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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]

This study aims to develop an optimal recipe of amendment (nutrients and electron acceptors) for anaerobic benzene bioremediation and identify the dominant indigenous benzene-degrading microorganisms in soil and groundwater collected from a fuel service station. Lessons learned in developing and optimizing the amendment recipe follow: (1) salinity and a high initial concentration of benzene were detrimental for benzene biodegradation, (2) a large dose of amendment can shorten the lag time for benzene biodegradation, (3) toluene was an essential co-substance for promoting benzene biodegradation. Stable isotope probing was used to identify microorganism incorporation of 13C from 13C– benzene. Under the experimental conditions, incorporation of 13C can be considered direct evidence of the occurrence of benzene biodegradation. Quantitative polymerase chain reaction showed the primary mechanism for benzene removal to be nitrate reduction. Microbial analyses (denaturing gradient gel electrophoresis and 16S ribosomal RNA) demonstrated that members of genus Dokdonella spp., Pusillimonas spp., and Advenella spp. were predominant in the microbial community and involved in anaerobic benzene bioremediation. [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.)

A major technical challenge for using optical imaging to analyze neuronal circuit functions is how to effectively load synthetic Ca(2+) dyes or neural tracers into the brain. We introduce here a simple but versatile approach to label many neurons and clearly visualize their axonal and dendritic morphology. The method uses a large-tip patch pipette filled with dextran-conjugated Ca(2+) dyes or fluorescent tracers. By inserting the pipette into a targeted brain area and passing microampere current pulses, dyes or tracers are electroporated into dendrites and axons near the pipette tip. The dyes are then transported to reveal the entire cell morphology, suitable for both functional Ca(2+) imaging and neuronal circuit tracing. This process requires basic physiological equipment normally available in a physiological laboratory., (© 2014 Cold Spring Harbor Laboratory Press.)