173 research outputs found
Point-Gap Bound States in Non-Hermitian Systems
In this paper, we systematically investigate the impurity-induced bound
states in 1D non-Hermitian systems. By establishing an exact relationship
between impurity potential and bound-state energy, we determine the minimum
impurity potential required to generate bound states within each point energy
gap. We demonstrate that the absence of Bloch saddle points necessitates a
finite threshold of impurity potential; otherwise, infinitesimal impurity
potential can create bound states. Furthermore, we show that the bound states
residing in the point gaps with nonzero spectral winding exhibit sensitivity to
boundary conditions and will be squeezed towards the edges when the boundaries
are opened, indicating the bulk-boundary correspondence in terms of point-gap
topology.Comment: 16 pages, 10 figure
Graphic characterization and clustering configuration descriptors of determinant space for molecules
Quantum Monte Carlo approaches based on the stochastic sampling of the
determinant space have evolved to be powerful methods to compute the electronic
states of molecules. These methods not only calculate the correlation energy at
an unprecedented accuracy but also provides insightful information on the
electronic structure of computed states, e.g. the population, connection, and
clustering of determinants, which have not been fully explored. In this work,
we devise a configuration graph for visualizing the determinant space,
revealing the nature of the molecule's electronic structure. In addition, we
propose two analytical descriptors to quantify the extent of configuration
clustering of multi-determinant wave functions. The graph and descriptors
provide us with a fresh perspective of the electronic structure of molecules
and can assist the further development of configuration interaction based
electronic structure methods
Tacchi: A Pluggable and Low Computational Cost Elastomer Deformation Simulator for Optical Tactile Sensors
Simulation is widely applied in robotics research to save time and resources.
There have been several works to simulate optical tactile sensors that leverage
either a smoothing method or Finite Element Method (FEM). However, elastomer
deformation physics is not considered in the former method, whereas the latter
requires a massive amount of computational resources like a computer cluster.
In this work, we propose a pluggable and low computational cost simulator using
the Taichi programming language for simulating optical tactile sensors, named
as Tacchi . It reconstructs elastomer deformation using particles, which allows
deformed elastomer surfaces to be rendered into tactile images and reveals
contact information without suffering from high computational costs. Tacchi
facilitates creating realistic tactile images in simulation, e.g., ones that
capture wear-and-tear defects on object surfaces. In addition, the proposed
Tacchi can be integrated with robotics simulators for a robot system
simulation. Experiment results showed that Tacchi can produce images with
better similarity to real images and achieved higher Sim2Real accuracy compared
to the existing methods. Moreover, it can be connected with MuJoCo and Gazebo
with only the requirement of 1G memory space in GPU compared to a computer
cluster applied for FEM. With Tacchi, physical robot simulation with optical
tactile sensors becomes possible. All the materials in this paper are available
at https://github.com/zixichen007115/Tacchi .Comment: 8 pages, 6 figures, accepted by IEEE Robotics and Automation Letter
A Hybrid Adaptive Controller for Soft Robot Interchangeability
Soft robots have been leveraged in considerable areas like surgery,
rehabilitation, and bionics due to their softness, flexibility, and safety.
However, it is challenging to produce two same soft robots even with the same
mold and manufacturing process owing to the complexity of soft materials.
Meanwhile, widespread usage of a system requires the ability to fabricate
replaceable components, which is interchangeability. Due to the necessity of
this property, a hybrid adaptive controller is introduced to achieve
interchangeability from the perspective of control approaches. This method
utilizes an offline trained recurrent neural network controller to cope with
the nonlinear and delayed response from soft robots. Furthermore, an online
optimizing kinematics controller is applied to decrease the error caused by the
above neural network controller. Soft pneumatic robots with different
deformation properties but the same mold have been included for validation
experiments. In the experiments, the systems with different actuation
configurations and the different robots follow the desired trajectory with
errors of 0.040 and 0.030 compared with the working space length, respectively.
Such an adaptive controller also shows good performance on different control
frequencies and desired velocities. This controller endows soft robots with the
potential for wide application, and future work may include different offline
and online controllers. A weight parameter adjusting strategy may also be
proposed in the future.Comment: 8 pages, 9 figures, 4 table
A Novel and Accurate BiLSTM Configuration Controller for Modular Soft Robots with Module Number Adaptability
Modular soft robots have shown higher potential in sophisticated tasks than
single-module robots. However, the modular structure incurs the complexity of
accurate control and necessitates a control strategy specifically for modular
robots. In this paper, we introduce a data collection strategy and a novel and
accurate bidirectional LSTM configuration controller for modular soft robots
with module number adaptability. Such a controller can control module
configurations in robots with different module numbers. Simulation cable-driven
robots and real pneumatic robots have been included in experiments to validate
the proposed approaches, and we have proven that our controller can be
leveraged even with the increase or decrease of module number. This is the
first paper that gets inspiration from the physical structure of modular robots
and utilizes bidirectional LSTM for module number adaptability. Future work may
include a planning method that bridges the task and configuration spaces and
the integration of an online controller.Comment: 10 figures, 4 table
Long-term high salt intake involves reduced SK Currents and Increased Excitability of PVN Neurons with projections to the rostral ventrolateral medulla in rats
