Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha. [electronic resource]
Producer: 20070327Description: 381-90 p. digitalISSN:- 1524-4571
- Aorta
- Aortic Diseases -- etiology
- Apolipoprotein C-III -- metabolism
- Arteriosclerosis -- etiology
- Arteritis -- etiology
- Cell Adhesion -- drug effects
- Cell Adhesion Molecules -- metabolism
- Cells, Cultured -- drug effects
- Chylomicrons -- blood
- Dietary Fats -- administration & dosage
- E-Selectin -- biosynthesis
- Endocytosis
- Endothelial Cells -- drug effects
- Endothelium, Vascular -- cytology
- Fat Emulsions, Intravenous -- pharmacology
- Gene Expression Regulation -- drug effects
- Humans
- Hypertriglyceridemia -- blood
- Hypoglycemia
- Intercellular Adhesion Molecule-1 -- biosynthesis
- LDL-Receptor Related Protein-Associated Protein -- pharmacology
- LDL-Receptor Related Proteins -- drug effects
- Leukocytes -- cytology
- Lipopolysaccharides -- pharmacology
- Lipoproteins, HDL -- blood
- Lipoproteins, LDL -- blood
- Lipoproteins, VLDL -- blood
- Low Density Lipoprotein Receptor-Related Protein-1 -- drug effects
- Membrane Transport Proteins -- drug effects
- Models, Cardiovascular
- Monocytes -- cytology
- NF-kappa B -- metabolism
- Oxidative Stress
- Receptors, LDL -- drug effects
- Rheology
- Signal Transduction -- drug effects
- Triglycerides -- blood
- Tumor Necrosis Factor-alpha -- pharmacology
- Vascular Cell Adhesion Molecule-1 -- biosynthesis
- p38 Mitogen-Activated Protein Kinases -- metabolism
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Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
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