Publications
160 results found
Macari DMT, Teixeira MM, Ansari T, et al., 1998, Priming and induction of eosinophil trafficking in guinea-pig cutaneous inflammation by tumour necrosis factor α, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 125, Pages: 1228-1235, ISSN: 0007-1188
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- Citations: 11
Erjefält JS, Andersson M, Greiff L, et al., 1998, Cytolysis and piecemeal degranulation as distinct modes of activation of airway mucosal eosinophils, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 102, Pages: 286-294, ISSN: 0091-6749
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- Citations: 73
Parameswaran K, Pizzichini MMM, Li D, et al., 1998, Serial sputum cell counts in the management of chronic airflow limitation, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 1405-1408, ISSN: 0903-1936
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- Citations: 15
Jeffery PK, 1998, The development of large and small airways, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 157, Pages: S174-S180, ISSN: 1073-449X
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- Citations: 79
Jeffery PK, 1998, Investigation and assessment of airway and lung inflammation: we now have the tools, what are the questions?, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 524-528, ISSN: 0903-1936
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- Citations: 13
Jeffery PK, Bousquet J, 1998, European respiratory society task force - Methods for assessment of airways inflammation - Foreword, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 1S-1S, ISSN: 0903-1936
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- Citations: 4
Frew AJ, Li D, Jeffery PK, 1998, In site hybridization and the polymerase chain reaction, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 30S-32S, ISSN: 0903-1936
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- Citations: 1
Miotla JM, Jeffery PK, Hellewell PG, 1998, Platelet-activating factor plays a pivotal role in the induction of experimental lung injury, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 18, Pages: 197-204, ISSN: 1044-1549
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- Citations: 62
Mulier B, Rahman I, Watchorn T, et al., 1998, Hydrogen peroxide-induced epithelial injury: the protective role of intracellular nonprotein thiols (NPSH), EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 384-391, ISSN: 0903-1936
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- Citations: 65
Jeffery PK, 1998, Structural and inflammatory changes in COPD: a comparison with asthma, THORAX, Vol: 53, Pages: 129-136, ISSN: 0040-6376
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- Citations: 243
Southcott AM, Hemingway I, Lorimer S, et al., 1998, Adhesion molecule expression in the lung: a comparison between normal and diffuse interstitial lung disease, EUROPEAN RESPIRATORY JOURNAL, Vol: 11, Pages: 91-98, ISSN: 0903-1936
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- Citations: 14
Stern M, Phillips J, Jaffe A, et al., 1997, A double blind placebo controlled trial of pulmonary and nasal administration of liposome-mediated CFTR gene transfer in CF subjects, Thorax, Vol: 52, ISSN: 0040-6376
We and others have previously shown functional changes folllowing liposome-mediated CFTR gene transfer to the nasal epithelium of CF subjects. We have now studied the safety and efficacy of this approach in the lungs and nose of CF subjects in a double blind placebo controlled study. 8 Subjects were randomised to receive DNA liposome complex or lipid alone by nebulisation into the lungs with 8 further subjects receiving the liposome alone. One week later, the same subjects received the same treatment by nasal administration. Safety was assessed clinically, radiographically, by pulmonary function and histological analysis. Efficacy was assessed by analysis of CFTR DNA, mRNA, in vivo potential difference, SPQ fluorescence, bacterial adherence and mucociliary clearance (nose only). The majority of subjects receiving the active complex noted mild flu-like symptoms which resolved within 36 hours. A proportion of both active and placebo subjects noted mild respiratory symptoms over a period of 12 hours following pulmonary administration. No specific treatment was required for either event. Pulmonary administration resulted in a significant (p<0.05) degree of correction of the chloride abnormality in the active, but not placebo treated subjects. No alterations in the sodium transport were detected. A similar pattern was observed following nasal administration. This study provides proof-of-principle that cationic liposome mediated CFTR gene transfer is able to influence significantly the underlying electrophysiological defect in the lungs of cystic fibrosis patients.
