Health hazards of work on visual display units (VDUs).
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Biomedical subjects
Publications and source records attributed to K T Tan.
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Familial porphyria cutanea tarda (PCT) is a photocutaneous disease in which subnormal activity of uroporphyrinogen decarboxylase is observed both in the liver and red cells. Hepatic iron plays a key role in the genesis of overt biochemical and clinical PCT. In this report, we have studied the properties of 10 000-fold purified erythrocyte uroporphyrinogen decarboxylase preparations from two familial PCT patients and a non-porphyric control subject. The apparent Michaelis constants (Km), determined by using uroporphyrinogen III substrate, were approx. 3.2-times higher for the enzyme from the diseased subjects (Km = approximately 1.0 microM) as compared to the normal (Km = 0.3 microM). Though both abnormal and normal enzymes were inhibited progressively with increasing concentrations of iron, the enzymes from diseased subjects exhibited greater susceptibility e.g. 0.1 mM Fe2+ inhibited the former about 50% and the latter about 20%. These observations suggest that the inherent biochemical defect in PCT is the reduced enzyme-substrate affinity and the intrinsic abnormal conformation renders the PCT enzyme particularly susceptible to inhibition by iron.
We describe the methodology used for quantifying and characterizing porphyrins in various tissues and in excreta, in the diagnosis and monitoring of the therapeutic modulation of biochemical disease activity in a 53-year-old white man who has a rare form of familial porphyria cutanea tarda with bone marrow rather than hepatic expression of the disease. Liquid-chromatographic and thin-layer chromatographic analyses of the patients's urine and skin showed predominantly heptacarboxylic porphyrin and uroporphyrin, whereas his stool and bile contained isocoproporphyrin and coproporphyrin as the major products. The data reflect defective uroporphyrinogen decarboxylation. Both analytical methods gave quantitatively similar results for urinary and fecal porphyrins. A triple-lumen perfusion study of samples procured both at the ampulla of Vater and 15 cm downstream provided data for porphyrins excreted in the bile and their reabsorption in the small intestine. We evaluated: suppression by hypertransfusion of bone marrow overproduction of porphyrins and reduction of enteral absorption of porphyrins by orally administered charcoal (Acta Char) and cholestyramine.
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The extent of cadmium exposure was studied in a cadmium-nickel battery factory and 8 PVC factories using cadmium stabilisers in the compounding of PVC. A total of 101 cadmium-exposed workers and 21 control subjects matched by sex, age, ethnic group and smoking history was investigated. Blood and urine cadmium levels were considerably elevated in the battery workers but were not raised in the PVC workers. These findings were consistent with the results of cadmium-in-air assessments. Among the female battery workers, urine cadmium excretion increased significantly with employment time. There was good correlation between blood and urine cadmium levels among the female subjects. A significant association between blood cadmium levels and prevalence of chest pain was also noted among the females. No low molecular weight proteinuria was detected, but two female battery workers had slight albuminuria and one male PVC worker had glucosuria but had abnormal GTT results.
118 patients with carcinoma of the lung seen in the Department of Cardiovascular and Thoracic Surgery, Tan Tock Seng Hospital, Singapore were followed for five years. The aim was to determine the survival of these patients in relation to the stage of the disease as well as the histologic type of carcinoma. 22 patients were in stage 1, 13 in Stage II and 83 in Stage III. Thoracotomy was performed in 62 patients and the rest had biopsy of distal lymph nodes. 43.3% of the carcinoma were squamous cell, 25% adenocarcinoma, 27% large cell, anaplastic, 2.9% oat cell and 1.8% bronchoalveolar cell carcinoma. Survival of the patients were found to be closely related to stage of the disease but not with the histologic type.
