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Journal articleTETLEY TD, DESAI R, HARWOOD JL, et al., 1977,
UTILIZATION OF (H-3)LEUCINE AND (C-14)HEXADECANOIC ACID BY ISOLATED PERFUSED RABBIT LUNG FOR BIOSYNTHESIS OF RADIOLABELED PULMONARY SURFACTANT
, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 5, Pages: 1310-1312, ISSN: 0300-5127- Author Web Link
- Cite
- Citations: 1
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Journal articleCAMPBELL EJM, DAVIS C, OPENSHAW P, et al., 1976,
DETERMINANTS OF RESIDUAL VOLUME IN NORMAL SUBJECTS
, CLINICAL RESEARCH, Vol: 24, Pages: A689-A689, ISSN: 0009-9279 -
Journal articleDAVIS C, OPENSHAW P, WOODROOF G, et al., 1976,
DETERMINANTS OF RESIDUAL VOLUME IN NORMAL SUBJECTS
, CLINICAL SCIENCE AND MOLECULAR MEDICINE, Vol: 51, Pages: P4-P4, ISSN: 0301-0538 -
Journal articleTETLEY TD, HEXT PM, RICHARDS RJ, et al., 1976,
CHRYSOTILE-INDUCED ASBESTOSIS - CHANGES IN FREE-CELL POPULATION, PULMONARY SURFACTANT AND WHOLE LUNG-TISSUE OF RATS
, BRITISH JOURNAL OF EXPERIMENTAL PATHOLOGY, Vol: 57, Pages: 505-514, ISSN: 0007-1021- Cite
- Citations: 68
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Journal articleRichards RJ, Hext PM, Desai R, et al., 1975,
Chrysotile asbestos: biological reaction potential.
, Inhaled Part, Vol: 4 Pt 2, Pages: 477-493, ISSN: 0301-1577Evidence is presented indicating that chrysotile asbestos induces rapid cellular ageing in lung fibroblast cultures. Depending on the dose of asbestos given to these cultures the formation of fibrous collagen is enhanced or suppressed. The reaction of chrysotile at the cellular and molecular level is discussed and is considered to be determined by the organic coating it receives or the manner in which the surface absorbed material is modified. Studies are included of the ability of chrysotile to adsorb and retain serum proteins, pulmonary surfactant and lysosomal enzymes. Finally, a critical appraisal is given of the theories accounting for chrysotile-induced fibrogenesis particularly related to the lung fibroblast system studied.
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Journal articleMcDermott M, Wagner JC, Tetley T, et al., 1975,
The effects of inhaled silica and chrysotile on the elastic properties of rat lungs; physiological, physical and biochemical studies of lung surfactant.
, Inhaled Part, Vol: 4 Pt 2, Pages: 415-427, ISSN: 0301-1577When rats breathed air containing approximately 70 mg m-3 of respirable crystalline silica 7 h daily for 10 days (2000 mg m-3 h) the surface tension forces of the alveolar lining film were reduced. This was shown both by surface tension measurements on lung extracts and by pressure-volume studies with air and saline filling of excised lungs. Larger quantities of inhaled silica produced similar effects. Chrysotile inhalation caused an even more marked decrease in the surface tension forces. In the chrysotile studies these findings were supported by biochemical estimations of the quantity of surfactant in the lungs, which was increased 10-fold by an inhalation of 6500 mg m-3 h. Electron microscopy showed an increased number of the type II alveolar cells which produce surfactant and of free phospholipid lattices in the air spaces of the lungs of rats exposed to chrysotile and silica. Both the surface tension and biochemical estimations on a control group of rats suggest that there is an increase in the amount of surfactant in the lungs up to about 12 months of age.
