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Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.

Diabetic cardiomyopathy (DCM) is a type of myocardial injury induced by diabetes. Under the stimulation of continuous hyperglycemia, cardiomyocytes will produce a series of stress responses include apoptosis and inflammation. Sterol regulatory element binding protein cleavage-activating protein (SCAP) is a cholesterol-regulating protein, which is related to diabetes and is abnormally expressed in a variety of complications of diabetes. The purpose of this study was to explore the role of SCAP on cardiomyocyte injury. H9C2 cells were exposed to 35 mmol glucose for 48 h to induce myocardial injury. The results of western blot and immunofluorescence staining showed that the expression of SCAP was increased in high glucose stimulated cells and cardiomyocyte apoptosis increased obviously after high glucose intervention. Then we transfected SCAP siRNA to inhibit SCAP. Our results showed that apoptosis of H9C2 cells induced by high glucose alleviated significantly after SCAP was silenced. And down-regulation of SCAP could also restrained reactive oxygen species (ROS) induced by high glucose. Meanwhile, the protein levels of NLRP3, Caspase-1, IL-1β, and p-NF-κB protein was decreased. This reminds us that down-regulation of SCAP can inhibit the apoptosis, ROS and inflammation of cardiomyocytes induced by high glucose. The above evidence speculates that SCAP might play a potential role in the cardiomyocytes injury under high glucose surroundings.

Aim Spinal cord injury (SCI) involves multiple pathological processes. Ferroptosis has been shown to play a critical role in the injury process. We wanted to explore whether zinc can inhibit ferroptosis, reduce inflammation, and then exert a neuroprotective effect. Methods The Alice method was used to establish a spinal cord injury model. The Basso Mouse Scale (BMS), Nissl staining, hematoxylin‐eosin staining, and immunofluorescence analysis were used to investigate the protective effect of zinc on neurons on spinal cord neurons and the recovery of motor function. The regulation of the nuclear factor E2/heme oxygenase‐1 (NRF2/HO‐1) pathway was assessed, the levels of essential ferroptosis proteins were measured, and the changes in mitochondria were confirmed by transmission electron microscopy and 5,5′,6,6′‐tetrachloro‐1,1′,3,3′‐tetraethyl‐imidacarbocyanine iodide (JC‐1) staining. In vitro experiments using VSC4.1 (spinal cord anterior horn motor neuroma cell line), 4‐hydroxynonenal (4HNE), reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), lipid peroxides, and finally the levels of inflammatory factors were detected to assess the effect of zinc. Results Zinc reversed behavioral and structural changes after SCI. Zinc increased the expression of NRF2/HO‐1, thereby increasing the content of glutathione peroxidase 4 (GPX4), SOD, and GHS and reducing the levels of lipid peroxides, MDA, and ROS. Zinc also rescued injured mitochondria and effectively reduced spinal cord injury and the levels of inflammatory factors, and the NRF2 inhibitor Brusatol reversed the effects of zinc. Conclusion Zinc promoted the degradation of oxidative stress products and lipid peroxides through the NRF2/HO‐1 and GPX4 signaling pathways to inhibit ferroptosis in neurons., Mechanisms underlying the repair of spinal cord injury through inhibiting ferroptosis with zinc.

Aim Spinal cord injury (SCI) is a serious disabling injury worldwide, and the excessive inflammatory response it causes plays an important role in secondary injury. Regulating the inflammatory response can be a potential therapeutic strategy for improving the prognosis of SCI. Zinc has been demonstrated to have a neuroprotective effect in experimental spinal cord injury models. In this study, we aimed to explore the neuroprotective effect of zinc through the suppression of the NLRP3 inflammasome. Method Allen's method was used to establish an SCI model in C57BL/6J mice. The Basso Mouse Scale (BMS), Nissl staining were employed to confirm the protective effect of zinc on neuronal survival and functional recovery in vivo. Western blotting (WB), immunofluorescence (IF), and enzyme‐linked immunosorbent assay (ELISA) were used to detect the expression levels of NLRP3 inflammasome and autophagy‐related proteins. Transmission electron microscopy (TEM) was used to confirm the occurrence of zinc‐induced autophagy. In vitro, lipopolysaccharide (LPS) and ATP polarized BV2 cells to a proinflammatory phenotype. 3‐Methyladenine (3‐MA) and bafilomycin A1 (BafA1) were chosen to explore the relationship between the NLRP3 inflammasome and autophagy. A coimmunoprecipitation assay was used to detect the ubiquitination of the NLRP3 protein. Results Our data showed that zinc significantly promoted motor function recovery after SCI. In vivo, zinc treatment inhibited the protein expression level of NLRP3 while increasing the level of autophagy. These effects were fully validated by the polarization of BV2 cells to a proinflammatory phenotype. The results showed that when 3‐MA and BafA1 were applied, the promotion of autophagy by zinc was blocked and that the inhibitory effect of zinc on NLRP3 was reversed. Furthermore, co‐IP confirmed that the promotion of autophagy by zinc also activated the protein expression of ubiquitin and suppressed high levels of NLRP3. Conclusion Zinc provides neuroprotection by regulating NLRP3 inflammasome through autophagy and ubiquitination after SCI., Zinc provides neuroprotection by regulating NLRP3 inflammasome through autophagy and ubiquitination after SCI.

