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Biomedical subjects

S M Sabesin

Publications and source records attributed to S M Sabesin.

At least 55 records · Page 3Linked to original sources
PubMed1981

Double-blind multicenter comparison of 1,200 mg. and 1,000 mg. cimetidine in hospitalized and ambulatory duodenal ulcer patients.

A multicenter double-blind study was made to compare whether 1,000 mg dosage of cimetidine, the dose commonly employed in the United Kingdom, was as effective as the 1,200 mg. dose recommended in the United States for the treatment of duodenal ulcer. Our second goal was to test whether hospitalization would enhance the efficacy of cimetidine in the healing of duodenal ulcer. There was no difference in healing rate after either one (40%) or four (86%) weeks of therapy. In addition, hospitalization (one week) did not enhance the efficacy of cimetidine therapy.

Adult↗
PubMed1980

Lipoprotein metabolism in liver disease.

In this review we have endeavored to emphasize the central role of the liver in normal lipoprotein metabolism and to demonstrate how derangements in these metabolic processes can lead to abnormalities characteristic of liver disease. Since changes in the concentration and composition of plasma lipids and lipoproteins occur frequently in liver disease, these findings may be useful in following the clinical course of patients with liver disease of various causes. It should be emphasized that elevated plasma triglycerides and cholesterol are due to underlying defects in lipoprotein metabolism and should not be confused with primary hyperlipidemia. Impaired cholesterol esterification, abnormal lipoprotein electrophoretic patterns and lipoprotein compositional changes, all reflect abnormalities of lipoprotein metabolism that are secondary to hepatocellular injury or cholestasis. These abnormalities are very sensitive indicators of fundamental metabolic defects that are related in part to LCAT and apoprotein activator deficiencies, impaired H-TGL and LPL activity and, perhaps, defective remnant lipoprotein clearance by the liver. Since these abnormalities tend to improve with clinical recovery they have proved to be reliable and sensitive indicators of hepatic function and thus, are useful in the assessment of liver disease.

Cholestasis↗
PubMed1977

Hepatic triglyceride lipase deficiency in liver disease.

The activity of post-heparin lipases in patients with alcoholic hepatitis and viral hepatitis was evaluated. Lipoprotein lipase and hepatic triglyceride lipase were differentiated by assay under high and low salt conditions and also by separation on heparin-agarose affinity chromatography columns. The mean activity of hepatic triglyceride lipase in the sera of liver disease patients was only 21-24% of the mean of controls, but lipoprotein lipase in patients' sera was not different from normal levels. Hepatic triglyceride lipase deficiency may partially account for the accumulation of a triglyceride-rich low density lipoprotein in liver disease.

Alcoholism↗
PubMed1977

Abnormal plasma lipoproteins and lecithin-cholesterol acyltransferase deficiency in alcoholic liver disease.

Serial studies of plasma lipids and lipoproteins were performed in 4 patients with acute alcoholic liver disease characterized by a massive fatty liver and laboratory evidence of intrahepatic cholestasis. There were striking alterations in the plasma lipoprotein electrophoretic patterns characterized by the absence of alpha- and pre-beta-lipoprotein bands and the presence of a single band of abnormal mobility. These changes were associated with an extreme decrease in plasma lecithin-cholesterol acyltransferase activity, resulting in greatly reduced levels of plasma cholesteryl esters and increased levels of unesterified cholesterol. In 2 patients hypertriglyceridemia and hypercholesterolemia were present, the latter because of an increase in unesterified cholesterol. Lipoproteins were isolated from the plasma by sequential ultracentrifugation at the densities used for separation of normal very low density, low density, and high density lipoproteins; however, the patients' lipoproteins were different from normal in lipid composition and ultrastructure. All of the lipoprotein fractions were decreased in cholesteryl esters and the major lipoprotein was a triglyceride-rich low density lipoprotein. Electron microscopic studies of the low and high density lipoprotein fractions revealed the presence of bilamellar vesicles and stacked discs. All of the changes in lipoprotein composition and ultrastructure gradually returned to normal with clinical improvement. These observations indicate that alcoholic liver injury is associated with profound alterations in lipoprotein composition and metabolism which may be related in part to lecithin-cholesterol acyltransferase deficiency.

Acyltransferases↗
PubMed1977

Electron microscopic studies of the assembly, intracellular transport, and secretion of chylomicrons by rat intestine.

A detailed ultrastructural investigation of the assembly, intracellular transport, and secretion of chylomicrons by rat proximal jejunal intestinal cells was performed in rats fed corn oil. Following fat feeding the smooth endoplasmic reticulum of the absorptive cells becomes laden with triglyceride droplets which are transported through channels of the endoplasmic reticulum to the Golgi apparatus. The Golgi zones become extremely prominent due to the accumulation of osmiophilic droplets, similar in size and configuration to chylomicrons, within proliferated Golgi vesicles. Golgi-derived secretory vesicles, containing nascent chylomicrons, migrate towards the lateral cell membrane. The secretory vesicle membranes fuse with the lateral plasmalemma and nascent chylomicrons are then discharged into the intercellular spaces. Alterations of specific domains of the secretory vesicles were prominent, appearing as coated pits. Coated pits were apparent in the lateral plasmalemma in areas of active chylomicron exocytosis suggesting their derivation from secretory vesicle-membrane fusion. Chylomicrons, within the intercellular spaces, pass through the basement membrane that lines the basal surfaces of the epithelial cells, traverse the cellular elements of the lamina propria, and finally gain access to the lymphatics entering these channels through gaps between adjacent endothelial cells. These observations indicate that nascent chylomicrons accumulate within Golgi vesicles as a pre-requisite to secretion and that secretion occurs by exocytosis resulting in the release of nascent chylomicrons from secretory vesicles.

Animals↗