Toward Controllable Hydraulic Coupling of Joints in a Wearable Robot

In this paper, we develop theoretical foundations for a new class of rehabilitation robot: body powered devices that route power between a user’s joints. By harvesting power from a healthy joint to assist an impaired joint, novel bimanual and self-assist therapies are enabled. This approach complements existing robotic therapies aimed at promoting recovery of motor function after neurological injury. We employ hydraulic transmissions for routing power, or equivalently for coupling the motions of a user’s joints. Fluid power routed through flexible tubing imposes constraints within a limb or between homologous joints across the body. Variable transmissions allow constraints to be steered on the fly, and simple valve switching realizes free space and locked motion. We examine two methods for realizing variable hydraulic transmissions: using valves to switch among redundant cylinders (digital hydraulics) or using an intervening electromechanical link. For both methods, we present a rigorous mathematical framework for describing and controlling the resulting constraints. Theoretical developments are supported by experiments using a prototype fluid-power exoskeleton

Self-Powered Robots to Reduce Motor Slacking During Upper-Extremity Rehabilitation: A Proof of Concept Study

Background: Robotic rehabilitation is a highly promising approach to recover lost functions after stroke or other neurological disorders. Unfortunately, robotic rehabilitation currently suffers from motor slacking , a phenomenon in which the human motor system reduces muscle activation levels and movement excursions, ostensibly to minimize metabolic- and movement-related costs. Consequently, the patient remains passive and is not fully engaged during therapy. To overcome this limitation, we envision a new class of body-powered robots and hypothesize that motor slacking could be reduced if individuals must provide the power to move their impaired limbs via their own body (i.e., through the motion of a healthy limb). Objective: To test whether a body-powered exoskeleton (i.e. robot) could reduce motor slacking during robotic training. Methods: We developed a body-powered robot that mechanically coupled the motions of the user\u27s elbow joints. We tested this passive robot in two groups of subjects (stroke and able-bodied) during four exercise conditions in which we controlled whether the robotic device was powered by the subject or by the experimenter, and whether the subject\u27s driven arm was engaged or at rest. Motor slacking was quantified by computing the muscle activation changes of the elbow flexor and extensor muscles using surface electromyography. Results: Subjects had higher levels of muscle activation in their driven arm during self-powered conditions compared to externally-powered conditions. Most notably, subjects unintentionally activated their driven arm even when explicitly told to relax when the device was self-powered. This behavior was persistent throughout the trial and did not wane after the initiation of the trial. Conclusions: Our findings provide novel evidence indicating that motor slacking can be reduced by self-powered robots; thus demonstrating promise for rehabilitation of impaired subjects using this new class of wearable system. The results also serve as a foundation to develop more sophisticated body-powered robots (e.g., with controllable transmissions) for rehabilitation purposes

Exclosures: An Experimental Technique for Protection of Northern Bobwhite Nests

Nest predation has been implicated as a factor affecting northern bobwhite (Colinus virginianus) recruitment rates. Public stakeholders are increasingly questioning use of lethal methods to manage predation. We evaluated a nonlethal method consisting of single nest treatments using an exclosure to protect nests from potential predators. The exclosure treatment also included use of Amdrot (hydramethylnon) and Snake-a-wayt repellents to deter red-imported fire ants (Solenopsis invicta) and snakes, respectively. We compared nest success of treated (n 1⁄4 8) to untreated nests (n 1⁄4 18). Treated nests were 88% successful which was a 2-fold increase over unprotected nests. We did not observe any difference in hen behavior between treatment and controls. This technique may be useful to study nest success of wild quail and is not intended to be a management technique to influence overall population growth

Quantum transport through a DNA wire in a dissipative environment

Electronic transport through DNA wires in the presence of a strong dissipative environment is investigated. We show that new bath-induced electronic states are formed within the bandgap. These states show up in the linear conductance spectrum as a temperature dependent background and lead to a crossover from tunneling to thermal activated behavior with increasing temperature. Depending on the strength of the electron-bath coupling, the conductance at the Fermi level can show a weak exponential or even an algebraic length dependence. Our results suggest a new environmental-induced transport mechanism. This might be relevant for the understanding of molecular conduction experiments in liquid solution, like those recently performed on poly(GC) oligomers in a water buffer (B. Xu et al., Nano Lett 4, 1105 (2004)).Comment: 5 pages, 3 figure

Vibrational Enhancement of the Effective Donor - Acceptor Coupling

The paper deals with a simple three sites model for charge transfer phenomena in an one-dimensional donor (D) - bridge (B) - acceptor (A) system coupled with vibrational dynamics of the B site. It is found that in a certain range of parameters the vibrational coupling leads to an enhancement of the effective donor - acceptor electronic coupling as a result of the formation of the polaron on the B site. This enhancement of the charge transfer efficiency is maximum at the resonance, where the effective energy of the fluctuating B site coincides with the donor (acceptor) energy.Comment: 5 pages, 3 figure

Green function techniques in the treatment of quantum transport at the molecular scale

The theoretical investigation of charge (and spin) transport at nanometer length scales requires the use of advanced and powerful techniques able to deal with the dynamical properties of the relevant physical systems, to explicitly include out-of-equilibrium situations typical for electrical/heat transport as well as to take into account interaction effects in a systematic way. Equilibrium Green function techniques and their extension to non-equilibrium situations via the Keldysh formalism build one of the pillars of current state-of-the-art approaches to quantum transport which have been implemented in both model Hamiltonian formulations and first-principle methodologies. We offer a tutorial overview of the applications of Green functions to deal with some fundamental aspects of charge transport at the nanoscale, mainly focusing on applications to model Hamiltonian formulations.Comment: Tutorial review, LaTeX, 129 pages, 41 figures, 300 references, submitted to Springer series "Lecture Notes in Physics

Diazepam actions in the VTA enhance social dominance and mitochondrial function in the nucleus accumbens by activation of dopamine D1 receptors.

