Splenic cyst diagnosed by percutaneous needle aspiration and splenography. Report of a case.
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Abdominal Neoplasms↗
Biomedical subjects
K Akdamar
Publications and source records attributed to K Akdamar.
Congenital dilation of the intrahepatic bile ducts.
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Adult↗
Modification of galactosamine-induced liver injury in rats by reticuloendothelial system stimulation or depression.
The reticuloendothelial system has been implicated in galactosamine-induced liver injury because of a correlation between phagocytic alterations induced by colloidal carbon or endotoxin, and development of liver necrosis. To evaluate this concept, the influence of galactosamine on liver function and histology was determined in rats in which the reticuloendothelial system was normal, stimulated, or depressed. Methyl palmitate was used as a reticuloendothelial system suppressant, and glucan was used as a reticuloendothelial system activating agent. Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein. Histological studies revealed hepatic necrosis, and a polymorphonuclear and lymphocytic cellular infiltrate in galactosamine-treated rats. Pretreatment of rats with methyl palmitate inhibited galactosamine-induced alterations in serum glucose concentration, glutamic oxalacetic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammatory reactions were also reduced in methyl palmitate-treated galactosamine-injected animals. In contrast, activation of the reticuloendothelial system by glucan increased galactosamine-induced alterations in serum bilirubin, glucose and cholesterol concentrations, glutamic oxalacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammation were also increased. These findings suggest that the degree of galactosamine-induced liver injury is directly correlated with macrophage function when specific macrophage-modifying agents are used.
Animals↗
Effects of somatostatin and a somatostatin agonist on diet-induced pancreatitis in mice.
We examined the effects of somatostatin-14 and the potent somatostatin agonist (N-acetyl-[Des(Ala1,Gly2),p-Cl-Phe6,D-Trp8]-somatostatin amide) on choline deficient, ethionine enriched diet (CDED)-induced acute pancreatitis in mice. Serum amylase determinations were performed, and specimens from the pancreas were examined by light and electron microscopy. No significant beneficial effects of somatostatin or its agonist were found in this model of acute pancreatitis.
Acute Disease↗