effective treatment for chronic inflammatory diseases such as asthma. Inflammation in asthma is characterized by the increased expression of multiple inflammatory genes, including those that encode cytokines, chemokines, adhesion molecules, and inflammatory enzymes and receptors. Increased expression of inflammatory genes is regulated by pro-inflammatory transcription factors, such as nuclear factor κB (NF-κB). These bind to, and activate, co-activator molecules that then acetylate core histones resulting in elevated gene transcription. Corticosteroids reverse histone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF-κB-associated co-activators or by recruitment of histone deacetylases to the activated transcription complex. Understanding how corticosteroids work in asthma may help in designing novel corticosteroids with fewer systemic effects, as well as novel anti-inflammatory approaches.
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