Benzodiazepines can ameliorate social disturbances and increase social competition, particularly in high-anxious individuals. However, the neural circuits and mechanisms underlying benzodiazepines' effects in social competition are not understood. Converging evidence points to the mesolimbic system as a potential site of action for at least some benzodiazepine-mediated effects. Furthermore, mitochondrial function in the nucleus accumbens (NAc) has been causally implicated in the link between anxiety and social competitiveness. Here, we show that diazepam facilitates social dominance, ameliorating both the competitive disadvantage and low NAc mitochondrial function displayed by high-anxious rats, and identify the ventral tegmental area (VTA) as a key site of action for direct diazepam effects. We also show that intra-VTA diazepam infusion increases accumbal dopamine and DOPAC, as well as activity of dopamine D1- but not D2-containing cells. In addition, intra-NAc infusion of a D1-, but not D2, receptor agonist facilitates social dominance and mitochondrial respiration. Conversely, intra-VTA diazepam actions on social dominance and NAc mitochondrial respiration are blocked by pharmacological NAc micro-infusion of a mitochondrial complex I inhibitor or an antagonist of D1 receptors. Our data support the view that diazepam disinhibits VTA dopaminergic neurons, leading to the release of dopamine into the NAc where activation of D1-signaling transiently facilitates mitochondrial function, that is, increased respiration and enhanced ATP levels, which ultimately enhances social competitive behavior. Therefore, our findings critically involve the mesolimbic system in the facilitating effects of diazepam on social competition and highlight mitochondrial function as a potential therapeutic target for anxiety-related social dysfunctions

Polyomic profiling reveals significant hepatic metabolic alterations in glucagon-receptor (GCGR) knockout mice: implications on anti-glucagon therapies for diabetes

<p>Abstract</p> <p>Background</p> <p>Glucagon is an important hormone in the regulation of glucose homeostasis, particularly in the maintenance of euglycemia and prevention of hypoglycemia. In type 2 Diabetes Mellitus (T2DM), glucagon levels are elevated in both the fasted and postprandial states, which contributes to inappropriate hyperglycemia through excessive hepatic glucose production. Efforts to discover and evaluate glucagon receptor antagonists for the treatment of T2DM have been ongoing for approximately two decades, with the challenge being to identify an agent with appropriate pharmaceutical properties and efficacy relative to potential side effects. We sought to determine the hepatic & systemic consequence of full glucagon receptor antagonism through the study of the glucagon receptor knock-out mouse (Gcgr^-/-) compared to wild-type littermates.</p> <p>Results</p> <p>Liver transcriptomics was performed using Affymetric expression array profiling, and liver proteomics was performed by iTRAQ global protein analysis. To complement the transcriptomic and proteomic analyses, we also conducted metabolite profiling (~200 analytes) using mass spectrometry in plasma. Overall, there was excellent concordance (R = 0.88) for changes associated with receptor knock-out between the transcript and protein analysis. Pathway analysis tools were used to map the metabolic processes in liver altered by glucagon receptor ablation, the most notable being significant down-regulation of gluconeogenesis, amino acid catabolism, and fatty acid oxidation processes, with significant up-regulation of glycolysis, fatty acid synthesis, and cholesterol biosynthetic processes. These changes at the level of the liver were manifested through an altered plasma metabolite profile in the receptor knock-out mice, e.g. decreased glucose and glucose-derived metabolites, and increased amino acids, cholesterol, and bile acid levels.</p> <p>Conclusions</p> <p>In sum, the results of this study suggest that the complete ablation of hepatic glucagon receptor function results in major metabolic alterations in the liver, which, while promoting improved glycemic control, may be associated with adverse lipid changes.</p

Can understanding reward help illuminate anhedonia?

Purpose of review: The goal of this paper is to examine how reward processing might help us understand the symptom of anhedonia. Recent findings: There are extensive reviews exploring the relationship between responses to rewarding stimuli and depression. These often include a discussion on anhedonia and how this might be underpinned in particular by dysfunctional reward processing. However, there is no specific consensus on whether studies to date have adequately examined the various sub-components of reward processing or how these might relate in turn to various aspects of anhedonia symptoms. Summary: The approach to understanding the symptom of anhedonia should be to examine all the sub-components of reward processing at the subjective and objective behavioural and neural level, with well validated tasks that can be replicated. Investigating real life experiences of anhedonia and how theses might be predicted by objective lab measures is also needed in future research