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Cervical spine tensile stiffness-to-failure and load-to-failure increased nonlinearly, whereas normalized displacement at failure decreased nonlinearly, from birth to adulthood. Pronounced ligamentous laxity observed at younger ages in the O-C2 segment quantitatively supports the prevalence of spinal cord injury without radiographic abnormality in the pediatric population. This study provides important and previously unavailable data for validating pediatric cervical spine models, for evaluating current scaling techniques and animal surrogate models, and for the development of more biofidelic pediatric crash test dummies.

Abstract-We tested the hypotheses that vascular cell adhesion molecule-1 (VCAM-1) expression on endothelium at lesion-prone sites in the rabbit aorta correlates with exposure to plasma cholesterol and that macrophage accumulation is associated with endothelial cells expressing VCAM-1. After rabbits were fed 0.25% cholesterol for 2 weeks, VCAM-1 expression was selectively increased at the distal and lateral portions of the major abdominal branches. In the arch and the celiac, superior mesenteric, and renal artery branches, VCAM-1 expression was positively correlated with the plasma cholesterol integrated over the duration of the experiments. After 2 weeks of cholesterol feeding, more macrophages were present around distal and lateral portions of the intercostal arteries and major abdominal branches relative to nonbranch regions. In the arch and around the intercostals and major abdominal branches, macrophage densities were positively correlated with the integrated plasma cholesterol. VCAM-1 and macrophage levels were correlated in lesion-prone regions. In normocholesterolemic rabbits, 23Ϯ4% (meanϮSEM) of the macrophages were directly associated with VCAM-1-positive endothelium. After 2 weeks of 0.25% cholesterol feeding, the association increased to 37Ϯ4% (PϽ0.015). Associations were highest around the lateral and distal regions of the major abdominal branches. These results suggest that (1) KeyWords: atherosclerosis Ⅲ endothelium Ⅲ monocyte Ⅲ hypercholesterolemia M acrophage and LDL accumulation in the arterial intima is the earliest event during atherogenesis. Before the first visible lesions appear around the lateral and distal portions of arterial branches in hypercholesterolemic animals, 1 lesion-prone sites differ from other arterial regions. In normocholesterolemic animals, lesion-prone regions exhibit elevated permeability to macromolecules. Within 2 weeks after onset of a hypercholesterolemic diet, lipoprotein and cholesterol accumulation begins and monocytes attach to endothelial cells. [1][2][3] Monocyte adhesion to endothelium is stimulated by the expression of adhesion molecules on the endothelium, such as VCAM-1, 4 -8 E-selectin, 6 P-selectin, 7-9 intercellular adhesion molecule-1 (ICAM-1), 8 and, a recently discovered glycoprotein, vascular monocyte adhesion-associated protein (VMAP-1). 10 Considerable interest exists in the role of VCAM-1 that is specific for monocytes and leukocytes. 4 Shortly after onset of a hypercholesterolemic diet, rabbits express VCAM-1 in the ascending aortic arch, 5 around the intercostal arteries, 7 and throughout the abdominal and thoracic aortas. 5 VCAM-1 expression appeared to precede macrophage accumulation. 5,7 Adhesion receptor expression and monocyte adhesion are affected by the local fluid dynamics 11 as well as normal 12 or oxidized 13 LDL.In the normal rabbit, the density of intimal macrophages is higher in the arch and around the lesion-prone regions of major orifices in the abdominal aorta than in nonbranch regions of the aorta. 14 In rabbits fed a hyperchol...