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Biomedical subjects

D S Harry

Publications and source records attributed to D S Harry.

31 records · Page 2Linked to original sources
PubMed1977

Screening for liver disease in vinyl chloride workers.

Following the occurrence of hepatic fibrosis and angiosarcoma in polyvinyl chloride autoclave workers, a screening programme was set up for workers at risk in a large production plant. There was no significant difference in liver function tests between workers and a control group of men in the same factory, not exposed to vinyl chloride. Four exposed workers out of 422 were found to have enlarged spleens compared with none out of 202 controls. Liver biopsies from selected cases showed no significant pathological changes, although there was minimal increase in portal tract and sinusoidal fibrosis in exposed workers.

Adult↗
PubMed1971

Cholesterol biosynthesis in transplantable hepatomas: evidence for impairment of uptake and storage of dietary cholesterol.

Cholesterol feeding inhibits cholesterol biosynthesis in normal but not in malignant liver tissue. It has been postulated that hepatomas have suffered a specific intracellular deletion of the cholesterol feedback control mechanism, but there is little direct evidence to support this hypothesis. Rats bearing Morris transplantable hepatomas were fed high cholesterol diets for periods of up to 21 days. Cholesterol biosynthesis, as expected, was suppressed in the normal liver but not in hepatomas. The livers accumulated large amounts of cholesteryl ester but the hepatomas showed little or no increase in ester content. Cholesterol-1alpha-(3)H was administered intragastrically to other tumor-bearing rats. Uptake of radioactivity by the tumors was much slower than by normal liver. Comparison of the specific activities of liver and tumor cholesterol with that of the plasma suggested that the liver took up dietary cholesterol selectively from the blood, while the appearance of radioactivity in the tumors could be explained by slow equilibration with plasma cholesterol. Our results suggest that the insensitivity of cholesterol biosynthesis to dietary cholesterol in hepatomas could be explained by an impairment in the uptake and storage of dietary cholesterol and that the concept of an intracellular deletion of the feedback mechanism requires further evidence.

Acetates↗
PubMedDate not supplied

Plasma lipid and lipoprotein response to fat feeding in alcoholic liver disease.

Serum lipids and lipoproteins were analyzed after an overnight fast, and following a fatty meal in 10 patients with cirrhosis, 5 with fatty liver, and 5 normal subjects. Cirrhotic patients were divided into two groups of five on the basis of serum lecithin-cholesterol acyltransferase activity. Fasting triglyceride levels were similar in all four groups. In all but cirrhotic patients with low lecithin-cholesterol acyltransferase activity, most fasting triglyceride was found in very low density lipoproteins; in the latter group, most of it was found in low density lipoproteins. We confirmed that patients with fatty liver have a higher serum triglyceride response to fat feeding than normal subjects, but we did not find higher levels in cirrhotic patients. Cirrhotic patients with "normal" lecithin-cholesterol acyltransferase activity had a normal triglyceride response to dietary fat. In patients with cirrhosis and low lecithin-cholesterol acyltransferase activity, the increase in triglyceride was less than in normal subjects. In this group, most of the extra triglyceride was carried in low density lipoprotein, and not in chylomicrons and very low density lipoprotein, as in the other groups.

Adult↗