Enhanced echo intensity (EI) on an ultrasound image of skeletal muscle indicates changes in muscle quality, including increases in intramuscular fibrous and adipose tissues. However, it is not known whether muscle quality assessed from the EI of computer-aided gray-scale analysis of an ultrasound image is associated with the muscle strength or body composition of a subject. The objectives of this study were to investigate whether muscle quality assessed from EI measured using gray-scale analysis is associated with muscle strength independently of age or muscle thickness (MT), and to examine the relationship between muscle EI and body composition. Ninety-two healthy women with a mean age of 70.4 ± 5.5 years (range, 51-87 years) dwelling in Kyoto, Japan, participated in the study. The MT, subcutaneous fat thickness (FT), and EI of the quadriceps femoris on the right extremity were assessed from transverse ultrasound images. Knee extensor isometric strength was used as a measure of the quadriceps femoris muscle strength. EI was significantly correlated with quadriceps strength independently of age or MT, and stepwise regression analysis revealed that MT and EI were independently associated with quadriceps strength. Importantly, EI showed no significant correlations with FT, percentage of body fat (%BF), or body mass index (BMI), while FT, BMI, and %BF did not significantly influence muscle strength. These data suggest that muscle quantity (i.e., MT) and muscle quality assessed from EI measured using computer-aided gray-scale analysis independently contribute to muscle strength in middle-aged and elderly persons.

These results suggest that lipid lowering with HMG-CoA reductase inhibitors alters plaque biology by reducing proliferation and activation of macrophages, prominent sources of molecules responsible for plaque instability and thrombogenicity.

Long-term solid-organ allografts typically develop diffuse arterial intimal lesions (graft arterial disease; GAD), consisting of smooth-muscle cells (SMC), extracellular matrix and admixed mononuclear leukocytes. GAD eventually culminates in vascular stenosis and ischemic graft failure. Although the exact mechanisms are unknown, chronic low-level alloresponses likely induce inflammatory cells and/or dysfunctional vascular wall cells to secrete growth factors that promote SMC intimal recruitment, proliferation and matrix synthesis. Although prior work demonstrated that the endothelium and medial SMCs lining GAD lesions in cardiac allografts are donor-derived, the intimal SMC origin could not be determined. They are generally presumed to originate from the donor media, leading to interventions that target donor medial SMC proliferation, with limited efficacy. However, other reports indicate that allograft vessels may contain host-derived endothelium and SMCs (refs. 8,9). Moreover, subpopulations of bone-marrow and circulating cells can differentiate into endothelium, and implanted synthetic vascular grafts are seeded by host SMCs and endothelium. Here we used murine aortic transplants to formally identify the source of SMCs in GAD lesions. Allografts in beta-galactosidase transgenic recipients showed that intimal SMCs derived almost exclusively from host cells. Bone-marrow transplantation of beta-galactosidase--expressing cells into aortic allograft recipients demonstrated that intimal cells included those of marrow origin. Thus, smooth-muscle--like cells in GAD lesions can originate from circulating bone--marrow-derived precursors.