ABSTRACT
F-actin fragments fluorescently labeled with rhodamine-phalloidin were copolymerized with non-labeled F-actin fragments. F-actin copolymer consisted of several bright (fluorescent) and dark (non-fluorescent) stripes of approximately 1 microm in width. Local motion of individual speckled F-actin was investigated by measuring translocation fluctuation of several tracing points marked on the actin filament. The tracing points included the borders between neighboring bright and dark stripes, as well as the tip and tail of the filament. For speckled F-actin with an average sliding speed of 4.6 microm/s at 23 degrees C, the translocation distance of the tracing points (per 0.1 s) showed significant fluctuation, of the order of +/-0.12 microm/s, approximately 25% of the sliding speed. The fluctuation correlation of the translocation distance between two tracing points decreased as the distance between them increased. Statistical analysis of the correlation length of the translocation distance L(c) showed that L(c) increased with the sliding speed of the actin filament. The sliding speed, however, saturated as the correlation length became close to the persistence length of the bending elasticity of F-actin. On the contrary, the correlation length of change in the translocation direction was essentially equal to the persistence length of F-actin, independent of the sliding speed. These results suggest that elasticity of the actin filament underlies the sliding velocity of F-actin.
Subject(s)
Actins/metabolism , Adenosine Triphosphate/pharmacology , Myosin Subfragments/metabolism , Actins/drug effects , Actins/physiology , Animals , Elasticity , Fluorescent Dyes , Humans , Microscopy, Fluorescence , Models, Chemical , Movement/drug effects , Myosin Subfragments/physiology , Myosins/metabolism , Myosins/physiology , Rhodamines , Surface PropertiesABSTRACT
Experiments were carried out in young adult monkeys to determine the influence of mechanical stress on degeneration of the lumbar facet joints. Eleven monkeys were used and divided into four groups, the control, upper lumbar laminectomy, discectomy and discectomy + rotation. The monkeys were given fluorochrome agents once a week. After sacrifice, undemineralised sections were studied under fluorescence microscopy. Contact microradiographs were also made. After laminectomy, subperiosteal bony proliferation was seen on the external surface of the superior and inferior articular processes. After discectomy there was localised bony proliferation on the anterior aspect of the superior articular processes. In the group with discectomy + rotation there was evidence of additional proliferation of the calcified cartilage zone at the insertion of the ligamentum flavum which had remodelled to bony tissue. We conclude that rotational stresses are mostly responsible for the development of spinal stenosis.
