27 results found
Hopkinson NS, Kemp SV, Toma TP, et al., 2011, Atelectasis and survival after bronchoscopic lung volume reduction for COPD, EUROPEAN RESPIRATORY JOURNAL, Vol: 37, Pages: 1346-1351, ISSN: 0903-1936
Hopkinson NS, Kemp SV, Toma TP, et al., 2010, ATELECTASIS FOLLOWING BRONCHOSCOPIC LUNG VOLUME REDUCTION (BLVR) IS ASSOCIATED WITH IMPROVED SURVIVAL IN COPD, British-Thoracic-Society-Winter-Meeting 2010, Publisher: B M J PUBLISHING GROUP, Pages: A137-A137, ISSN: 0040-6376
Fidler KJ, Hilliard TN, Bush A, et al., 2009, Mannose-binding lectin is present in the infected airway: a possible pulmonary defence mechanism, THORAX, Vol: 64, Pages: 150-155, ISSN: 0040-6376
Geddes D, 2008, Segregation is not good for patients with cystic fibrosis., J R Soc Med, Vol: 101 Suppl 1, Pages: S36-S38, ISSN: 0141-0768
Larsen MDB, Griesenbach U, Goussard S, et al., 2008, Bactofection of lung epithelial cells in vitro and in vivo using a genetically modified Escherichia coli, GENE THERAPY, Vol: 15, Pages: 434-442, ISSN: 0969-7128
Ferrari S, Griesenbach U, Iida A, et al., 2007, Sendai virus-mediated CFTR gene transfer to the airway epithelium, GENE THERAPY, Vol: 14, Pages: 1371-1379, ISSN: 0969-7128
Elston C, Geddes D, 2007, Inflammation in cystic fibrosis - When and why? Friend or foe?, SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 28, Pages: 286-294, ISSN: 1069-3424
Xenariou S, Griesenbach U, Liang H-D, et al., 2007, Use of ultrasound to enhance nonviral lung gene transfer in vivo, GENE THERAPY, Vol: 14, Pages: 768-774, ISSN: 0969-7128
Aziz ZA, Davies JC, Alton EW, et al., 2007, Computed tomography and cystic fibrosis: promises and problems, THORAX, Vol: 62, Pages: 181-186, ISSN: 0040-6376
Horsley A, Macleod K, Saunders C, et al., 2007, UKCF gene therapy consortium tracking study: Lung clearance index improves with treatment of an infective exacerbation, PEDIATRIC PULMONOLOGY, Pages: 335-336, ISSN: 8755-6863
Xenariou S, Griesenbach U, Ferrari S, et al., 2006, Using magnetic forces to enhance non-viral gene transfer to airway epithelium in vivo, GENE THERAPY, Vol: 13, Pages: 1545-1552, ISSN: 0969-7128
Lim E, Ali A, Cartwright N, et al., 2006, Effect and duration of lung volume reduction surgery: Mid-term results of the Brompton trial, THORACIC AND CARDIOVASCULAR SURGEON, Vol: 54, Pages: 188-192, ISSN: 0171-6425
Que C, Cullinan P, Geddes D, 2006, Improving rate of decline of FEV1 in young adults with cystic fibrosis, THORAX, Vol: 61, Pages: 155-157, ISSN: 0040-6376
Geddes D, 2005, Translational research - from gene to treatment: lessons from cystic fibrosis, CLINICAL MEDICINE, Vol: 5, Pages: 258-263, ISSN: 1470-2118
McShane D, Davies JC, Wodehouse T, et al., 2004, Normal nasal mucociliary clearance in CF children: evidence against a CFTR-related defect, EUROPEAN RESPIRATORY JOURNAL, Vol: 24, Pages: 95-100, ISSN: 0903-1936
Elkin S, Geddes D, 2003, Pseudomonal infection in cystic fibrosis: the battle continues., Expert Rev Anti Infect Ther, Vol: 1, Pages: 609-618, ISSN: 1478-7210
Pseudomonas aeruginosa lung infection is the major cause of morbidity and mortality in patients with cystic fibrosis. Infection usually begins in childhood and is responsible for respiratory failure and death in most patients with cystic fibrosis. The organism triggers an exuberant chronic inflammatory reaction which damages the airways and leads to progressive loss of lung function. Over the last decade significant advances have been made in the understanding of the pathophysiology of cystic fibrosis airways disease. These should assist the development of new and better therapies to treat this pathogen. This review provides an overview of pseudomonal infection in cystic fibrosis, including mechanisms by which the bacteria may colonize the cystic fibrosis airway, persistence of pseudomonal infection and the biofilm mode of growth. Available treatments and possible novel approaches to therapy will be discussed.