Nicholson AG, Li DC, Pastorino U, et al., 1997, Full thickness eosinophilia in oesophageal leiomyomatosis and idiopathic eosinophilic oesophagitis. A common allergic inflammatory profile?, JOURNAL OF PATHOLOGY, Vol: 183, Pages: 233-236, ISSN: 0022-3417
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- Citations: 39
Li D, Wang D, GriffithsJohnson DA, et al., 1997, Eotaxin protein and gene expression in guinea-pig lungs: constitutive expression and upregulation after allergen challenge, EUROPEAN RESPIRATORY JOURNAL, Vol: 10, Pages: 1946-1954, ISSN: 0903-1936
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- Citations: 61
Humbles AA, Conroy DM, Marleau S, et al., 1997, Kinetics of eotaxin generation and its relationship to eosinophil accumulation in allergic airways disease: Analysis in a guinea pig model in vivo, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 186, Pages: 601-612, ISSN: 0022-1007
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- Citations: 212
Jeffery PK, 1997, Airway mucose: Secretory cells, mucus and mucin genes, EUROPEAN RESPIRATORY JOURNAL, Vol: 10, Pages: 1655-1662, ISSN: 0903-1936
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- Citations: 108
Gizycki MJ, Adelroth E, Rogers AV, et al., 1997, Myofibroblast involvement in the allergen-induced late response in mild atopic asthma., Am J Respir Cell Mol Biol, Vol: 16, Pages: 664-673, ISSN: 1044-1549
We undertook a detailed cellular and ultrastructural examination of bronchial biopsies from seven allergic asthmatic patients and 10 nonasthmatic control subjects (five atopic and five nonatopic) to determine the nature of the inflammation that occurs during allergen-induced late-phase responses (LPRs). The asthmatic subjects had mild asthma (FEV1 = 94 +/- 9% predicted; mean +/- SEM) and required only intermittent use of beta 2-agonists. Airway mucosal biopsy specimens were obtained on a single occasion from the nonasthmatic controls and on two occasions from the asthmatic subjects, at 24 h after diluent challenge and 24 h after challenge with allergen 3 wk later. The mean maximal decrease in FEV1 during the late response after allergen challenge was 30%, and that after administration of diluent was 4%. In coded plastic sections, subepithelial cells were counted with both light and electron microscopy, and the numbers present were expressed per 0.1 mm2 of tissue. Light microscopy revealed statistically significant increases in the total number of inflammatory cells (P < 0.02) and in "activated fibroblasts" after allergen challenge (P < 0.05). Electron microscopy showed significant increases after allergen challenge in the total number of eosinophils (P < 0.05) and cells with the ultrastructural features of myofibroblasts. The latter cells constituted 1.5% of cells after administration of diluent, and this increased to 15.5% after allergen challenge (P < 0.05). Mast cells were significantly more abundant in the atopic nonasthmatic controls than in the asthmatic subjects after allergen challenge. The study demonstrates that the profile of inflammatory cells in asthma at 24 h after allergen challenge is distinct from that in stable asthma and in nonasthmatic controls, and that migratory cells with a contractile phenotype appear in greater numbers in the late response. We propose that subjects who repeatedly develop a late response have increased n
Chanez P, Vignola AM, OShaugnessy T, et al., 1997, Corticosteroid reversibility in COPD is related to features of asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 155, Pages: 1529-1534, ISSN: 1073-449X
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- Citations: 212
Li D, Wang D, Majumdar S, et al., 1997, Localization and up-regulation of mucin (MUC2) gene expression in human nasal biopsies of patients with cystic fibrosis, Journal of Pathology, Vol: 181, Pages: 305-310, ISSN: 0022-3417
Using digoxigenin-UTP-labelled human HAM-1 (92 bp) or SMUC41 (850 bp) cRNA probes, the expression and localization of MUC2 gene transcripts were determined by in situ hybridization in human nasal tissues obtained as biopsies from 12 patients with cystic fibrosis (CF): all had been part of a gene therapy trial in which CFTR cDNA-liposome complexes had been delivered by topical application to eight and liposome alone to four as a placebo control. For comparison, there were nasal tissues taken at surgical resection from four non-CF subjects and a further four biopsies taken from normal healthy volunteer controls. Both SMUC41 and HAM-1 probes provided a strong signal. MUC2 mRNA transcripts were present in serous and mucous acini of submucosal glands, ciliated and basal cells of the surface epithelium, and occasional mononuclear inflammatory cells. The percentages (mean ± SEM) of serous and mucous acini showing positivity for MUC2 gene expression in the four samples surgically resected from non-CF subjects were 25.4 ± 5.6 and 26.7 ± 3.3 per cent, respectively. Compared with the non-CF subjects, the mean percentage of acini showing MUC2 gene expression in the four placebo-treated CF subjects was significantly higher for serous (80.5 ± 12.7 per cent; P < 0.05, t-test), but not for mucous acini (53.1 ± 16.8 per cent; P = 0.38). In CF and non-CF groups, where present, MUC2 positivity was strongly expressed and constituted approximately 84 per cent of the cell area in serous acini, whereas it was less obvious and was confined to the perinurclear area of cells in mucous acini. A significantly greater proportion of the surface epithelium was positive for MUC2 mRNA transcripts in the CF subjects (89.0 ± 1.4 per cent) than in the surgically resected tissues of the four non-CF subjects (19.4 ± 4.0 per cent) (P = 0.02). In the eight CFTR-cDNA-treated subjects, there was an overall trend to reduction, but no statistically significa
