Whole body vibration on people with sequelae of polio.

PURPOSE: The purpose was to explore the feasibility of whole body vibration (WBV) on polio survivors with/without post-polio syndrome (PPS) by studying its effects on walking speed (10-m walk test), endurance (2-min walk test), pain severity/interference (Brief Pain Inventory [BPI]), sleep quality (Pittsburg Sleep Quality Index), fatigue (Fatigue Severity Scale), leg strength (manual muscle testing and hand-held dynamometry), and muscle cramping (written logs). METHODS: Fifteen individuals completed the study, participating in eight sessions in two 4-week blocks. Participants started with ten 1-min vibration bouts/session, increasing to 20 min. Low (amplitude 4.53 mm, g force 2.21) and higher (amplitude 8.82 mm, g force 2.76) intensity blocked intervention occurred in random order crossover design. Blinded testing ensued before/after intervention blocks and at follow-up. RESULTS: No study-related adverse events occurred. Participants starting first with higher intensity intervention improved in walking speed (p = 0.017). BPI pain severity significantly improved (p = 0.049) after higher intensity intervention. No significant changes were found after low intensity vibration or in other outcome measures. CONCLUSIONS: WBV appears to be a safe exercise for this population. Long-term use in polio survivors needs to be researched, particularly in reducing barriers to participation to promote the physical aspects of health.

Anthrax Toxin Receptor 1 Is Essential for Arteriogenesis in a Mouse Model of Hindlimb Ischemia.

Anthrax toxin receptor 1/tumor endothelial marker 8 (Antxr1 or TEM8) is up-regulated in tumor vasculature and serves as a receptor for anthrax toxin, but its physiologic function is unclear. The objective of this study was to evaluate the role of Antxr1 in arteriogenesis. The role of Antxr1 in arteriogenesis was tested by measuring gene expression and immunohistochemistry in a mouse model of hindlimb ischemia using wild-type and ANTXR1(-/-) mice. Additional tests were performed by measuring gene expression in in vitro models of fluid shear stress and hypoxia, as well as in human muscle tissues obtained from patients having peripheral artery disease. We observed that Antxr1 expression transiently increased in ischemic tissues following femoral artery ligation and that its expression was necessary for arteriogenesis. In the absence of Antxr1, the mean arterial lumen area in ischemic tissues decreased. Antxr1 mRNA and protein expression was positively regulated by fluid shear stress, but not by hypoxia. Furthermore, Antxr1 expression was elevated in human peripheral artery disease requiring lower extremity bypass surgery. These findings demonstrate an essential physiologic role for Antxr1 in arteriogenesis and peripheral artery disease, with important implications for managing ischemia and other arteriogenesis-dependent vascular diseases.