Computer interaction via visually guided hand or finger movements is a ubiquitous part of daily computer usage in work or gaming. Surprisingly, however, little is known about the performance effects of using virtual limb representations versus simpler cursors. In this study 26 healthy right-handed adults performed cued index finger flexion-extension movements towards an on-screen target while wearing a data glove. They received each of four different types of real-time visual feedback: a simple circular cursor, a point light pattern indicating finger joint positions, a cartoon hand and a fully shaded virtual hand. We found that participants initiated the movements faster when receiving feedback in the form of a hand than when receiving circular cursor or point light feedback. This overall difference was robust for three out of four hand versus circle pairwise comparisons. The faster movement initiation for hand feedback was accompanied by a larger movement amplitude and a larger movement error. We suggest that the observed effect may be related to priming of hand information during action perception and execution affecting motor planning and execution. The results may have applications in the use of body representations in virtual reality applications.

Little is known about the mechanistic significance of the ubiquitin proteasome system (UPS) in a kidney autoimmune environment. In membranous nephropathy (MN), autoantibodies target podocytes of the glomerular filter resulting in proteinuria. Converging biochemical, structural, mouse pathomechanistic, and clinical information we report that the deubiquitinase Ubiquitin C-terminal hydrolase L1 (UCH-L1) is induced by oxidative stress in podocytes and is directly involved in proteasome substrate accumulation. Mechanistically, this toxic gain-of-function is mediated by non-functional UCH-L1, which interacts with and thereby impairs proteasomes. In experimental MN, UCH-L1 becomes non-functional and MN patients with poor outcome exhibit autoantibodies with preferential reactivity to non-functional UCH-L1. Podocyte-specific deletion of UCH-L1 protects from experimental MN, whereas overexpression of non-functional UCH-L1 impairs podocyte proteostasis and drives injury in mice. In conclusion, the UPS is pathomechanistically linked to podocyte disease by aberrant proteasomal interactions of non-functional UCH-L1.