Exodex Adam—A Reconfigurable Dexterous Haptic User Interface for the Whole Hand

Applications for dexterous robot teleoperation and immersive virtual reality are growing. Haptic user input devices need to allow the user to intuitively command and seamlessly “feel” the environment they work in, whether virtual or a remote site through an avatar. We introduce the DLR Exodex Adam, a reconfigurable, dexterous, whole-hand haptic input device. The device comprises multiple modular, three degrees of freedom (3-DOF) robotic fingers, whose placement on the device can be adjusted to optimize manipulability for different user hand sizes. Additionally, the device is mounted on a 7-DOF robot arm to increase the user’s workspace. Exodex Adam uses a front-facing interface, with robotic fingers coupled to two of the user’s fingertips, the thumb, and two points on the palm. Including the palm, as opposed to only the fingertips as is common in existing devices, enables accurate tracking of the whole hand without additional sensors such as a data glove or motion capture. By providing “whole-hand” interaction with omnidirectional force-feedback at the attachment points, we enable the user to experience the environment with the complete hand instead of only the fingertips, thus realizing deeper immersion. Interaction using Exodex Adam can range from palpation of objects and surfaces to manipulation using both power and precision grasps, all while receiving haptic feedback. This article details the concept and design of the Exodex Adam, as well as use cases where it is deployed with different command modalities. These include mixed-media interaction in a virtual environment, gesture-based telemanipulation, and robotic hand–arm teleoperation using adaptive model-mediated teleoperation. Finally, we share the insights gained during our development process and use case deployments

Crowdsourcing hypothesis tests: Making transparent how design choices shape research results

To what extent are research results influenced by subjective decisions that scientists make as they design studies? Fifteen research teams independently designed studies to answer fiveoriginal research questions related to moral judgments, negotiations, and implicit cognition. Participants from two separate large samples (total N > 15,000) were then randomly assigned to complete one version of each study. Effect sizes varied dramatically across different sets of materials designed to test the same hypothesis: materials from different teams renderedstatistically significant effects in opposite directions for four out of five hypotheses, with the narrowest range in estimates being d = -0.37 to +0.26. Meta-analysis and a Bayesian perspective on the results revealed overall support for two hypotheses, and a lack of support for three hypotheses. Overall, practically none of the variability in effect sizes was attributable to the skill of the research team in designing materials, while considerable variability was attributable to the hypothesis being tested. In a forecasting survey, predictions of other scientists were significantly correlated with study results, both across and within hypotheses. Crowdsourced testing of research hypotheses helps reveal the true consistency of empirical support for a scientific claim.</div

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Combined Inhibition of the Renin-Angiotensin System and Neprilysin Positively Influences Complex Mitochondrial Adaptations in Progressive Experimental Heart Failure.

BACKGROUND:Inhibitors of the renin angiotensin system and neprilysin (RAS-/NEP-inhibitors) proved to be extraordinarily beneficial in systolic heart failure. Furthermore, compelling evidence exists that impaired mitochondrial pathways are causatively involved in progressive left ventricular (LV) dysfunction. Consequently, we aimed to assess whether RAS-/NEP-inhibition can attenuate mitochondrial adaptations in experimental heart failure (HF). METHODS AND RESULTS:By progressive right ventricular pacing, distinct HF stages were induced in 15 rabbits, and 6 animals served as controls (CTRL). Six animals with manifest HF (CHF) were treated with the RAS-/NEP-inhibitor omapatrilat. Echocardiographic studies and invasive blood pressure measurements were undertaken during HF progression. Mitochondria were isolated from LV tissue, respectively, and further worked up for proteomic analysis using the SWATH technique. Enzymatic activities of citrate synthase and the electron transfer chain (ETC) complexes I, II, and IV were assessed. Ultrastructural analyses were performed by transmission electron microscopy. During progression to overt HF, intricate expression changes were mainly detected for proteins belonging to the tricarboxylic acid cycle, glucose and fat metabolism, and the ETC complexes, even though ETC complex I, II, or IV enzymatic activities were not significantly influenced. Treatment with a RAS-/NEP-inhibitor then reversed some maladaptive metabolic adaptations, positively influenced the decline of citrate synthase activity, and altered the composition of each respiratory chain complex, even though this was again not accompanied by altered ETC complex enzymatic activities. Finally, ultrastructural evidence pointed to a reduction of autophagolytic and degenerative processes with omapatrilat-treatment. CONCLUSIONS:This study describes complex adaptations of the mitochondrial proteome in experimental tachycardia-induced heart failure and shows that a combined RAS-/NEP-inhibition can beneficially influence mitochondrial key pathways

Enzymatic activity of succinate dehydrogenase (ETC complex II).

<p>Enzymatic activity of succinate dehydrogenase (ETC complex II).</p

Enzymatic activity of NADH dehydrogenase (ETC complex I).

<p>Enzymatic activity of NADH dehydrogenase (ETC complex I).</p

Protein expression level of carnitine palmitoyltransferase 1 A normalized to the expression of the outer mitochondrial membrane protein VDAC.

<p>Protein expression level of carnitine palmitoyltransferase 1 A normalized to the expression of the outer mitochondrial membrane protein VDAC.</p

Synopsis of different pathway regulation patterns.

<p>Synopsis of different pathway regulation patterns.</p