Incubation of mouse peritoneal macrophages with very low density lipoproteins (VLDL) from normal rats or rhesus monkeys markedly increased the levels of intracellular triglycerides by 10- to 56-fold and was accompanied by the production of oil red O positive vacuoles. The stimulation of triglyceride accumulation in macrophages was time- and concentration-dependent and was specific for VLDL. Three possible mechanisms for the VLDL-stimulated triglyceride accumulation in macrophages were explored: receptor-mediated uptake, action of lipoprotein lipase, and phagocytosis. Macrophage uptake and degradation of 125I-monkey and rat VLDL demonstrated saturable and nonsaturable components. Uptake of 125I-VLDL could be inhibited by unlabeled normal VLDL, although hyperlipemic VLDL was more effective. HDL did not compete to a significant extent. Heparin released lipoprotein lipase-like activity from peritoneal macrophages. Addition of heparin with VLDL resulted in a greater, more rapid elevation in intracellular triglycerides, which was partially inhibited by albumin. Free fatty acid and Intralipid also produced triglyceride accumulation in macrophages. The data showed that all three of the mechanisms examined could contribute to the metabolism of VLDL by macrophages and cause the production of triglyceride-rich cells with a "foamy" appearance, although the evidence suggested that the action of lipoprotein lipase was probably the most important in this process.

Animals↗

PubMedDate not supplied

CT evaluation of gastric cancer: depth of tumor invasion and pancreas invasion.

PURPOSE: To compare the internal structure of tumor and the contiguous organ configuration on computed tomography (CT) with the depth of tumor invasion on the pathological specimen. METHODS: Sixty-four gastric cancers depicted on incremental dynamic CT were classified according to the internal structure of the tumor, and correlated with the depth of tumor invasion. In addition, the cancers were classified according to the contiguous pancreatic configuration, and correlated with the degree of pancreatic invasion. RESULTS: Eleven tumors with thickened gastric wall consisting of both a thick inner layer of high attenuation and a thin outer layer of low attenuation (two-layered tumor with a thin outer layer) did not invade the serosa: mucosa (n = 5) and submucosa (n = 6). Of 59 gastric cancers with a regular margin to the contiguous pancreas, pancreatic invasion was absent in 58 and present in one. Pancreatic invasion was present in all of five gastric cancers with an irregular margin. CONCLUSIONS: Our results indicate that two-layered gastric tumors with a thin outer layer never invade the serosa. Furthermore, pancreatic invasion is predicted only when the margin of the contiguous pancreas is irregular.

Adult↗