Search PubMed⌕ Search

Biomedical subjects

B J Sweetman

Publications and source records attributed to B J Sweetman.

80 records · Page 5Linked to original sources
PubMedDate not supplied

Occupational hazards and low back pain.

In a cross-sectional study of 2684 males from a range of occupations the prevalence rate for back pain was 20% (11% disc disease and 9% undetermined pain) and about half of these had pain related to the lower back with the remainder being located in the dorsoscapular or cervical regions. Follow up study of a cohort of 1249 of these workers over a two year period indicated that the incidence rate of low back pain in that group was about 1% per annum. When sickness absence certificates were studied the annual absence from back pain (all sites) was 1323 days per thousand employees. However, when confirmation was obtained from general practitioners about non-specific rheumatic diagnoses this figure rose to 1707 days. The prevalence of disc disease is higher among those engaged in heavy rather than among those in light work, and also among those required to adopt a chronic stooping posture at the place of work. A device designed to record lumbar EMG, antero-posterior and lateral posture of the lumbar spine and intra-abdominal pressure designed to be used in work places over a complete shift is described and traces obtained under laboratory conditions are presented.

Absenteeism↗
PubMedDate not supplied

Metabolism of procainamide to a hydroxylamine by rat and human hepatic microsomes.

We have previously demonstrated that procainamide is oxidized to a reactive metabolite. We speculated that this reactive metabolite might be a hydroxylamine and further that it might be responsible for the syndrome of procainamide-induced lupus. We now report that procainamide is metabolized to a hydroxylamine by rat and human hepatic microsomes. The extent of this metabolic oxidation was quantitated by HPLC after conversion of the hydroxylamine to the more stable nitro derivative of procainamide. Formation of the hydroxylamine required NADPH, active microsomes, and oxygen and was inhibited by carbon monoxide, SKF 525-A, and cimetidine. Formation of the hydroxylamine was also studied as a function of time, microsomal protein concentration, and procainamide concentration.

Adult↗
PubMedDate not supplied

Metabolism of procainamide in the perfused rat liver.

We have previously produced evidence that procainamide forms a reactive metabolite. This study of the metabolism of procainamide in a perfused rat liver was aimed at providing clues to the identity of this reactive metabolite. Several metabolites were found that had not been previously described and three of these were identified. Probably the most significant of these metabolites is the phenol, N-acetyl-3-hydroxyprocainamide. This phenol could have been formed from either a hydroxylamine or an arene oxide intermediate and either of these could represent a reactive metabolite. In contrast to the metabolism of procainamide, the phenol metabolite, N-acetyl-3-hydroxyprocainamide, is not formed in significant quantities from N-acetylprocainamide. This implies that oxidation of procainamide to 3-hydroxyprocainamide precedes acetylation to give N-acetyl-3-hydroxyprocainamide. As N-acetylation of procainamide decreases both its toxicity and the formation of the oxidative phenol metabolite, among the hypotheses to be explored is relationship between the formation of the phenol metabolite and the toxicity of procainamide. The other metabolites that were identified were N-acetylprocainamide N-oxide and N-acetyl-4-aminohippuric acid.

Acecainide↗