Iron Loss and Temperature Rise Analysis of a Transformer Core Considering Vector Magnetic Hysteresis Characteristics under Direct Current Bias.

Direct current (DC) bias induced by the DC transmission and geomagnetically induced current is a critical factor in the abnormal operation of electrical equipment and is widely used in the field of power transmission and distribution system state evaluation. As the main affected component, the vector magnetization state of a transformer core under DC bias has rarely been studied, resulting in inaccurate transformer operation state estimations. In this paper, a dynamic vector hysteresis model that considers the impact of rotating and DC-biased fields is introduced into the numerical analysis to simulate the distribution of magnetic properties, iron loss and temperature of the transformer core model and a physical 110 kV single-phase autotransformer core. The maximum values of B, H and iron loss exist at the corners and T-joint of the core under rotating and DC-biased fields. The corresponding maximum value of the temperature increase is found in the main core limb area. The temperature rise of the 110 kV transformer core under various DC-biased conditions is measured and compared with the FEM (Finite Element Method) results of the proposed model and the model solely based on the magnetization curve B||H. The calculation error of the temperature rise obtained by the improved model is approximately 3.76-15.73% and is much less than the model solely based on magnetization curve B||H (approximately 50.71-66.92%).

Demagnetization Parameters Evaluation of Magnetic Shields Based on Anhysteretic Magnetization Curve.

To achieve the nearly zero-field environment, demagnetization is an indispensable step for magnetic shields composed of high-permeability material, which adjusts the magnetization of the material to establish magnetic equilibrium with the environmental field and improve the shielding performance. The ideal demagnetization can make the high-permeability material on the anhysteretic magnetization curve to have a higher permeability than on the initial magnetization curve. However, inappropriate parameters of degaussing field cause the magnetization state to deviate from the anhysteretic magnetization curve. Therefore, this article proposes a new assessment criterion to analyze and evaluate the parameters of degaussing field based on the difference between the final magnetization state after demagnetization and theoretical anhysteretic state of the shielding material. By this way, the magnetization states after demagnetizations with different initial amplitude, frequency, period number and envelope attenuation function are calculated based on the dynamic Jiles-Atherton (J-A) model, and their magnetization curves under these demagnetization conditions are also measured and compared, respectively. The lower frequency, appropriate amplitude, sufficient period number and logarithmic envelope attenuation function can make the magnetization state after demagnetization closer to the ideal value, which is also consistent with the static magnetic-shielding performance of a booth-type magnetically shielded room (MSR) under different demagnetization condition.

MicroRNA-328 is involved in the effect of selenium on hydrogen peroxide-induced injury in H9c2 cells.

Oxidative stress induces apoptosis in cardiac cells, and antioxidants attenuate the injury. MicroRNAs (miRNAs) are also involved in cell death; therefore, this study aimed to investigate the role of miRNAs in the effect of selenium on oxidative stress-induced apoptosis. The effects of sodium selenite were analyzed via cell viability, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) concentration. Flow cytometry was used to evaluate cell apoptosis. Fura-2AM was used to calculate intracellular Ca2+ concentration. Sodium selenite could ameliorate hydrogen peroxide (H2 O2 )-induced cell apoptosis and improve expression levels of glutathione peroxidase and thioredoxin reductase. Pretreatment with sodium selenite improved SOD activity and reduced MDA concentration. Treatments with H2 O2 or sodium selenite decreased miR-328 levels. MiR-328 overexpression enhanced cell apoptosis, reduced ATP2A2 levels, and increased intracellular Ca2+ concentration, while inhibition produced opposite effects. MiR-328 might be involved in the effect of sodium selenite on H2 O2 -induced cell death in H9c2 cells.

Role of tRNA selenocysteine 1 associated protein 1 in the proliferation and apoptosis of cardiomyocyte­like H9c2 cells.

Transfer RNA selenocysteine 1 associated protein 1 (Trnau1ap) serves an essential role in the synthesis of selenoproteins, which have critical functions in numerous biological processes. Selenium deficiency results in a variety of diseases, including cardiac disease. However, the mechanisms underlying myocardial injury induced by selenium deficiency remain unclear. The present study examined the effects of Trnau1ap under­ and overexpression in cardiomyocyte­like H9c2 cells, by transfection with small interfering RNA and an overexpression plasmid, respectively. Expression levels of glutathione peroxidase, thioredoxin reductase and selenoprotein K were decreased in Trnau1ap­underexpressing cells, and increased in Trnau1ap­overexpressing cells. Using MTT, proliferating cell nuclear antigen, annexin V and caspase­3 activity assays, it was demonstrated that reducing Trnau1ap expression levels inhibited the proliferation of H9c2 cells and induced apoptosis. Conversely, increasing Trnau1ap expression levels promoted cell growth. Western blot analysis revealed that the phosphoinositide 3­kinase/protein kinase B signaling pathway was activated in Trnau1ap­underexpressing cells. Furthermore, the apoptotic pathway was activated in these cells, evidenced by relatively greater expression levels of B­cell lymphoma (Bcl­2)­associated X protein and reduced expression levels of Bcl­2. Taken together, these findings suggest that Trnau1ap serves a key role in the proliferation and apoptosis of H9c2 cells. The present study provides insight into the underlying mechanisms of myocardial injury induced by selenium deficiency.