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The insulation defects in Opening/Closing coil of circuit breaker were studied in this paper by analysing the structure of coil, the current of coil when operating, causes and characteristics of internal defects. The results show that the insulation defects caused as coil manufacturing will produce local overheating or inter-turn short circuit under the operating current. Faulty coil does not affect performances of circuit breaker. However the DC resistance decreases, coil current increases and waveform is abnormal, and the correctness of the analysis was verified by return test and anatomy. Finally, effective protection measures to the Opening/Closing coil of circuit breaker were proposed and a pulse detection method which can effectively detect defects in coils was introduced. The practice shows that the pulse detection method significantly improves the qualified rate of the coil.

Comparing voltage and reactive power exchange before and after reactive power optimization, the effect of reactive power optimization of converter station is verified. This article presents reactive power balance method of converter station on account of reactive power compensation equipment at low voltage side of main transformer, and proposes a strategy of changing reactive power control region. Taking one local converter station as an example, the real operation condition is simulated in RTDS, and the two proposed methods are applied to reactive power control. The simulation results verify the beneficial effect of the proposed methods on optimizing the switching of reactive power equipment and improving the voltage control ability of converter station. It provides important reference for engineering application of reactive power control strategies optimization.

In an HVDC system, the power line carrier noise filter, or the PLC filter for short, is mainly used to eliminate the interference of high-frequency harmonics generated by the converter valve to AC line carrier communication. There had been several burning accidents of PLC filter tuning elements in HVDC projects, which profoundly reduced the availability of the HVDC system. To solve this problem, in this paper, the operating parameters of PLC filter components were simulated and analyzed with the variation of harmonic power supply frequency firstly, with the fault weak points of tuned components being found. Then, according to the structures of the PLC communication filters and the tuning elements, three optimization schemes of the PLC filter were proposed. The feasibility of these schemes are compared by simulation and calculation from two aspects: the effect of reducing high-frequency harmonic interference and the influence on the running capacity of the equipment. Finally the risk of these schemes are pointed out.

Dexamethasone is a commonly used synthetic glucocorticoid in the clinic. As a compound that can cross the placental barrier to promote fetal lung maturation, dexamethasone is extensively used in pregnant women at risk of premature delivery. However, the use of glucocorticoids during pregnancy increases the risk of neurodevelopmental disorders. In the present study, we observed anxiety- and depressive-like behavior changes and hyperexcitability of hippocampal neurons in adult rat offspring with previous prenatal dexamethasone exposure (PDE); the observed changes were related to in utero damage of parvalbumin interneurons. A programmed change in neuregulin 1 (NRG1)-Erb-b2 receptor tyrosine kinase 4 (ErbB4) signaling was the key to the damage of parvalbumin interneurons in the hippocampus of PDE offspring. Anxiety- and depressive-like behavior, NRG1-ErbB4 signaling activation, and damage of parvalbumin interneurons in PDE offspring were aggravated after chronic stress. The intervention of NRG1-ErbB4 signaling contributed to the improvement in dexamethasone-mediated injury to parvalbumin interneurons. These results suggested that PDE might cause anxiety- and depressive-like behavior changes in male rat offspring through the programmed activation of NRG1-ErbB4 signaling, resulting in damage to parvalbumin interneurons and hyperactivity of the hippocampus. Intrauterine programming of neuregulin 1 (NRG1)-Erb-b2 receptor tyrosine kinase 4 (ERBB4) overactivation by dexamethasone mediates anxiety- and depressive-like behavior in male rat offspring.

Epidemiological investigations have suggested that periodic use of dexamethasone during pregnancy is a risk factor for abnormal behavior in offspring, but the potential mechanism remains unclear. In this study, we investigated the changes in the glutamatergic system and neurobehavior in female offspring with prenatal dexamethasone exposure (PDE) to explore intrauterine programing mechanisms. Compared with the control group, rat offspring with PDE exhibited spatial memory deficits and anxiety-like behavior. The expression of hippocampal glucocorticoid receptors (GR) and histone deacetylase 2 (HDAC2) increased, whereas histone H3 lysine 14 acetylation (H3K14ac) of brain-derived neurotrophic factor (BDNF) exon IV (BDNF IV) and expression of BDNF decreased. The glutamatergic system also changed. We further observed that changes in the fetal hippocampus were consistent with those in adult offspring. In vitro, the administration of 0.5 μM dexamethasone to the H19-7 fetal hippocampal neuron cells directly led to a cascade of changes in the GR/HDAC2/BDNF pathway, whereas the GR antagonist RU486 and the HDAC2 inhibitor romidepsin (Rom) reversed changes caused by dexamethasone to the H3K14ac level of BDNF IV and to the expression of BDNF. The increase in HDAC2 can be reversed by RU486, and the changes in the glutamatergic system can be partially reversed after supplementation with BDNF. It is suggested that PDE increases the expression of HDAC2 by activating GR, reducing the H3K14ac level of BDNF IV, inducing alterations in neurobehavior and hippocampal glutamatergic system balance. The findings suggest that BDNF supplementation and glutamatergic system improvement are potential therapeutic targets for the fetal origins of abnormal neurobehavior.

Epidemiological investigations have confirmed that prenatal caffeine intake could increase the incidence rate of intrauterine growth retardation (IUGR) and multiple diseases after birth. Based on liquid chromatography-mass spectrometry, we analyzed serum metabolic profiles of offspring rats before and after birth in IUGR model induced by prenatal caffeine exposure (PCE). We discovered that differential metabolites in PCE fetuses mainly manifested as amino acids and lipid metabolism. In adulthood, PCE offspring showed less and inconsistent types of differential metabolites compared to those in utero, which still exhibited gender differences. The main differential metabolites induced by PCE, including phospholipids, platelet-activating factor, arachidonic acid, bile acid, sphingosine-1-phosphoric acid, indoxyl sulfuric acid, and cortexolone, may participate in the pathological and physiological processes of organ toxicities. This study demonstrated the short- and long-term developmental toxicity and gender differences of caffeine, providing new ideas for exploring the early warning and drug intervention targets of IUGR offspring.

Nuclear receptors (NRs) belong to a family of ligand-dependent transcription factors. The target genes of NRs include many drug metabolizing enzymes and transporters. The central nervous system (CNS) bears the expression of NRs, drug metabolizing enzymes and transporters. NRs that express in the brain can be divided into three groups according to their characteristics of ligand binding: steroid hormone receptors, non-steroid hormone receptors, and orphan receptors. The NR-mediated regulation of drug metabolizing enzymes and transporters plays important roles in the metabolism and disposition of drugs in the CNS and the penetration of endogenous and exogenous substances through the blood-brain barrier (BBB). NR-mediated regulation of drug metabolizing enzymes and transporters can cause the toxicological effects of xenobiotics in the CNS and also lead to drug resistance in the centrum. The regulatory pathways of drug metabolizing enzymes and transporters can provide new strategies for selective regulation of the BBB permeability and drug metabolism in the brain. This review focuses on the importance of NR-mediated regulation of drug metabolizing enzymes and transporters in the CNS and the implications of this regulation in the therapeutic effect of CNS drugs and CNS side effects of drugs and other xenotoxicants.