Griesenbach U, Kitson C, Garcia SE, et al., 2003, Gene silencing through RNA interference and antisense strategies in the lung, 6th Annual Meeting of the American-Society-of-Gene-Therapy, Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE, Pages: S389-S389, ISSN: 1525-0016
Toma T, Hopkinson N, Hillier J, et al., 2003, Bronchoscopic volume reduction with valve implants in patients with severe emphysema, Lancet, Vol: 361, Pages: 931-933
Ulrich K, Stern M, Goddard M, et al., 2002, Characterisation of a murine model of oleic acid-induced acute lung injury, Winter Meeting of the British-Thoracic-Society, Publisher: BRITISH MED JOURNAL PUBL GROUP, ISSN: 0040-6376
Geddes D, Davies M, Koyama H, et al., 2000, Effect of lung-volume-reduction surgery in patients with severe emphysema., NEW ENGLAND JOURNAL OF MEDICINE, Vol: 343, Pages: 239-245, ISSN: 0028-4793
Stern M, Ulrich K, Robinson C, et al., 2000, Pretreatment with cationic lipid-mediated transfer of the Na+K+-ATPase pump in a mouse model in vivo augments resolution of high permeability pulmonary oedema, GENE THERAPY, Vol: 7, Pages: 960-966, ISSN: 0969-7128
Hillery E, Cheng S, Geddes D, et al., 1999, Effects of altering dosing on cationic liposome-mediated gene transfer to the respiratory epithelium., Gene Ther, Vol: 6, Pages: 1313-1316, ISSN: 0969-7128
Liposome-mediated gene transfer is currently sub-optimal with respect to both the extent and duration of transgene expression. We investigated whether simple changes in DNA dosing could enhance either of these outcomes. Increasing DNA doses produced highest transgene expression at an intermediate dose with toxicity observed at higher doses, thereby likely limiting expression. Adminis- tering an equivalent DNA dose in aliquots over a 1-3 day period resulted in significantly lower gene expression and did not increase the duration of expression. Administration at different times of the day (and hence wake/sleep cycles of the animals) did not alter gene expression. We conclude that such simple changes in dosing regimes are unlikely to contribute to improvements in gene transfer efficiency.
Geddes D, Alton E, 1998, Cystic fibrosis clinical trials, ADVANCED DRUG DELIVERY REVIEWS, Vol: 30, Pages: 205-217, ISSN: 0169-409X
Stern M, Geddes D, 1996, Cystic fibrosis: Basic chemical and cellular mechanisms, BRITISH JOURNAL OF HOSPITAL MEDICINE, Vol: 55, Pages: 237-240, ISSN: 0007-1064
Cramer D, Ward S, Geddes D, 1996, Assessment of oxygen supplementation during air travel, THORAX, Vol: 51, Pages: 202-203, ISSN: 0040-6376
Alton E, Geddes D, 1995, The prospects for gene therapy in cystic fibrosis., Curr Opin Pulm Med, Vol: 1, Pages: 471-477, ISSN: 1070-5287
Gene therapy provides the best prospect of a fundamental new treatment for cystic fibrosis. The lungs are the most important target, because this organ is the most severely affected by the disease and is also accessible for topical treatment. Advances in this field have been very rapid, and the prospects remain good although a number of problems need to be overcome. The two main approaches to gene transfer, namely adenoviruses and liposomes, are efficient in vitro, but early clinical trials have shown that they work less well in vivo. A number of proof of concept studies have shown that gene transfer is possible, but full functional correction of the cystic fibrosis defect has not yet been achieved. Adenoviruses have provoked an inflammatory response, and new viral vectors are being developed to overcome this. Existing lipids are relatively inefficient, but new liposomes are being developed to enhance gene transfer. Much work needs to be done to improve safety and efficacy of gene transfer before materials are ready for large scale clinical trials. However, progress is very rapid, and there is a real prospect of developing an effective gene therapy for cystic fibrosis within the next decade.
Ranasinha C, Assoufi B, Shak S, et al., 1993, Efficacy and safety of short-term administration of aerosolised recombinant human DNase I in adults with stable stage cystic fibrosis., Lancet, Vol: 342, Pages: 199-202, ISSN: 0140-6736
Chronic pulmonary infection is the major cause of morbidity and mortality in cystic fibrosis. High levels of DNA in the sputum make the sputum viscous and difficult to expectorate. Recombinant human deoxyribonuclease (rhDNase) in vitro has been shown to reduce the viscoelasticity of the sputum from CF patients. We have done a phase II double-blind randomised placebo-controlled trial in which patients received either 2.5 mg rhDNase twice daily or placebo for 10 days. All patients had forced vital capacity (FVC) above 40% predicted and were clinically stable. Patients were followed up for 42 days from the start of drug/placebo administration. All 71 randomised patients, aged 16-55, completed every aspect of the study and baseline characteristics were similar in the two groups. Baseline forced expiratory volume in one second (FEV1) was 46% of predicted for patients randomised to rhDNase, and 48% for those randomised to placebo; and baseline FVC was 76% of predicted for both groups. The mean percentage change in FEV1 from baseline was a 13.3% rise on rhDNase and a 0.2% fall on placebo (p < 0.001). FVC rose 7.2% in the rhDNase group and 2.3% in the placebo group (not significant). There were no life-threatening adverse events and no anaphylactic reactions. There was no significant difference in side-effects between the groups. This study confirms that short-term administration of rhDNase in stable patients with cystic fibrosis is safe and improves lung function.
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