Foams cells

CellgeometTy is governed predominantly by the final foam density and the external forces exerted on the cellular stmcture prior to its stabilization in the expanded state. In a foam prepared without such external forces, the cells tend to be spherical or ellipsoidal at gas volumes less than 70—80% of the total volume, and they tend toward the shape of packed regular dodecahedra at greater gas volumes. These shapes have been shown to be consistent with surface chemistry arguments (144,146,147). Photographs of actual foam cells (Fig. 2) show a broad range of variations in shape. 

Fig. 2ab. Photomicrographs of foam cell stmcture (a) extmded polystyrene foam, reflected light, 26 x (b) polyurethane foam, transmitted light, 26 x (c) polyurethane foam, reflected light, 12 x (d) high density plastic foam, transmitted light, 50x (22).

Density and polymer composition have a large effect on compressive strength and modulus (Fig. 3). The dependence of compressive properties on cell size has been discussed (22). The cell shape or geometry has also been shown important in determining the compressive properties (22,59,60,153,154). In fact, the foam cell stmcture is controlled in some cases to optimize certain physical properties of rigid cellular polymers. 

Probucol. Probucol is an antioxidant that is effective in lowering LDL cholesterol. Whereas probucol was known to lower cholesterol after relatively simple clinical trials (160), its mechanism of action as an antioxidant in the treatment of atherosclerosis is quite novel. Probucol has been shown to have the abiUty to produce regression of atherosclerotic lesions in animal models (161). Probucol therefore represents a novel class of pharmaceutical agent for the treatment of atherosclerosis. This effect occurs mechanistically, in part, by preventing oxidation of LDL, a necessary step in foam cell formation. This antioxidant activity has been shown in laboratory experiments and its activity in lowering LDL cholesterol in human studies is well documented (162). 

Wood, then, is a foamed fibrous composite. Both the foam cells and the cellulose fibres in the cell wall are aligned predominantly along the grain of the wood (i.e. parallel to the axis of the trunk). Not surprisingly, wood is mechanically very anisotropic the properties along the grain are quite different from those across it. But if all woods are made of the same stuff, why do the properties range so widely from one sort of wood to another The differences between woods are primarily due to the differences in their relative densities (see Table 26.1). This we now examine more closely. 

Macrophage/athero- t Reverse cholesterol transport from foam cells l Progression of atherosclerosis... 

Numbers without circles = largest foam cell size (pm) fEstimated... 

Figure 2. Results for emulsion and foam cell size in PS foam RSM experiment.

It is accepted that oxidation of LDL is a key event in endothelial injury and dysfunction. Oxidised LDL (oxLDL) may directly injure the endothelium and trigger the expression of migration and adhesion molecules. Monocytes and lymphocytes interact with oxLDL and the phagocytosis which follows leads to the formation of foam cells, which in turn are associated with the alteration of the expression pattern of growth regulatory molecules, cytokines and pro-inflammatory signals. The proposed role of oxLDL in atherogenesis, based on studies in vitro, is shown in Fig. 2.1. 

Fig. 2.1 Sequence of events in atherogenesis and role of low-density lipoprotein. Native LDL, in the subendothelial space, undergoes progressive oxidation (mmLDL) and activates the expression of MCP-1 and M-CSF in the endothelium (EC). MCP-1 and M-CSF promote the entry and maturation of monocytes to macrophages, which further oxidise LDL (oxLDL). Ox-LDL is specifically recognised by the scavenger receptor of macrophages and, once internalised, formation of foam cells occurs. Both mmLDL and oxLDL induce endothelial dysfunction, associated with changes of the adhesiveness to leukoc)des or platelets and to wall permeability.

KAPLAN M and AVIRAM M (1999) Oxidized low density lipoprotein atherogenic and proinflammatoiy characteristics during macrophage foam cell formation. An inhibitory role for nutritional antioxidants and serum paraoxonase Clinical Chemistry Laboratory Medicine 37,111-9,1. 

Brown, M. S. and Goldstein, J.L. (1980). The cholesteryl ester cycle in macrophage foam cells. J. Biol. Chem. 255, 9344-9352. 

It is unlikely that the damaging effects of ox-LDL are relevant only to the walls of blood vessels and there is no reason to suppose they are confined to one disease. The initial histopathologjcal sign of coronary heart disease is the appearance of the fetty streak on the luminal surfece of arteries. Fatty streaks are composed of aggregated macrophages that have taken up ox-LDL via the scavenger receptor. Recently, we have detected such foam cells in the rheumatoid synovium (Section 5.5). 

In atherosclerosis, ox-LDL is taken up ultimately by macrophages and smooth muscle cells in the arterial intima. Once loaded with lipid, these cells have a foamy appearance when examined histologically. The accumulation of these so-called foam cells in the artery wall leads to the formation of fatty streaks , which can lead to atheromatous plaque formation and consequent coronary heart disease. 

Winyard, P.G., Tatzber, F., Esterbauer, H., Kus, M.L., Blake, D.R. and Morris, C.J. (1993). Presence of foam cells containing oxidised low density lipoprotein in the synovial membrane from patients with rheumatoid arthritis. Ann. Rheum. Dis. 52, 677-680. 

Figure 12.7 Schematic diagram showing the role of LDL glycatlon and oxidation in foam-cell formation [adapted from Lyons (1991) and Esterbauer et al. (1992)]. C, cholesterol CE, cholesterol ester.

Dysfunction of the endothelium allows lipoproteins, predominantly low-density lipoprotein (LDL) cholesterol, and inflammatory cells, namely monocytes and T lymphocytes, to migrate from the plasma to the sub-endothelial space. Monocyte-derived macrophages ingest lipoproteins to form foam cells. Macrophages also secrete growth factors that promote smooth muscle cell migration from the media to the intima. A fatty streak consists of lipid-laden macrophages and smooth muscle cells and is the earliest type of atherosclerotic lesion. 

Lipid-laden macrophages, smooth muscle cells, and necrotic debris from the death of foam cells accumulate in the subendothelial space, leading to enlargement of the fatty streak. A collagen matrix forms a fibrous cap that covers the lipid core of the lesion to establish a fibrous plaque called an atherosclerotic plaque. Initially, the diameter of the coronary artery lumen is... 

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