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Biomedical subjects

R J Hancox

Publications and source records attributed to R J Hancox.

22 records · Page 2Linked to original sources
PubMed1998

Polymorphism of the beta2-adrenoceptor and the response to long-term beta2-agonist therapy in asthma.

Polymorphisms affecting amino acids 16 and 27 of the beta2-adrenoceptor alter receptor regulation in vitro. Whether these polymorphisms alter the response to beta2-agonist therapy in asthma is unknown. In a previous study of 64 asthmatics, most experienced a deterioration in asthma control during regular inhaled beta2-agonist (fenoterol) treatment, while a minority improved. We have determined the beta2-adrenoceptor genotypes in these subjects, to establish whether changes in asthma control during the earlier study were influenced by beta2-adrenoceptor polymorphism. The genotypes coding for amino acids 16 and 27 were identified in 60 subjects using allele-specific polymerase chain reaction. The effects of regular beta2-agonist treatment on asthma control were compared between genotypes. There was no association between genotype and change in overall asthma control during regular beta2-agonist treatment. Only two of 10 markers of asthma control showed changes that were significantly associated with genotype: subjects homozygous for glycine at position 16 had no increase in bronchial responsiveness to methacholine during regular treatment; subjects homozygous for glutamic acid at position 27 had no increase in evening peak expiratory flow rates during regular treatment. These differences are the opposite of those that would have been predicted by the results of in vitro studies. In these subjects, the deleterious response to regular inhaled beta2-agonist treatment was not related to beta2-receptor polymorphism.

Administration, Inhalation↗
PubMed1997

The efficacy of inhaled corticosteroids in the management of non asthmatic chronic airflow obstruction.

AIMS: The aims of this investigation were to evaluate the efficacy of regular inhaled beclomethasone in the control of symptoms and lung function with non-asthmatic smoking related obstructive pulmonary disease and to evaluate the relationship between clinical responses to a short course of oral prednisone and longer term outcomes using inhaled steroid. METHODS: The study was a randomised, double blind, placebo controlled, crossover investigation in 18 patients. The active treatment was inhaled beclomethasone 1000 micrograms given twice daily for three months by metered dose inhaler. At the end of each treatment period, patients received oral prednisone 30 mg/day for ten days. The two treatment phases were separated by a one month washout interval. Peak flow rates, symptom scores and "rescue" bronchodilator use were recorded twice daily. Lung function (FEV1, FVC and lung volumes) and bronchial hyperresponsiveness (PC20 methacholine) were measured at monthly visits. The number of exacerbations requiring intervention therapy were also recorded. RESULTS: There were no consistent benefits attributable to beclomethasone. Lung function was not significantly better as a result of active treatment. Sputum production improved but other symptom scores were similar during active and placebo therapy. Three patients exhibited an increase in FEV1 of 15% or more during active treatment but did not do so when oral prednisone was administered immediately after the period of placebo treatment. A further three patients showed an improvement in FEV1 of 15% or more with oral prednisone but failed to improve during treatment with inhaled beclomethasone. The predictive value of the "trial of steroid" was 0% and 81.3% for positive and negative outcomes respectively. CONCLUSIONS: Our results indicate that in non-asthmatic chronic obstructive pulmonary disease inhaled corticosteroid fails to achieve significant improvements in either lung function or symptoms. The response to a "trial of steroid" using oral prednisone is not clinically helpful in selecting the small number of patients who may subsequently benefit from this form of therapy.

Administration, Inhalation↗
PubMed1987

Cortical generators of the CI component of the pattern-onset visual evoked potential.

Thirteen-channel visual evoked potentials (VEPs) to pattern-onset were recorded with stimuli restricted to individual octants of the peripheral field, to halves and to quadrants of the fovea. The voltage of the CI component was measured in each channel to define its topography for each stimulated sector. The potential fields so obtained were then analysed to find the orientation and location of a dipole that would produce a corresponding pattern of voltages at the scalp. The locations of the computed dipoles are consistent with the hypothesis that CI is generated in striate cortex. The computed locations and orientations are not compatible with alternative arrangements of sources in extrastriate cortex. A significant problem remains. If CI is indeed generated by the striate cortex then the orientation of the dipoles excited by stimulation of the peripheral field indicates that the cortex is surface negative. This leads to the prediction that foveal stimuli will elicit a CI which is negative at posterior electrodes. The experiments reported here confirm that CI is positive with such stimuli, and its source is calculated as a horizontal dipole with its positive pole oriented posterolaterally. Two possible explanations are considered for the reversed polarity of foveal CI: (a) that macropotentials associated with stimulation of the fovea are opposite in polarity from those associated with stimulation of the peripheral field; (b) that the foveal area of the retinotopic map extends into the lateral calcarine fissure with the effect that much of it faces in the reverse direction from the cortex at the pole.

Adolescent↗