Kinegami: Algorithmic Design of Compliant Kinematic Chains From Tubular Origami

Origami processes can generate both rigid and compliant structures from the same homogeneous sheet material. In this article, we advance the origami robotics literature by showing that it is possible to construct an arbitrary rigid kinematic chain with prescribed joint compliance from a single tubular sheet. Our “Kinegami” algorithm converts a Denavit–Hartenberg specification into a single-sheet crease pattern for an equivalent serial robot mechanism by composing origami modules from a catalogue. The algorithm arises from the key observation that tubular origami linkage design reduces to a Dubins path planning problem. The automatically generated structural connections and movable joints that realize the specified design can also be endowed with independent user-specified compliance. We apply the Kinegami algorithm to a number of common robot mechanisms and hand-fold their algorithmically generated single-sheet crease patterns into functioning kinematic chains. We believe this is the first completely automated end-to-end system for converting an abstract manipulator specification into a physically realizable origami design that requires no additional human input

The evolution of dystonia-like movements in TOR1A rats after transient nerve injury is accompanied by dopaminergic dysregulation and abnormal oscillatory activity of a central motor network

TOR1A is the most common inherited form of dystonia with still unclear pathophysiology and reduced penetrance of 30–40%. ∆ETorA rats mimic the TOR1A disease by expression of the human TOR1A mutation without presenting a dystonic phenotype. We aimed to induce dystonia-like symptoms in male ∆ETorA rats by peripheral nerve injury and to identify central mechanism of dystonia development. Dystonia-like movements (DLM) were assessed using the tail suspension test and implementing a pipeline of deep learning applications. Neuron numbers of striatal parvalbumin+, nNOS+, calretinin+, ChAT+ interneurons and Nissl+ cells were estimated by unbiased stereology. Striatal dopaminergic metabolism was analyzed via in vivo microdialysis, qPCR and western blot. Local field potentials (LFP) were recorded from the central motor network. Deep brain stimulation (DBS) of the entopeduncular nucleus (EP) was performed. Nerve-injured ∆ETorA rats developed long-lasting DLM over 12 weeks. No changes in striatal structure were observed. Dystonic-like ∆ETorA rats presented a higher striatal dopaminergic turnover and stimulus-induced elevation of dopamine efflux compared to the control groups. Higher LFP theta power in the EP of dystonic-like ∆ETorA compared to wt rats was recorded. Chronic EP-DBS over 3 weeks led to improvement of DLM. Our data emphasizes the role of environmental factors in TOR1A symptomatogenesis. LFP analyses indicate that the pathologically enhanced theta power is a physiomarker of DLM. This TOR1A model replicates key features of the human TOR1A pathology on multiple biological levels and is therefore suited for further analysis of dystonia pathomechanism