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Journal articleHARWOOD JL, DESAI R, HEXT P, et al., 1975,
CHARACTERIZATION OF PULMONARY SURFACTANT FROM OX, RABBIT, RAT AND SHEEP
, BIOCHEMICAL JOURNAL, Vol: 151, Pages: 707-714, ISSN: 0264-6021- Author Web Link
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- Citations: 101
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Patent,
Specific Inhibition of Gene expression by small double stranded RNAs
, PCT/US02/24226 -
Patent,
Specific Inhibition of Gene Expression by small double-stranded RNAs
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Patent,
Paramyoxovirus Vector for Gene transfer to the Cardiovascular System
, TOKUGAN 2000-339942 -
Patent,
Paramyoxovirus Vector for Gene Transfer to the Cardiovascular System
, TOKUGAN 2000-339942 -
Journal articleLalvani A, Newton P, Conlon CP,
Salmonella enteritidis and acute renal failure: Report of five cases and review
, INFECTIOUS DISEASES IN CLINICAL PRACTICE, Vol: 6, Pages: 193-195, ISSN: 1056-9103 -
Book chapterPérez-Gil J, Cruz A, Bernardino de la Serna J,
Lateral Membrane Structure and Lipid-Protein Interactions
, Springer Series in Biophysics, Publisher: Springer-Verlag, Pages: 127-140, ISBN: 3540284001 -
Journal articleLukacs KV, Pardo OE, Steel RM, et al.,
Cancer gene therapy with a heat shock protein gene
, CANCER GENE THERAPY, Vol: 4, Pages: 310-310, ISSN: 0929-1903 -
Journal articleBaussano I, Mercadante S, Lalvani A, et al.,
THE CONTROL OF TUBERCULOSIS AMONG MARGINAL IMMIGRANTS: A DYNAMIC APPROACH
, EPIDEMIOLOGIA & PREVENZIONE, Vol: 35, Pages: 105-105, ISSN: 1120-9763 -
Conference paperJohnston SL,
Impact of meal timing and frequency on nutrient utilization and metabolism: Adaptive implications
, Publisher: WILEY-BLACKWELL, Pages: 230-230, ISSN: 1042-0533 -
PosterPeel T, Jackson D, Johnston S, et al.,
IL-23, Increased In Asthmatics, Licences IL-17 Secretion In Response To Rhinovirus Infection
, American Thoracic Society 2014 International Conference: While the main axis of allergic inflammation in asthmatics has been considered Th2-driven eosinophilia and IgE, recentRATIONALEobservations have shown that, especially in moderate-to-severe asthmatics, IL-17 and neutrophils may also significantly contribute todisease. The cytokine IL-23, produced by dendritic cells and macrophages, is a main driver of IL-17 responses from T helper, γδ and innatelymphoid cells and has been shown to be increased in the serum of asthmatic subjects.The greatest clinical burden of asthma is associated with exacerbations, the majority of which are induced by rhinovirus. Rhinovirusinfection recruits significantly higher levels of neutrophils into the airways of asthmatics compared to healthy controls, which correlatewith loss of lung function. In addition, we have recently observed that IL-17 is higher in the airways of asthmatics both at baseline andfollowing experimental rhinovirus infection.We hypothesise that the presence of IL-23 drives IL-17 responses to rhinovirus, leading to increased neutrophilia andHYPOTHESIS:worsened lung function.: C57BL/6 mice were infected intranasally with rhinovirus serotype 1B. Neutrophils were recruited by 8 hoursMETHODS AND RESULTSand peaked at 24 hours, while CD4 IFNγ Th1 cells were recruited by day 7. Unlike in human subjects, no IL-17 responses to rhinovirus+ +were seen by ELISA, flow or qPCR. To investigate the effect of IL-23, infection was supplemented with 1µg of recombinant IL-23 (rIL-23).Alone, rIL-23 had no effect but elicited significant levels of IL-17 (mean 290pg/ml) and IL-17F (1917pg/ml) in the airways following arhinovirus infection. IL-17 secretion was associated with significant increases in airway neutrophilia (3-fold increase, <0.001). Additionally,Pinfection with rhinovirus caused increased persistence of rIL-23 in the airways 24 hours after infection compared to rIL-23 dosing alone (97vs. 660 pg/ml, <0.001).PIn the mouse, approximately two-thirds of &
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Journal articleLukacs KV, Steel RM, Oakley RE, et al.,
Cancer gene therapy with a heat shock protein gene
, CANCER GENE THERAPY, Vol: 4, Pages: O133-O133, ISSN: 0929-1903
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