Publications
1032 results found
Huang TJ, Adcock IM, Chung KF, 2001, A novel transcription factor inhibitor, SP100030, inhibits cytokine gene expression, but not airway eosinophilia or hyperresponsiveness in sensitized and allergen-exposed rat, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 134, Pages: 1029-1036, ISSN: 0007-1188
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- Citations: 28
Kagoshima M, Wilcke T, Ito K, et al., 2001, Glucocorticoid-mediated transrepression is regulated by histone acetylation and DNA methylation, EUROPEAN JOURNAL OF PHARMACOLOGY, Vol: 429, Pages: 327-334, ISSN: 0014-2999
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- Citations: 63
Payne DNR, Adcock IM, Wilson NM, et al., 2001, Relationship between exhaled nitric oxide and mucosal eosinophilic inflammation in children with difficult asthma, after treatment with oral prednisolone, American Journal of Respiratory and Critical Care Medicine, Vol: 164, Pages: 1376-1381, ISSN: 1073-449X
Exhaled nitric oxide (FeNO) has been proposed as a noninvasive marker of airway inflammation in asthma, and may reflect airway eosinophilia. We examined the relationship between FeNO and eosinophilic inflammation in endobronchial biopsies from 31 children with difficult asthma (mean age [range] 11.9 [6-17] yr), following 2 wk of prednisolone (40 mg/d). Endobronchial biopsy was also performed in seven children without asthma. Biopsy eosinophils were detected using antibody to major basic protein, and point-counting used to derive an "eosinophil score." FeNO readings and suitable biopsies for analysis were both obtained in 21 of 31 children with asthma. Adherence to prednisolone was demonstrated in 17 of these 21. Within this group, there was a correlation between FeNO and eosinophil score (r = 0.54, p = 0.03). The relationship was strongest in patients with persistent symptoms after prednisolone, in whom FeNO > 7 ppb was associated with a raised eosinophil score. For all patients, FeNO < 7 ppb was associated with an eosinophil score within the nonasthmatic range, regardless of symptoms. We propose that FeNO is associated with eosinophilic inflammation in children with difficult asthma, following prednisolone, and may help in identifying patients in whom persistent symptoms are associated with airway eosinophilia.
Payne DNR, Adcock IM, Wilson NM, et al., 2001, Relationship between exhaled nitric oxide and mucosal eosinophilic inflammation in children with difficult asthma, after treatment with oral prednisolone, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 164, Pages: 1376-1381, ISSN: 1073-449X
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- Citations: 337
Caramori G, Lim S, Ito K, et al., 2001, Expression of GATA family of transcription factors in T-cells, monocytes and bronchial biopsies, EUROPEAN RESPIRATORY JOURNAL, Vol: 18, Pages: 466-473, ISSN: 0903-1936
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- Citations: 66
Adcock I, 2001, Mechanistic qualities of steroids in chronic-severe asthma, Pages: 45-50, ISSN: 1472-9725
Ito K, Jazrawi E, Cosio BJ, et al., 2001, p65-activated histone acetyltransferase activity is repressed by glucocorticoids, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 276, Pages: 30208-30215
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- Citations: 108
Lim S, Tomita K, Carramori G, et al., 2001, Low-dose theophylline reduces eosinophilic inflammation but not exhaled nitric oxide in mild asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 164, Pages: 273-276, ISSN: 1073-449X
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- Citations: 89
Chung KF, Adcock IM, 2001, Pathophysiological mechanisms of asthma -: <i>Application of cell and molecular biology techniques</i>, MOLECULAR BIOTECHNOLOGY, Vol: 18, Pages: 213-232, ISSN: 1073-6085
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- Citations: 11
Adcock IM, Caramori G, 2001, Cross-talk between pro-inflammatory transcription factors and glucocorticoids, IMMUNOLOGY AND CELL BIOLOGY, Vol: 79, Pages: 376-384, ISSN: 0818-9641
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- Citations: 273
