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Central sensitization and network hyperexcitability of the nociceptive system is a basic mechanism of neuropathic pain. We hypothesize that development of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in response to lesion-induced somatosensory deprivation and activity loss, and can be controlled by enhancing cortical activity. In a mouse model of neuropathic pain, in vivo two-photon imaging and patch clamp recording showed initial loss and subsequent recovery and enhancement of spontaneous firings of somatosensory cortical pyramidal neurons. Unilateral optogenetic stimulation of cortical pyramidal neurons both prevented and reduced pain-like behavior as detected by bilateral mechanical hypersensitivity of hindlimbs, but corpus callosotomy eliminated the analgesic effect that was ipsilateral, but not contralateral, to optogenetic stimulation, suggesting involvement of inter-hemispheric excitatory drive in this effect. Enhancing activity by focally blocking cortical GABAergic inhibition had a similar relieving effect on the pain-like behavior. Patch clamp recordings from layer V pyramidal neurons showed that optogenetic stimulation normalized cortical hyperexcitability through changing neuronal membrane properties and reducing frequency of excitatory postsynaptic events. We conclude that development of neuropathic pain involves abnormal homeostatic activity regulation of somatosensory cortex, and that enhancing cortical excitatory activity may be a novel strategy for preventing and controlling neuropathic pain.

We describe results from a channel measurement and modeling campaign for the airport surface environment in the 5-GHz band. Using a 50-MHz bandwidth test signal, thousands of power delay profiles (PDPs) were obtained and processed to develop empirical tapped-delay line statistical channel models for large airports. A log-distance path loss model was also developed. The large airport surface channel is classified into three propagation regions, and models are presented for each of the regions for two values of bandwidth. Values of the median root-mean-square (RMS) delay spread range from 500 to 1000 ns for these airports, with the 90th percentile RMS delay spreads being approximately 1.7 ms. Corresponding correlation bandwidths (i.e., correlation value 1/2) range from approximately 1.5 MHz in non-line-of-sight (NLOS) settings to 17.5 MHz in line-of-sight (LOS) settings. Two types of statistical nonstationarity were also observed: 1) multipath component persistence and 2) propagation region transitions. We provide the multipath component probability of occurrence models and describe Markov chains that are used for modeling both phenomena. Channel tap amplitude statistics are also provided, using the flexible Weibull probability density function (pdf). This pdf was found to best fit fading tap amplitude data, particularly for frequently observed severe fading, which is characterized by fade probabilities that are worse than the commonly used Rayleigh model. Fading parameters equivalent to Nakagami-m-model values of m near 0.7 were often observed (with ra = 1 being Rayleigh and m < 1 being worse than Rayleigh). We also provide channel tap amplitude correlation coefficients, which typically range from 0.1 to 0.4 but occasionally take values greater than 0.7. Index Terms--Channel impulse response (CIR), fading, radio propagation.

In this paper, a new modulation scheme that is called spectrally shaped generalized multitone direct sequence spread spectrum (SSG-MT-DS-SS) is proposed. This scheme enables moderate shaping of the transmitted spectrum without the use of spectral-shaping filters; instead, the spectrum is shaped by appropriate selection of the parameters of each subcarrier. These parameters are amplitude, data rate, processing gain, and the frequency separation between adjacent subcarriers. Since these parameters are selectable, this scheme is a completely generalized MT-DS-SS approach. Analysis and simulation results show that by properly choosing these parameters, the level of the spectral sidelobes can be reduced, while slightly changing the width of the mainlobe and simultaneously obtaining a good error-probability performance, on both additive white Gaussian noise and dispersive fading channels. For even a small number of subcarriers (e.g., 3-5), spectral sidelobes can be reduced by 3-6 dB from those of the conventional MT-DS-SS spectrum, with little or no degradation in error-probability performance. For larger numbers of subcarriers, additional sidelobe reductions are attainable. In addition, the SSG-MT-DS-SS system has a smaller peak-to-average power ratio than the conventional MT-DS-SS when the amplitudes of each subcarrier are not identical. Index Terms--Bit error ratio (BER) performance, multitone, spectrum shaping, spread spectrum (SS).

We report a novel Ni3S2 carbon coated (denoted as NCC) rod-like structure prepared by a facile one-pot hydrothermal method and employ it as a binder free electrode in supercapacitor. We coated carbon with glucose as carbon source on the surface of samples and investigated the suitable glucose concentration. The as-obtained NCC rod-like structure demonstrated great performance with a huge specific capacity of 657 C g−1 at 1 A g−1, preeminent rate capability of 87.7% retention, the current density varying to 10 A g−1, and great cycling stability of 76.7% of its original value through 3500 cycles, which is superior to the properties of bare Ni3S2. The result presents a facile, general, viable strategy to constructing a high-performance material for the supercapacitor applications. [ABSTRACT FROM AUTHOR]

Objective: Posttraumatic epilepsy (PTE) that develops after a traumatic brain injury (TBI) cannot be prevented by current treatments. Although neuroinflammation is involved in epileptogenesis, a potential role for cellular immunity in this process is largely unknown. Natural killer T (NKT) cells are innate-like T lymphocytes that recognize lipid antigens presented by the major histocompatibility complex class I-like CD1d molecule and play a crucial role in regulating immune responses. Herein we examined the role of the CD1d/NKT cell axis in PTE., Methods: We used an undercut surgery to induce TBI in wild-type (WT) and CD1d-deficient (CD1d knockout [KO], CD1d KO) or NKT cell-deficient (Traj18 KO) mice. A pentylenetetrazol (PTZ) test was used to determine seizure susceptibility in vivo, and field potential recordings were made from cortical slices in vitro. Continuous video and wireless EEG monitoring was undertaken of WT and CD1d KO mice between 5 and 8 weeks after brain injury. Because statins are known to impair antigen presentation by CD1d to NKT cells, we also treated WT mice with simvastatin for 10 days after injury and performed the PTZ test. Immunofluorescence and flow cytometry were used to determine changes in immune cells in brain tissue., Results: CD1d KO or Traj18 KO TBI mice had a significantly lower seizure susceptibility than WT mice on the PTZ test. CD1d KO mice had a significantly lower rate of detectable epileptiform activities during field potential recording. Video and EEG monitoring showed that CD1d KO TBI mice had a significantly lower frequency of spontaneous epileptic seizures. There was increased infiltration of immune cells, but reduced microgliosis in the brains of these mice. Simvastatin treatment significantly reduced seizure susceptibility in TBI mice., Significance: Neuroinflammation initiated by the CD1d/NKT cell axis is involved in the development of cortical hyperexcitability and PTE; early treatment with simvastatin following a TBI exerts a prophylactic effect on posttraumatic epileptogenesis by blocking this axis., (© 2025 The Author(s). Epilepsia published by Wiley Periodicals LLC on behalf of International League Against Epilepsy.)