Evidence indicates that high salt (HS) intake activates presympathetic paraventricular nucleus (PVN) neurons, which contributes to sympathoexcitation of salt-sensitive hypertension. The present study determined whether 5 weeks of HS (2% NaCl) intake alters the small conductance Ca2+-activated potassium channel (SK) current in presympathetic PVN neurons and whether this change affects the neuronal excitability. In whole-cell voltage-clamp recordings, HS-treated rats had significantly decreased SK currents compared to rats with normal salt (NS, 0.4% NaCl) intake in PVN neurons. The sensitivity of PVN neuronal excitability in response to current injections was greater in HS group compared to NS controls. The SK channel blocker apamin augmented the neuronal excitability in both groups but had less effect on the sensitivity of the neuronal excitability in HS group compared to NS controls. In the HS group, the interspike interval (ISI) was significantly shorter than that in NS controls. Apamin significantly shortened the ISI in NS controls but had less effect in the HS group. This data suggests that HS intake reduces SK currents, which contributes to increased PVN neuronal excitability at least in part through a decrease in spike frequency adaptation and may be a precursor to the development of salt-sensitive hypertension
Deletion of TRPC6 attenuates NMDA receptor-mediated Ca\u3csup\u3e2+\u3c/sup\u3e Entry and Ca\u3csup\u3e2+\u3c/sup\u3e-induced neurotoxicity following cerebral ischemia and oxygen-glucose deprivation
Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na+ and Ca2+ and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca2+ levels ([Ca2+]i), we found that OGD induced a significant higher increase in glutamate-evoked Ca2+ influx compared to untreated control and such an increase was reduced by TRPC6 deletion. Enhancement of TRPC6 expression using AdCMV-TRPC6-GFP infection in WT neurons increased [Ca2+]i in response to glutamate application compared to AdCMV-GFP control. Inhibition of N-methyl-d-aspartic acid receptor (NMDAR) with MK801 decreased TRPC6-dependent increase of [Ca2+]i in TRPC6 infected cells, indicating that such a Ca2+ influx was NMDAR dependent. Furthermore, TRPC6-dependent Ca2+ influx was blunted by blockade of Na+ entry in TRPC6 infected cells. Finally, OGD-enhanced Ca2+ influx was reduced, but not completely blocked, in the presence of voltage-dependent Na+ channel blocker tetrodotoxin (TTX) and dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) blocker CNQX. Altogether, we concluded that I/R-induced brain damage was, in part, due to upregulation of TRPC6 in cortical neurons. We postulate that overexpression of TRPC6 following I/R may induce neuronal death partially through TRPC6-dependent Na+ entry which activated NMDAR, thus leading to a damaging Ca2+ overload. These findings may provide a potential target for future intervention in stroke-induced brain damage
Deletion of TRPC6 attenuates NMDA receptor-mediated Ca\u3csup\u3e2+\u3c/sup\u3e Entry and Ca\u3csup\u3e2+\u3c/sup\u3e-induced neurotoxicity following cerebral ischemia and oxygen-glucose deprivation
Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na+ and Ca2+ and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca2+ levels ([Ca2+]i), we found that OGD induced a significant higher increase in glutamate-evoked Ca2+ influx compared to untreated control and such an increase was reduced by TRPC6 deletion. Enhancement of TRPC6 expression using AdCMV-TRPC6-GFP infection in WT neurons increased [Ca2+]i in response to glutamate application compared to AdCMV-GFP control. Inhibition of N-methyl-d-aspartic acid receptor (NMDAR) with MK801 decreased TRPC6-dependent increase of [Ca2+]i in TRPC6 infected cells, indicating that such a Ca2+ influx was NMDAR dependent. Furthermore, TRPC6-dependent Ca2+ influx was blunted by blockade of Na+ entry in TRPC6 infected cells. Finally, OGD-enhanced Ca2+ influx was reduced, but not completely blocked, in the presence of voltage-dependent Na+ channel blocker tetrodotoxin (TTX) and dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) blocker CNQX. Altogether, we concluded that I/R-induced brain damage was, in part, due to upregulation of TRPC6 in cortical neurons. We postulate that overexpression of TRPC6 following I/R may induce neuronal death partially through TRPC6-dependent Na+ entry which activated NMDAR, thus leading to a damaging Ca2+ overload. These findings may provide a potential target for future intervention in stroke-induced brain damage
Responses of Nucleus Tractus Solitarius (NTS) early and late neurons to blood pressure changes in anesthetized F344 rats
Previously, many different types of NTS barosensitive neurons were identified. However, the time course of NTS barosensitive neuronal activity (NA) in response to arterial pressure (AP) changes, and the relationship of NA-AP changes, have not yet been fully quantified. In this study, we made extracellular recordings of single NTS neurons firing in response to AP elevation induced by occlusion of the descending aorta in anesthetized rats. Our findings were that: 1) Thirty-five neurons (from 46 neurons) increased firing, whereas others neurons either decreased firing upon AP elevation, or were biphasic: first decreased firing upon AP elevation and then increased firing during AP decrease. 2) Fourteen neurons with excitatory responses were activated and rapidly increased their firing during the early phase of AP increase (early neurons); whereas 21 neurons did not increase firing until the mean arterial pressure changes (ΔMAP) reached near/after the peak (late neurons). 3) The early neurons had a significantly higher firing rate than late neurons during AP elevation at a similar rate. 4) Early neuron NA-ΔMAP relationship could be well fitted and characterized by the sigmoid logistic function with the maximal gain of 29.3. 5) The increase of early NA correlated linearly with the initial heart rate (HR) reduction. 6) The late neurons did not contribute to the initial HR reduction. However, the late NA could be well correlated with HR reduction during the late phase. Altogether, our study demonstrated that the NTS excitatory neurons could be grouped into early and late neurons based on their firing patterns. The early neurons could be characterized by the sigmoid logistic function, and different neurons may differently contribute to HR regulation. Importantly, the grouping and quantitative methods used in this study may provide a useful tool for future assessment of functional changes of early and late neurons in disease models
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