Di Stefano A, Capelli A, Lusuardi M, et al., 2001, Decreased T lymphocyte infiltration in bronchial biopsies of subjects with severe chronic obstructive pulmonary disease, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 31, Pages: 893-902, ISSN: 0954-7894
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- Citations: 64
Vigushin DM, Ali S, Pace PE, et al., 2001, Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer <i>in vivo</i>, CLINICAL CANCER RESEARCH, Vol: 7, Pages: 971-976, ISSN: 1078-0432
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- Citations: 367
Ito K, Lim S, Caramori G, et al., 2001, Cigarette smoking reduces histone deacetylase 2 expression, enhances cytokine expression, and inhibits glucocorticoid actions in alveolar macrophages., FASEB J, Vol: 15, Pages: 1110-1112, ISSN: 0892-6638
Finney PA, Donnelly LE, Belvisi MG, et al., 2001, Chronic systemic administration of salmeterol to rats promotes pulmonary β<sub>2</sub>-adrenoceptor desensitization and down-regulation of G<sub>sα</sub>, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 132, Pages: 1261-1270, ISSN: 0007-1188
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- Citations: 25
Payne DNR, Adcock IM, 2001, Molecular mechanisms of corticosteroid actions, Paediatr Respir Rev, Vol: 2, Pages: 145-150, ISSN: 1526-0542
Adcock IM, 2001, Glucocorticoid-regulated transcription factors, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 14, Pages: 211-219, ISSN: 1094-5539
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- Citations: 130
Matthews JG, Irusen E, Smith S, et al., 2000, Altered steroid binding in PBMC corellates strongly with steroid in-sensitivity in patients with difficult asthma, THORAX, Vol: 55, Pages: A22-A22, ISSN: 0040-6376
Lim S, Groneberg D, Fischer A, et al., 2000, Expression of heme oxygenase isoenzymes 1 and 2 in normal and asthmatic airways - Effect of inhaled corticosteroids, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 162, Pages: 1912-1918, ISSN: 1073-449X
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- Citations: 92
Ito K, Barnes PJ, Adcock IM, 2000, Glucocorticoid receptor recruitment of histone deacetylase 2 inhibits interleukin-1β-induced histone H4 acetylation on lysines 8 and 12, MOLECULAR AND CELLULAR BIOLOGY, Vol: 20, Pages: 6891-6903, ISSN: 0270-7306
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- Citations: 543
Finney PA, Belvisi MG, Donnelly LE, et al., 2000, Albuterol-induced downregulation of Gsα accounts for pulmonary β<sub>2</sub>-adrenoceptor desensitization in vivo, JOURNAL OF CLINICAL INVESTIGATION, Vol: 106, Pages: 125-135, ISSN: 0021-9738
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- Citations: 58
Adcock IM, Ito K, 2000, Molecular mechanisms of corticosteroid actions., Monaldi Arch Chest Dis, Vol: 55, Pages: 256-266, ISSN: 1122-0643
Corticosteroids are the most effective therapy for the treatment of inflammatory diseases such as asthma. Functionally, they act partly by inducing anti-inflammatory genes such as secretary leukocyte proteinase inhibitor, Lipocortin-1 and interleukin-1 receptor antagonist, but mainly by repression of inflammatory genes, such as cytokines, adhesion molecules, inflammatory enzymes and receptors. They act by binding to a cytosolic glucocorticoid receptor (GR), which upon binding is activated and rapidly translocates to the nucleus. Within the nucleus, the GR either induces gene transcription by binding to specific deoxyribonucleic acid elements in the promoter/enhancer regions of responsive genes or reduces gene transcription by transrepression. The GR reduces gene transcription by interaction with pro-inflammatory transcription factors such as activation protein-1 and nuclear factor-kappa B. These effects of the GR on gene expression involve changes in the chromatin structure localized to the promoter sites of responsive genes. Many of the detrimental side-effects of corticosteroids are believed to be due to gene induction, leading to the search for novel corticosteroids which can repress inflammatory genes without inducing gene transcription.
