Correction to: Cluster identification, selection, and description in Cluster randomized crossover trials: the PREP-IT trials

An amendment to this paper has been published and can be accessed via the original article

Costs and Radiographic Outcomes of Rotational Ankle Fractures Treated by Orthopaedic Surgeons With or Without Trauma Fellowship Training

Introduction: We evaluated the radiographic outcomes and surgical costs of surgically treated rotational ankle fractures in our health system between providers who had completed a trauma fellowship and those who had not. Methods: We grouped patients into those treated by trauma-trained orthopaedic surgeons (TTOS) and non–trauma-trained orthopaedic surgeons (NTTOS). We graded the quality of fracture reductions and calculated implant-related costs of treatment. Results: A total of 208 fractures met the inclusion criteria, with 119 in the TTOS group and 89 in the NTTOS group. Five patients lost reduction during the follow-up period. The adequacy of fracture reduction at final follow-up did not differ (P = 0.29). The median surgical cost was $2,940 for the NTTOS group and$1,233 for the TTOS group (P < 0.001). Discussion: We found no notable differences in radiographic outcomes between the TTOS and NTTOS groups. Cost analysis demonstrated markedly higher implant-related costs for the NTTOS group, with the median surgical cost being more than twice that for the TTOS group. Level of Evidence: Level II

Dual Roles for RHOA/RHO-Kinase In the Regulated Trafficking of a Voltage-sensitive Potassium Channel

Kv1.2 is a member of the Shaker family of voltage-sensitive potassium channels and contributes to regulation of membrane excitability. The electrophysiological activity of Kv1.2 undergoes tyrosine kinase-dependent suppression in a process involving RhoA. We report that RhoA elicits suppression of Kv1.2 ionic current by modulating channel endocytosis. This occurs through two distinct pathways, one clathrin-dependent and the other cholesterol-dependent. Activation of Rho kinase (ROCK) via the lysophosphatidic acid (LPA) receptor elicits clathrin-dependent Kv1.2 endocytosis and consequent attenuation of its ionic current. LPA-induced channel endocytosis is blocked by the ROCK inhibitor Y27632 or by clathrin RNA interference. In contrast, steady-state endocytosis of Kv1.2 in unstimulated cells is cholesterol dependent. Inhibition of basal ROCK signaling with Y27632 increased surface Kv1.2, an effect that persists in the presence of clathrin small interfering RNA and that is not additive to the increase in surface channel levels elicited by the cholesterol sequestering drug filipin. Temperature block experiments show that ROCK affects cholesterol-dependent trafficking by modulating the recycling of endocytosed channel back to the plasma membrane. Both receptor-stimulated and steady-state Kv1.2 trafficking modulated by RhoA/ROCK required the activation of dynamin as well as the ROCK effector Lim-kinase, indicating a key role for actin remodeling in RhoA-dependent Kv1.2 regulation