49 research outputs found
Visual Tactile Sensor Based Force Estimation for Position-Force Teleoperation
Vision-based tactile sensors have gained extensive attention in the robotics
community. The sensors are highly expected to be capable of extracting contact
information i.e. haptic information during in-hand manipulation. This nature of
tactile sensors makes them a perfect match for haptic feedback applications. In
this paper, we propose a contact force estimation method using the vision-based
tactile sensor DIGIT, and apply it to a position-force teleoperation
architecture for force feedback. The force estimation is done by building a
depth map for DIGIT gel surface deformation measurement and applying a
regression algorithm on estimated depth data and ground truth force data to get
the depth-force relationship. The experiment is performed by constructing a
grasping force feedback system with a haptic device as a leader robot and a
parallel robot gripper as a follower robot, where the DIGIT sensor is attached
to the tip of the robot gripper to estimate the contact force. The preliminary
results show the capability of using the low-cost vision-based sensor for force
feedback applications.Comment: IEEE CBS 202
Cellularly-Driven Differences in Network Synchronization Propensity Are Differentially Modulated by Firing Frequency
Spatiotemporal pattern formation in neuronal networks depends on the interplay between cellular and network synchronization properties. The neuronal phase response curve (PRC) is an experimentally obtainable measure that characterizes the cellular response to small perturbations, and can serve as an indicator of cellular propensity for synchronization. Two broad classes of PRCs have been identified for neurons: Type I, in which small excitatory perturbations induce only advances in firing, and Type II, in which small excitatory perturbations can induce both advances and delays in firing. Interestingly, neuronal PRCs are usually attenuated with increased spiking frequency, and Type II PRCs typically exhibit a greater attenuation of the phase delay region than of the phase advance region. We found that this phenomenon arises from an interplay between the time constants of active ionic currents and the interspike interval. As a result, excitatory networks consisting of neurons with Type I PRCs responded very differently to frequency modulation compared to excitatory networks composed of neurons with Type II PRCs. Specifically, increased frequency induced a sharp decrease in synchrony of networks of Type II neurons, while frequency increases only minimally affected synchrony in networks of Type I neurons. These results are demonstrated in networks in which both types of neurons were modeled generically with the Morris-Lecar model, as well as in networks consisting of Hodgkin-Huxley-based model cortical pyramidal cells in which simulated effects of acetylcholine changed PRC type. These results are robust to different network structures, synaptic strengths and modes of driving neuronal activity, and they indicate that Type I and Type II excitatory networks may display two distinct modes of processing information
Sparse Gamma Rhythms Arising through Clustering in Adapting Neuronal Networks
Gamma rhythms (30â100 Hz) are an extensively studied synchronous brain state responsible for a number of sensory, memory, and motor processes. Experimental evidence suggests that fast-spiking interneurons are responsible for carrying the high frequency components of the rhythm, while regular-spiking pyramidal neurons fire sparsely. We propose that a combination of spike frequency adaptation and global inhibition may be responsible for this behavior. Excitatory neurons form several clusters that fire every few cycles of the fast oscillation. This is first shown in a detailed biophysical network model and then analyzed thoroughly in an idealized model. We exploit the fact that the timescale of adaptation is much slower than that of the other variables. Singular perturbation theory is used to derive an approximate periodic solution for a single spiking unit. This is then used to predict the relationship between the number of clusters arising spontaneously in the network as it relates to the adaptation time constant. We compare this to a complementary analysis that employs a weak coupling assumption to predict the first Fourier mode to destabilize from the incoherent state of an associated phase model as the external noise is reduced. Both approaches predict the same scaling of cluster number with respect to the adaptation time constant, which is corroborated in numerical simulations of the full system. Thus, we develop several testable predictions regarding the formation and characteristics of gamma rhythms with sparsely firing excitatory neurons