Over the last three decades there has been a world-wide decline in the incidence and severity of rheumatic fever and rheumatic heart disease, but the death rate in Singapore from chronic rheumatic heart disease has risen from 3.6 per 100,000 population in 1966 to 4.4 per 100,000 in 1977. Valvular lesions from rheumatic heart disease are very common, and between 1967 to 1979, 715 surgical procedures were performed for rheumatic valvular disease, and of these, 654 procedures involved the mitral valve which was most commonly affected by the disease process. Since many of the patients were female and in the child-bearing age, conservative procedures on the mitral valve were performed whenever possible. Mitral valvotomy for mitral stenosis relieved symptoms effectively; and for restenosis of the mitral valve, more than half of the patients underwent a second valvotomy with functional improvement. Mitral valve replacement was reserved for the severely distorted valve, sometimes calcified, and where there was stenosis associated with incompetence. Between 1971 to 1979, 162 mitral valves were replaced and actuarial studies showed 80% survival five years after surgery. 30 aortic and mitral valve replacements were performed in this same period with an operative mortality of 16.7%. Only 75 aortic valves were replaced for rheumatic valvular disease and 14 of these also had associated mitral and triscuspid valve disease. The prosthetic valves commonly used for replacement were the Starr-Edwards non-cloth covered valves, models 6120 and 1260. All patients that had valve replacements were treated with long-term anticoagulation with Warfarin. The incidence of thromboembolism was low, being 8% for mitral valve replacement and the majority of these episodes occurred in the first three months after surgery.
Symptomatic ventricular septal defects in infants who responded poorly to intensive medical therapy require surgical intervention. This paper aims to compare the results of the two stage approach of initial pulmonary artery banding followed by debanding and ventricular septal defect closure with primary intracardiac repair in infancy. Thirty-six infants underwent pulmonary artery banding between 1968-1979 with two operative deaths (5.6%). Eighteen patients underwent pulmonary artery debanding and closure of ventricular septal defect between 1971-1979 with five operative deaths (25.6%). However during 1978-1979 ten patients underwent 2nd stage repair with no operative death. During the same period primary intracardiac repair in infancy was carried out in nine infants with three operative deaths (33.3%). There appears to be still a place for two stage treatment of symptomatic ventricular-septal defect in critically ill infants certain situation.
Four hundred and twenty-five patients underwent mitral valvotomy between 1960 and 1979, the majority by the closed method. Thirty-two patients required another operation for mitral restenosis. There was high incidence of reoperation after the 6th and 7th years (23.3%) and after the 9th and 10th years (26.4%) postoperatively. Sixteen patients (47%) with restenosis underwent a second closed mitral valvotomy with a satisfactory result, 12 patients (35.4%) required valve replacement, and 6 patients (17.6%) had an open valvotomy. Another valvotomy for pure mitral restenosis can give satisfactory results, but where the valve is severely deformed or incompetent, valve replacement is preferred.
Three groups of patients are identified in the series of secumdum atrial septal defect with left axis deviation in an analysis of 910 patients of secundum atrial septal defect with or without other accompanying anomalies: 1) 12 patients with isolated ostium secumdum defect; 2) 5 patients with associated prolapse of posterior leaflet of the mitral valve; 3) 4 patients with associated hypertrophic cardiomyopathy and/or single (left) coronary artery. The findings of these 21 patients with proved secumdum atrial septal defect are analysed. The combination of such anomalies should be considered in the differential diagnosis of primum endocardial cushion defect from the electrocardiographic viewpoints.
Genes play a very important role in the etiology of hypertension. This paper reviews the current pool of candidate genes for human hypertension. Some of the genes studied in rat models of hypertension are also discussed. The methods for studying the genetics of hypertension are reviewed. A discussion of the role of cardiac gene libraries and gene databases in the characterization of cardiovascular disease is also included. This review is concluded by a discussion on the future role of genomics and cardiovascular gene databases in medical research.
A simple and sensitive method for determining urinary cyclohexanol, the main metabolite of cyclohexanone, by hydrolysis and gas chromatography (GC) with a flame ionization detector was developed. A 2-mL urine sample was hydrolyzed with 0.4 mL of concentrated HCl and followed by extracting twice with diethylether. Two microL of the filtrate was injected into the GC with a methyl silicone column. The detection limit is estimated to be 0.4 mg/L. The coefficient of variation for the procedure is 8% and 10% for the range of concentration 5 and 50 mg/L, respectively. The within-run variation was 5.4% and between-day variation was 9.67%. The method was verified with urine samples collected from workers exposed to cyclohexanone. An excellent correlation (r = 0.88) was observed between environmental cyclohexanone exposure and cyclohexanol in urine. The procedure is relatively simple and reproducible and it can be applied for occupational health measurement of cyclohexanone exposure.