RESUMO
One-dimensional diffusion along long atomic chains of the Si(553)-Au surface is studied with scanning tunneling microscopy. Ab initio calculations reveal aligned preferential adsorption sites between Si step edge atomic chain and double Au atomic chain on each terrace. At 220 K the Pb atoms hop between shallow potential basins forming a potential groove and move parallel to the atomic chains. By combining the results of measurements with the model calculations of the Pb atoms static energy on the Si(553)-Au surface the attempt frequency ν0 is determined.
RESUMO
Most experimental studies of spinal cord injury have centered on the rat as an experimental model. A shift toward a mouse model has occurred in recent years because of its usefulness as a genetic tool. While many studies have concentrated on motor function and the inflammatory response following spinal cord injury in the mouse, the development of autonomic dysreflexia after injury has yet to be described. Autonomic dysreflexia is a condition in which episodic hypertension develops after injuries above the mid-thoracic segment of the spinal cord. In this study 129Sv mice received a spinal cord transection at the second thoracic segment. The presence of autonomic dysreflexia was assessed 2 weeks later. Blood pressure responses to stimulation were as follows: moderate cutaneous pinch caudal to the injury (35+/-6 mm Hg), tail pinch (25+/-7 mm Hg), and a 0.3 ml balloon distension of the colon (37+/-4 mm Hg). Previous reports have suggested that small diameter primary afferent fiber sprouting after spinal cord injury may be responsible for the development of autonomic dysreflexia. In order to determine whether autonomic dysreflexia in the mouse may be caused by a similar mechanism, the size of the small diameter primary afferent arbor in spinal cord-injured and sham-operated animals was assessed by measuring the area occupied by calcitonin gene-related peptide-immunoreactive fibers. The percentage increase in the area of the small diameter primary afferent arbor in transected over sham-operated spinal cords was 46%, 45% and 80% at spinal segments thoracic T5-8, thoracic T9-12 and thoracic T13-lumbar L2 respectively. This study demonstrates the development of autonomic dysfunction in a mouse model of spinal cord injury that is associated with sprouting of calcitonin gene-related peptide fibers. These results provide strong support for the use of this mouse model of spinal cord injury in the study of autonomic dysreflexia.