"The Tobacco Products Research Trust 1982-1996".
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Biomedical subjects
Publications and source records attributed to P Froggatt.
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For more than 20 years there has been a coherent programme of product modification in the UK, involving the introduction of low tar brands of cigarettes and the gradual reduction in average tar yields over the whole range of manufactured cigarettes. The sales-weighted average tar yield has declined from 20.8 mg/cigarette in 1972 to 11.0 mg/cigarette in 1993. To some extent potential benefits to established smokers have been offset by their tendency to 'compensate' for reduced nicotine yields. Investigating such aspects has formed one part of a wide-ranging research programme to monitor effects of modified products on health. Collectively the studies show benefits in terms of smoke intake and health outcome related to reduced tar cigarettes, but the success achieved in reducing average tar yields and narrowing the range has limited opportunities to detect differential effects.
Thomas Ferrar was the second professor of surgery in the short-lived (1835-1849) medical school of the Royal Belfast Academical Institution. Appointed on 5 July 1836 he failed to turn up for the winter session and was accordingly discharged on 29 November. He died in Sligo in the following June aged 39. Nothing has been written about Ferrar who survives as a mere foot-note in Belfast medical history. The events leading to his dismissal are, however, unusual, equivocal, and worth recounting. The facts suggest that the Institution was clearly justified in its action but that Ferrar emerges with some credit for a certain if misplaced high-mindedness though overshadowed by his patent derelictions.
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Eight patients (different families) with syncopal attacks and a long QT interval in the ECG died suddenly. Five heard normally and three were born deaf. At postmortem examination of all eight hearts the single consistent abnormality was focal neuritis and neural degeneration within the sinus node, A-V node, His bundle and ventricular myocardium. Although the etiology of this intracardiac neural disease is uncertain, a chronic viral infection or some noninfectious degenerative process are among the plausible causes discussed. If intracardiac neuritis and neural degeneration prove to be a prevalent finding among other victims dying from the long QT syndromes, further consideration should be given to whether there is any genuine hereditary component in the pathogenesis. Because of the asymmetrical and focal distribution of the cardioneural lesions, the response to present forms of medical or surgical treatment of the lung QT syndromes may vary from benefit to harm. Until more is known of the true etiology of the neural disease, treatment will probably remain empirical in nature and should be conducted with cautious clinical observation.