Short Conduction Delays Cause Inhibition Rather than Excitation to Favor Synchrony in Hybrid Neuronal Networks of the Entorhinal Cortex
How stable synchrony in neuronal networks is sustained in the presence of conduction delays is an open question. The Dynamic Clamp was used to measure phase resetting curves (PRCs) for entorhinal cortical cells, and then to construct networks of two such neurons. PRCs were in general Type I (all advances or all delays) or weakly type II with a small region at early phases with the opposite type of resetting. We used previously developed theoretical methods based on PRCs under the assumption of pulsatile coupling to predict the delays that synchronize these hybrid circuits. For excitatory coupling, synchrony was predicted and observed only with no delay and for delays greater than half a network period that cause each neuron to receive an input late in its firing cycle and almost immediately fire an action potential. Synchronization for these long delays was surprisingly tight and robust to the noise and heterogeneity inherent in a biological system. In contrast to excitatory coupling, inhibitory coupling led to antiphase for no delay, very short delays and delays close to a network period, but to near-synchrony for a wide range of relatively short delays. PRC-based methods show that conduction delays can stabilize synchrony in several ways, including neutralizing a discontinuity introduced by strong inhibition, favoring synchrony in the case of noisy bistability, and avoiding an initial destabilizing region of a weakly type II PRC. PRCs can identify optimal conduction delays favoring synchronization at a given frequency, and also predict robustness to noise and heterogeneity
Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets
Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is the third leading cause of death globally. Through genome-wide association discovery in 48,943 individuals, selected from extremes of the lung function distribution in UK Biobank, and follow-up in 95,375 individuals, we increased the yield of independent signals for lung function from 54 to 97. A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (âŒ6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 Ă 10âŸâŽâč), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest genetic risk score deciles in UK Biobank. The 97 signals show enrichment in genes for development, elastic fibers and epigenetic regulation pathways. We highlight targets for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and describe targets for potential drug repositioning from other clinical indications.This work was funded by a Medical Research Council (MRC) strategic award to M.D.T., I.P.H., D.S. and L.V.W. (MC_PC_12010). This research has been conducted using the UK Biobank Resource under application 648. This article presents independent research funded partially by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the UK Department of Health. This research used the ALICE and SPECTRE High-Performance Computing Facilities at the University of Leicester. Additional acknowledgments and funding details can be found in the Supplementary Note
Cholestérol alimentaire et morbi/mortalité cardiovasculaire
Si lâhypercholestĂ©rolĂ©mie est un facteur de risque avĂ©rĂ© des maladies cardiovasculaires,
le rĂŽle du cholestĂ©rol alimentaire dans la survenue de ces maladies reste discutĂ©. Ă
lâorigine, les travaux dâAnitshkow chez le lapin ont montrĂ© quâune alimentation riche en
cholestĂ©rol se traduit par le dĂ©veloppement de plaques dâathĂ©rome. Les Ă©tudes
dâintervention chez lâhomme ont examinĂ© lâeffet du cholestĂ©rol alimentaire et/ou des Ćufs
sur les lipides plasmatiques, aboutissant à des résultats contradictoires. Elles ont
Ă©galement fait Ă©merger la notion complexe dâhypo- et dâhyper-rĂ©pondeur au cholestĂ©rol.
LâĂ©pidĂ©miologie observationnelle ne permet pas non plus de conclure Ă un effet dĂ©lĂ©tĂšre du
cholestĂ©rol alimentaire chez lâhomme. NĂ©anmoins, chez les sujets diabĂ©tiques, une
association positive entre la consommation et lâincidence des Ă©vĂ©nements cardiovasculaires
est retrouvĂ©e assez constamment, sans que lâon puisse lâexpliquer de maniĂšre convaincante.