Coker RK, Laurent GJ, Shahzeidi S, et al., 1997, Transforming growth factors-beta(1), -beta(2), and -beta(3) stimulate fibroblast procollagen production in vitro but are differentially expressed during bleomycin-induced lung fibrosis, AMERICAN JOURNAL OF PATHOLOGY, Vol: 150, Pages: 981-991, ISSN: 0002-9440
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- Citations: 221
OShaughnessy TC, Ansari TW, Barnes NC, et al., 1997, Inflammation in bronchial biopsies of subjects with chronic bronchitis: Inverse relationship of CD8(+) T lymphocytes with FEV(1), AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 155, Pages: 852-857, ISSN: 1073-449X
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- Citations: 518
Coker RK, Laurent GJ, Shahzeidi S, et al., 1996, Diverse cellular TGF-beta(1) and TGF-beta(3) gene expression in normal human and murine lung, EUROPEAN RESPIRATORY JOURNAL, Vol: 9, Pages: 2501-2507, ISSN: 0903-1936
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- Citations: 74
Jeffery PK, 1996, Bronchial biopsies and airway inflammation, EUROPEAN RESPIRATORY JOURNAL, Vol: 9, Pages: 1583-1587, ISSN: 0903-1936
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- Citations: 38
Alton EWFW, KingsleighSmith DJ, Munkonge FM, et al., 1996, Asthma prophylaxis agents alter the function of an airway epithelial chloride channel, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 14, Pages: 380-387, ISSN: 1044-1549
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- Citations: 30
Miotla JM, Williams TJ, Hellewell PG, et al., 1996, Role for the beta(2) integrin CD11b in mediating experimental lung injury in mice, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 14, Pages: 363-373, ISSN: 1044-1549
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- Citations: 27
Godfrey RW, Lorimer S, Majumdar S, et al., 1995, Airway and lung elastic fibre is not reduced in asthma nor in asthmatics following corticosteroid treatment., Eur Respir J, Vol: 8, Pages: 922-927, ISSN: 0903-1936
By morphometric investigation of the relative content of elastic and collagen fibres, we have tested the hypothesis that loss of elastic fibres in the conducting airways and lung parenchyma may reduce tissue elastic recoil, resulting in increased airway maximal closure and apparent increased responsiveness. The study groups comprised: Group A (n = 11) with relatively mild atopic asthma using inhaled bronchodilators prn (i.e. short-term corticosteroids users); Group B (n = 9) with more severe asthma requiring inhaled bronchodilators regularly, and daily inhaled glucocorticosteroids (i.e. longterm corticosteroid users); Group C (n = 12) normal healthy workers. Bronchial biopsy samples were taken from three sites from the left lung. Group A biopsy samples were taken before and after a 4 wk treatment period with inhaled corticosteroids (200 micrograms b.i.d.) and the relative elastic and collagen fibre content of a subepithelial zone was determined from electron micrographs. In a parallel study, the relative proportion of elastic fibre in post mortem lung tissue samples (inner aspect of the bronchial wall, alveolar wall, and points of attachment of surrounding alveoli to intrapulmonary bronchi) from subjects suffering a fatal asthma attack (n = 11), and non-asthmatic suffering sudden death (n = 9), were determined using Miller's elastic and eosin counterstain for light microscopy. In bronchial biopsies of normal subjects, 4.6 (SEM 1.1)% of subepithelial connective tissue was elastic fibre, similar to mild asthmatic subjects, 1.9 (SEM 0.48)%. Neither short-term (4 weeks) inhaled corticosteroid (200 micrograms b.i.d.) nor long-term (< 6 months) treatment with variable doses of inhaled steroids (100-1000 micrograms b.i.d.) significantly altered the elastic or collagen content of the tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
GODFREY RWA, LORIMER S, MAJUMDAR S, et al., 1995, AIRWAY AND LUNG ELASTIC FIBER IS NOT REDUCED IN ASTHMA NOR IN ASTHMATICS FOLLOWING CORTICOSTEROID TREATMENT, EUROPEAN RESPIRATORY JOURNAL, Vol: 8, Pages: 922-927, ISSN: 0903-1936
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- Citations: 33
SOUTHCOTT AM, JONES KP, LI D, et al., 1995, INTERLEUKIN-8 - DIFFERENTIAL EXPRESSION IN LONE FIBROSING ALVEOLITIS AND SYSTEMIC-SCLEROSIS, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 151, Pages: 1604-1612, ISSN: 1073-449X
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- Citations: 83
Sharma RK, Addis BJ, Jeffery PK, 1995, The distribution and density of airway vasoactive intestinal polypeptide (VIP) binding sites in cystic fibrosis and asthma, PULMONARY PHARMACOLOGY, Vol: 8, Pages: 91-96, ISSN: 0952-0600
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- Citations: 12
MIOTLA JM, PERRETTI M, FLOWER RJ, et al., 1995, SUPPRESSION OF EXPERIMENTAL ACUTE LUNG INJURY IN THE MOUSE BY DEXAMETHASONE AND THE ROLE OF LIPOCORTIN-1, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 114, Pages: P62-P62, ISSN: 0007-1188
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- Citations: 3
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