Adcock IM, 2000, Role of transcription factors in mediating cytokine-induced inflammation, Pages: 289-293, ISSN: 0905-9180
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- Citations: 3
Hart L, Lim S, Adcock I, et al., 2000, Effects of inhaled corticosteroid therapy on expression and DNA-binding activity of nuclear factor κB in asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 161, Pages: 224-231, ISSN: 1073-449X
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- Citations: 87
Ito K, J Barnes P, M Adcock I, 2000, Histone acetylation and deacetylation., Methods Mol Med, Vol: 44, Pages: 309-319, ISSN: 1543-1894
In the resting cell, DNA is tightly compacted to prevent transcription factor accessibility. During activation of the cell, this compact inaccessible DNA is made available to DNA-binding proteins, thus allowing the induction of gene transcription (1 ,2). DNA is packaged into chromatin, a highly organized and dynamic protein-DNA complex. The fundamental subunit of chromatin, the nucleosome, is composed of an octomer of four core histones, an H3/H4 tetramer and two H2A/H2B dimers, surrounded by 146 bp DNA (2,3). The packaging of DNA into nucleosomes acts as a barrier to the initiation of transcription by preventing the access of transcriptional factors, and RNA polymerase II, to their cognate recognition sequences (4). Specific lysine residues in the N-terminal tails of the core histone can be post-translationally modified by acetylation of the ε-amino group. The dynamic equilibrium of core histone acetylation is established and maintained by histone acetyltransferase (HAT) and histone deacetylase (HDAC). Several transcriptional regulators possess intrinsic HAT and HDAC activities, strongly suggesting that histone acetylation and deacetylation play a causal role in regulating transcription (5-8). There is compelling evidence that increased gene transcription is associated with an increase in histone acetylation; hypoacetylation of histone is correlated with reduced transcription or gene silencing (2 ,7,8; Fig 1).
Chung F, Adcock I, 2000, Asthma: application of cell and molecular biology techniques to unravel causes and pathophysiological mechanisms., Methods Mol Med, Vol: 44, Pages: 1-29, ISSN: 1543-1894
The condition termed "asthma" has been difficult to define satisfactorily. Much of this problem arises from poor understanding of its causes, natural history, and pathophysiology, and also from a lack of a specific marker(s) of the disease. To the clinician, the diagnosis of asthma is not difficult in most cases, particularly if patients present early with symptoms of intermittent wheeze and chest tightness, and if their symptoms respond to particular treatments, such as β-adrenergic agonists. Early definitions of asthma included the presence of airway obstruction that could spontaneously reverse with treatment, and also the increased narrowing of the airways to non-specific bronchoconstrictor stimuli, i.e., bronchial hyperresponsiveness (BHR). The essential elements of this definition were useful in separating asthma from other conditions, such as chronic bronchitis, chronic obstructive pulmonary disease, and emphysema, which could sometimes be diagnostically confused with asthma. More recently, the definition of asthma has been enhanced by the recognition that the airway submucosa of patients with asthma are chronically inflamed with a typical inflammatory infiltrate, and that inflammatory processes are important causes of the chief characteristics of asthma: airway obstruction and BHR. In addition, the loss of reversibility of airway obstruction as a long-term effect of the chronic inflammatory process is recognized:
Chung KF, Adcock IM, 2000, Induction of nuclear factor-κB by exposure to ozone and inhibition by glucocorticoids, SINGLET OXYGEN, UV-A, AND OZONE, Vol: 319, Pages: 551-562, ISSN: 0076-6879
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- Citations: 8
Adcock IM, 2000, Molecular mechanisms of glucocorticosteroid actions, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 13, Pages: 115-126, ISSN: 1094-5539
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- Citations: 128
Newton R, Adcock IM, 2000, Analysis of Transcription Factor Activation: NFκB as a Regulator of Inflammatory Genes in Epithelial Cells., Methods Mol Med, Vol: 44, Pages: 143-159, ISSN: 1543-1894
In addition to being essential for differentiation and maturation, regulated gene expression governs many cellular responses to their local environment. For example, cytokines, viral infection, and numerous other inflammatory stimuli elicit the expression of specific response genes. Such signals are generally.
Payne DNR, Adcock IM, McKenzie SA, et al., 1999, Corticosteroid insensitive asthma in children, THORAX, Vol: 54, Pages: A6-A6, ISSN: 0040-6376
Vigushin DM, Ali S, Pace P, et al., 1999, Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer <i>in vivo</i>., CLINICAL CANCER RESEARCH, Vol: 5, Pages: 3777S-3777S, ISSN: 1078-0432
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