Il nâexiste pas dâessai clinique examinant lâimpact des aliments riches en cholestĂ©rol sur
la survenue des événements cardiovasculaires. Toutefois, les résultats des études MRFIT et
PREDIMED ne vont pas dans le sens dâun effet dĂ©lĂ©tĂšre du cholestĂ©rol alimentaire. Ă
lâinverse, les travaux rĂ©alisĂ©s sur le transporteur intestinal du cholestĂ©rol NPC1L1 sont
en faveur de lâintĂ©rĂȘt dâinhiber lâabsorption du cholestĂ©rol pour rĂ©duire lâincidence des
maladies cardiovasculaires. Lâensemble des donnĂ©es disponibles nâest pas en faveur dâun
rÎle clé du cholestérol alimentaire dans la survenue des maladies cardiovasculaires. Elles
ne permettent donc pas dâen faire une cible prioritaire du rĂ©gime Ă proposer pour prĂ©venir
les maladies cardiovasculaires
Etude quantitative et qualitative des HDL chez des patients à risque cardiovasculaire (impact thérapeutique d'interventions nutritionnelles et pharmacologiques)
La concentration sĂ©rique du HDL-CholestĂ©rol (HDL-C) est un facteur de risque indĂ©pendant de maladie cardio-vasculaire (CV). Augmenter le taux du HDL-C, reflet de la quantitĂ© des HDL, et amĂ©liorer la qualitĂ© des activitĂ©s biologiques des HDL sont donc des approches thĂ©rapeutiques prometteuses pour rĂ©duire le risque CV. Bien que les principaux facteurs qui dĂ©terminent la concentration du HDL-C soient assez bien connus, il n'en est pas de mĂȘme de la quantification de leur rĂŽle relatif, ni du bĂ©nĂ©fice CV de l'augmentation du HDL-C liĂ©e Ă chacun de ces facteurs en particulier. En second lieu, peu de travaux ont tentĂ© d'amĂ©liorer la qualitĂ© des particules HDL par des thĂ©rapeutiques usuelles. Notre travail nous a permis de progresser dans deux aspects diffĂ©rents : 1) Nous avons mis en Ă©vidence, chez 14 000 sujets dyslipidĂ©miques, huit paramĂštres associĂ©s de façon indĂ©pendante Ă la concentration de HDL-C. Par ordre d'importance, ce sont les triglycĂ©rides plasmatiques, le sexe, l'Ăąge, le tour de taille, la consommation d'alcool, la CRPus, l'index HOMA et le tabagisme. Dans une seconde Ă©tude, centrĂ©e spĂ©cifiquement sur le " dĂ©terminant alcool ", effectuĂ©e chez prĂšs de 150 000 sujets, nous Ă©tablissons des relations statistiques en J entre la consommation d'alcool et la plupart des facteurs de risque, traditionnels ou non, des maladies CV. Cependant il ressort de l'Ă©tude que ces relations ne sont pas nĂ©cessairement causales. L'effet cardioprotecteur supposĂ© de l'alcool peut ĂȘtre liĂ© Ă des facteurs de confusion non pris en compte dans les Ă©tudes Ă©pidĂ©miologiquesPARIS-BIUSJ-Biologie recherche (751052107) / SudocSudocFranceF
Etude de la relation entre le tour de taille et les sous-fractions de HDL
LE KREMLIN-B.- PARIS 11-BU MĂ©d (940432101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
Cholestérol alimentaire et morbi/mortalité cardiovasculaire
Si lâhypercholestĂ©rolĂ©mie est un facteur de risque avĂ©rĂ© des maladies cardiovasculaires,
le rĂŽle du cholestĂ©rol alimentaire dans la survenue de ces maladies reste discutĂ©. Ă
lâorigine, les travaux dâAnitshkow chez le lapin ont montrĂ© quâune alimentation riche en
cholestĂ©rol se traduit par le dĂ©veloppement de plaques dâathĂ©rome. Les Ă©tudes
dâintervention chez lâhomme ont examinĂ© lâeffet du cholestĂ©rol alimentaire et/ou des Ćufs
sur les lipides plasmatiques, aboutissant à des résultats contradictoires. Elles ont
Ă©galement fait Ă©merger la notion complexe dâhypo- et dâhyper-rĂ©pondeur au cholestĂ©rol.
LâĂ©pidĂ©miologie observationnelle ne permet pas non plus de conclure Ă un effet dĂ©lĂ©tĂšre du
cholestĂ©rol alimentaire chez lâhomme. NĂ©anmoins, chez les sujets diabĂ©tiques, une
association positive entre la consommation et lâincidence des Ă©vĂ©nements cardiovasculaires
est retrouvĂ©e assez constamment, sans que lâon puisse lâexpliquer de maniĂšre convaincante.
Il nâexiste pas dâessai clinique examinant lâimpact des aliments riches en cholestĂ©rol sur
la survenue des événements cardiovasculaires. Toutefois, les résultats des études MRFIT et
PREDIMED ne vont pas dans le sens dâun effet dĂ©lĂ©tĂšre du cholestĂ©rol alimentaire. Ă
lâinverse, les travaux rĂ©alisĂ©s sur le transporteur intestinal du cholestĂ©rol NPC1L1 sont
en faveur de lâintĂ©rĂȘt dâinhiber lâabsorption du cholestĂ©rol pour rĂ©duire lâincidence des
maladies cardiovasculaires. Lâensemble des donnĂ©es disponibles nâest pas en faveur dâun
rÎle clé du cholestérol alimentaire dans la survenue des maladies cardiovasculaires. Elles
ne permettent donc pas dâen faire une cible prioritaire du rĂ©gime Ă proposer pour prĂ©venir
les maladies cardiovasculaires