RESUMO
Cooling based on the electrocaloric effect (ECE) is a promising solution to environmental and energy efficiency problems of vapor-compression refrigeration. Ferroelectric polymer-ceramics nanocomposites, integrating high electric breakdown of organic ferroelectrics and large EC strength of ceramics, are attractive EC materials. Here, we tuned the orientation of Ba0.67Sr0.33TiO3 nanofibers (BST nfs) in the P(VDF-TrFE-CFE) polymer. When the nfs were aligned parallel to the field, a ΔT of 11.3 K with an EC strength of 0.16 K·m/MV was achieved in the blends. The EC strength not only surpasses advanced nanocomposites but also is comparable to ferroelectric ceramics. The simulation indicates that a significantly higher electric field is concentrated in polymer regions around the ends of the orientated nfs, contributing to easier flipping of polymer chains for large ECE. This work provides a new method to obtain large ECE in composites for next-generation refrigeration.
RESUMO
Microwave-absorbing materials have attracted enormous attention for electromagnetic (EM) pollution. Herein, hollow beaded Fe3C/N-doped carbon fibers (Fe3C/NCFs) were synthesized through convenient electrospinning and subsequent thermal treatment. The special hollow morphology of the samples is conducive to achieve lightweight and broadband microwave absorption properties. The thermal treatment temperatures exhibit a significant impact on conductivity and EM properties. The broadest effective absorption bandwidth (EAB) is 5.28 GHz at 2.16 mm when the thermal treatment temperature is 700 °C, and the EAB can cover 13.13 GHz with a tunable absorber thickness from 1.0 to 3.5 mm when the thermal treatment temperature is 750 °C. The excellent microwave absorption properties of the samples are due to the synergistic effect of impedance matching and strong EM energy attenuation abilities. Hence, the magnetic hollow beaded Fe3C/NCFs are expected to be an attractive candidate material as a lightweight and efficient microwave absorber in the future.
RESUMO
Chronic neuropathic pain is one of the primary causes of disability subsequent to spinal cord injury. Patients experiencing neuropathic pain after spinal cord injury suffer from poor quality of life, so complementary therapy is seriously needed. Dehydrocorybulbine is an alkaloid extracted from Corydalis yanhusuo. It effectively alleviates neuropathic pain. In the present study, we explored the effect of dehydrocorybulbine on neuropathic pain after spinal cord injury and delineated its possible mechanism. Experiments were performed in rats to evaluate the contribution of dehydrocorybulbine to P2X4 signaling in the modulation of pain-related behaviors and the levels of pronociceptive interleukins and proteins after spinal cord injury. In a rat contusion injury model, we confirmed that chronic neuropathic pain is present on day 7 after spinal cord injury and P2X4R expression is exacerbated after spinal cord injury. We also found that administration of dehydrocorybulbine by tail vein injection relieved pain behaviors in rat contusion injury models without affecting motor functions. The elevation in the levels of pronociceptive interleukins (IL-1ß, IL-18, MMP-9) after spinal cord injury was mitigated by dehydrocorybulbine. Dehydrocorybulbine significantly mitigated the upregulation of P2X4 receptor and reduced ATP-evoked intracellular Ca2+ concentration. Both P2XR and dopamine receptor2 agonists antagonized dehydrocorybulbine's antinociceptive effects. In conclusion, we propose that dehydrocorybulbine produces antinociceptive effects in spinal cord injury models by inhibiting P2X4R.
Assuntos
Isoquinolinas/uso terapêutico , Neuralgia/tratamento farmacológico , Neuralgia/etiologia , Receptores Purinérgicos P2X4/metabolismo , Traumatismos da Medula Espinal/complicações , Animais , Linhagem Celular , Regulação para Baixo/efeitos dos fármacos , Interleucinas/metabolismo , Isoquinolinas/farmacologia , Masculino , Camundongos , Atividade Motora/efeitos dos fármacos , Neuralgia/fisiopatologia , Nociceptividade/efeitos dos fármacos , Ratos Sprague-Dawley , Receptores de Dopamina D2/metabolismo , Traumatismos da Medula Espinal/fisiopatologiaRESUMO
Spinal cord injury (SCI) is one major cause of death and results in long-term disability even in the most productive periods of human lives with few efficacious drugs. Autophagy is a potential therapeutic target for SCI. In the present study, we examined the role of lithium in functional recovery in the rat model of SCI and explored the related mechanism. Locomotion tests were employed to assess the functional recovery after SCI, Western blotting and RT-PCT to determine the level of p-ERK and LC3-II as well as p62, immunofluorescence imaging to localize LC3 and p62. Here, we found that both the expression of LC3-II and p62 were increased after SCI. However, lithium chloride enhanced the level of LC3-II while abrogated the abundance of p62. Furthermore, lithium treatment facilitated ERK activation in vivo, and inhibition of MEK/ERK signaling pathway suppressed lithium-evoked autophagy flux. Taken together, our results illustrated that lithium facilitated functional recovery by enhancing autophagy flux.