Spinal cord injury (SCI) causes immune activation of resident macrophages/microglia. Activated macrophages/microglia have two different phenotypes, the pro-inflammatory classically activated (M1) phenotype and the anti-inflammatory alternatively activated (M2) phenotype. M1 phenotype macrophages/microglia are the key factor in inflammation. The treatment of SCI remains a huge challenge due to the nontargeting and inefficiency of anti-inflammatory drugs through the blood-brain barrier (BBB). The purpose of this experiment was to design M2-type primary peritoneal macrophages exosomes (Exos) as a drug carrier for berberine (Ber), which can be efficiently targeted to deliver drugs to the injured spinal cord due to the natural advantage of Exos across the BBB. The Exos with particle size of 125±12 nm were loaded with by an ultrasonic method and the drug loading reached 17.13 ±1.64%. The Ber release experiment showed that the loaded sample (Exos-Ber) exhibited sustained release effect, and the cumulative release amount reached 71.44±2.86% within 48 h. In vitro and in vivo experiments confirmed that the Exos-Ber could decrease the M1 protein marker iNOS, elevate the M2 protein marker CD206 and reduce inflammatory and apoptotic cytokines (TNF-α, IL-1β, IL-6, Caspase 9, Caspase 8), which showed that Exos-Ber had a good anti-inflammatory and anti-apoptotic effect by inducing macrophages/microglia from the M1 phenotype to M2 phenotype polarization. Moreover, the motor function of SCI mice was significantly improved after Exos-Ber treatment, indicating that Exos-Ber is a potential agent for SCI therapy. STATEMENT OF SIGNIFICANCE: Efficient targeting strategy for drug delivery. In addition to good biocompatibility and stealth ability, M2 macrophage-derived Exosomes present natural inflammatory targeting ability. The inflammatory microenvironment after spinal cord injury provides motivation for the targeting of exosomes. Natural drug carrier with higher safety. With the rapid development of nanomaterials, drug carriers have become more selective. However, due to the special microenvironment after central nervous system damage, some non-degradable inorganic materials will increase the pressure of self-healing and even secondary damage to neurons, which has been solved by the emergence of exosomes. Some previous studies used tumor cell line exosomes as drug carriers, but the carcinogenic factors carried by themselves have extremely high hidden dangers, and endogenous macrophage exosomes have absolute advantages over their safety.

Spinal cord injury (SCI) causes immune activation of resident microglia. Activated microglia have two different phenotypes, the pro-inflammatory classically activated (M1) phenotype and the anti-inflammatory alternatively activated (M2) phenotype. M1 phenotype microglia are the key factor in inflammation. The treatment of SCI remains a huge challenge due to the nontargeting and inefficiency of anti-inflammatory drugs through the blood-brain barrier (BBB). The purpose of this experiment was to design M2-type primary peritoneal macrophages exosomes (Exos) as a drug carrier for berberine (Ber), which can be efficiently targeted to deliver drugs to the injured spinal cord due to the natural advantage of Exos across the BBB. The Exos were loaded with Ber by an ultrasonic method. In vitro and in vivo experiments confirmed that the loaded sample (Exos-Ber) could decrease the M1 protein marker iNOS, elevate the M2 protein marker CD206 and reduce inflammatory and apoptotic cytokines (TNF-α, IL-1β, IL-6, Caspase 9, Caspase 8), which showed that Exos-Ber had a good anti-inflammatory and anti-apoptotic effect by inducing microglia from the M1 phenotype to M2 phenotype polarization. Moreover, the motor function of SCI mice was significantly improved after Exos-Ber treatment, indicating that Exos-Ber is a potential agent for SCI therapy.

The SVPWM technique plays an important role in the DC-AC transform. The modeling and simulation for SVPWM were proposed in this paper. The sector calculating model and basic vector working time model were set up. The effective vector function of time was set up. The triangle wave symmetry modulation was established too. The simulation results show that the model proposed in this paper is effective and has application value.

Airfield lighting circuit is an important part of airfield lighting system, and the insulation resistance value of this circuit is affected by humidity, temperature, the quality and the number of the Isolation Transformers and many other factors, so it is difficult to accurately predict the resistance size by using traditional methods. In the light of insulation resistance values of airfield lighting circuit, this paper put forward adopting Gray System Theory to make the prediction, and then build GM(2,1) model to analyze and forecast the resistance values according to the actually measured values of the insulation resistance at Shanghai Pudong International Airport. Finally, the research shows that there is only a little difference between predicted values and the actually measured values. In other words, the prediction of insulation resistance based on Gray System Theory is viable.

Navigation light monitoring system is designed to detect the working condition of each light with circuit cable carrier. However, the real-time detecting information could be inaccurate as a result of the existence of disturbances such as noise, multi-path effect and channel decline, when the data transmission happens in light cable as the channel. In this paper, OFDM (Orthogonal Frequency Division Multiplexing) is presented to be used in circuit cable communication. And the reason and capability of the resistance to these disturbances in OFDM are analyzed. Finally, the result is concluded that OFDM used in navigation light cable channel is feasible.