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Biomedical subjects

L C Smith

Publications and source records attributed to L C Smith.

At least 217 records · Page 12Linked to original sources
PubMed1972

Hydrolysis of glyceryl tri(1- 14 C)octanoate and glyceryl tri(1- 14 C)oleate monolayers by postheparin lipolytic activity.

The hydrolysis of monomolecular films of glyceryl tri[1-(14)C]octanoate and glyceryl tri[1-(14)C]oleate has been demonstrated by measurement of the decrease in surface radio-activity that occurs in the presence of postheparin plasma. The hydrolysis displayed first order kinetics and was proportional to enzyme concentration over a 10-fold range. No hydrolysis was observed in the absence of enzyme, and only slight activity (1%) was found in plasma taken from subjects before heparin administration. The hydrolysis was stimulated to a variable extent by Ca(2+). The first product of hydrolysis of the monolayer was identified as 1,2-diglyceride, which was subsequently converted to 2-monoglyceride. Inhibition of triglyceride hydrolysis was observed when postheparin plasma was preincubated in 2 m NaCl, 10(-4) m protamine, 10 mm Na(4)P(2)O(7), and 0.1 m NaF. Monolayer techniques avoid some but not all of the problems associated with emulsified lipid substrates and appear to be applicable for study of post-heparin lipolytic activities.

Carbon Isotopes↗
PubMedDate not supplied

Lipopolysaccharide activates the sea urchin immune system.

Profilin is a small, actin-binding protein that functions at the intersection of signal transduction and cytoskeletal modifications. Increases in the number of profilin messages per cell correlate with sea urchin coelomocytes activation in response to injury. Here we show that coelomocytes respond to immune challenge from lipopolysaccharide with significant elevations in profilin transcripts per coelomyocyte.

Animals↗
PubMedDate not supplied

Echinoderm immunity and the evolution of the complement system.

Our understanding of inflammatory responses in humans has its roots in the comparative approach to immunology. In the late 1900s, research on echinoderms provided the initial evidence for the importance of phagocytic cells in reactions to foreign material. Studies of allograft rejection kinetics have shown that echinoderms have a non-adaptive, activation type of immune response. Coelomocytes mediate the cellular responses to immune challenges through phagocytosis, encapsulation, cytotoxicity, and the production of antimicrobial agents. In addition, a variety of humoral factors found in the coelomic fluid, including lectins, agglutinins, and lysins, are important in host defense against pathogens and other foreign substances. Recently, a simple complement system has been identified in the purple sea urchin that is homologous to the alternative pathway in vertebrates. The sea urchin [corrected] homologue of C3, is inducible by challenge with lipopolysaccharide, which is known to activate coelomocytes. Complement components have been identified in all vertebrate classes, and now have been characterized in protochordates and echinoderms indicating the primordial nature of the complement system. Because it is thought that the complement system evolved from a few primordial genes by gene duplication and divergence, the origin of this system appears to have occurred within the common ancestor of the deuterostomes.

Animals↗
PubMedDate not supplied

Enhanced hepatic uptake and processing of cholesterol esters from low density lipoprotein by specific lactosaminated Fab fragments.

Reduction of the blood levels of low density lipoprotein (LDL) is important for lowering the incidence of atherosclerosis. In this study, LDL was directed to rat parenchymal liver cells by lactosaminated Fab fragments of anti-apolipoprotein B antibodies (LacFab). We followed the fate of intravenously injected complexes of LacFab and [3H]cholesteryl oleate-labeled LDL. Complexing of LacFab to LDL led to rapid disappearance of LDL from the circulation. At 30 minutes after injection, the liver contained 58.5 +/- 9.0% of the injected dose (at that time the liver contained only 5.7 +/- 2.2% of an injected dose of free LDL). Liver uptake was blocked by N-acetylgalactosamine but not by N-acetylglucosamine, which indicates that galactose-specific recognition sites are responsible for the LacFab-induced hepatic uptake. By isolating liver cells, it was found that parenchymal, endothelial, and Kupffer cells account for 87%, 3%, and 10% of the total hepatic uptake, respectively. Subcellular fractionation of the liver indicated that the complexes are rapidly internalized and transported to lysosomes. Within 1 hour after injection, virtually all the [3H]cholesteryl oleate of the internalized LDL was hydrolyzed; hydrolysis was followed by excretion of radioactivity into the bile. Compared with rats injected with native [3H]cholesteryl oleate-labeled LDL, eight times as much radioactivity was excreted into the bile during the first 4 hours after the injection of LacFab-complexed [3H]cholesteryl oleate-labeled LDL. Thus, LacFab induces enhanced hepatic uptake of LDL via galactose receptors on the parenchymal cells, followed by processing in lysosomes and excretion into the bile. In this way, LacFab induces an increased irreversible removal of LDL cholesterol from the body.

Amino Sugars↗