prominences that correspond to the ACL tibial footprint and three surrounding 1 5 landmarks: anterior ridge, lateral groove, and intertubercular fossa. In the first study, findings and three-dimensional (3D) CT images of these bony landmarks. In the second 2 0 study, the morphology of the bony prominence and incidence of their bony landmarks 2 1 were evaluated from the preoperative CT data of 60 knee joints.

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During development, axons elongate vigorously, carefully controlling their speed, to connect with their targets. In general, rapid axon growth is correlated with active growth cones driven by dynamic actin filaments. For example, when the actin-driven tip is collapsed by repulsive guidance molecules, axon growth is severely impaired. In this study, we report that axon growth can be suppressed, without destroying the actin-based structure or motility of the growth cones, when antibodies bind to the four-transmembrane glycoprotein M6a concentrated on the growth cone edge. Surprisingly, M6a-deficient axons grow actively but are not growth suppressed by the antibodies, arguing for an inductive action of the antibody. The binding of antibodies clusters and displaces M6a protein from the growth cone edge membrane, suggesting that the spatial rearrangement of this protein might underlie the unique growth cone behavior triggered by the antibodies. Molecular dissection of M6a suggested involvement for the N-terminal intracellular domain in this antibody-induced growth cone arrest.

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