An accurate calculation method for inductor air gap length in high power DC-DC converters.

High-power inductors are fundamental components in high-power DC-DC converters, with their performance being a crucial metric of converter efficiency. This paper presents an in-depth analysis of a novel calculation method for the air gap length in such inductors. Taking into account the effects of air gap diffusion and the winding magnetic field, an expression for the air gap diffusion radius is derived, focusing on a distributed air gap structure. Furthermore, models for calculating the air gap and winding reluctance are developed, grounded in electromagnetic field theory. An equivalent magnetic circuit model, formulated based on Kirchhoff's second law, facilitates the proposed method for air gap length calculation. This study also involves the development of 3D models for both discrete and decoupled integrated inductors. The comparison between simulation outcomes and calculated air gap lengths indicates a maximum error of less than 8%, with the minimum error being as low as - 0.79%. Compared with traditional methods, the calculation method proposed in this paper has significant advantages. Additionally, the discrepancy between calculated values and experimental measurements is found to be 1.11%. These results validate the accuracy and applicability of the theoretical analysis and calculation method, underscoring their significance in the design and optimization of high-power DC-DC converters.

Winding loss analysis of planar spiral coil and its structure optimization technique in wireless power transfer system.

Circular planar spiral coils are wildly used for the magnetic coupling system in a high-frequency wireless power transfer system. The loss of the magnetic coupling system usually takes dominance in the whole system. This paper built the calculation model of magnetic field strength and coil loss, the proposed calculation model can effectively consider the mutual influence between the transmitter and receiver coil and accurately calculated the AC loss of WPT coils. Then, the effect of turn spacing on the AC resistance of coil is analyzed. It reveals that the proximity effect loss is greater when the coil is tightly wound, and the AC loss can be optimized by designing the turn spacing. Based on the above analysis, a double-layer coil method is proposed. This method can reduce the AC loss and improve the quality factor (Q) without changing the mutual inductance and footprint of coil at high frequency. The AC resistance of the double-layer coil method can be greatly reduced compared with the general method through simulation and experiment. The work efficiency of WPT system is increased by 4.3%, which verifies the accuracy and flexibility of theoretical analysis.

Natural variation and domestication selection of ZmSULTR3;4 is associated with maize lateral root length in response to salt stress.

Soil salinity is a major constraint that restricts crop productivity worldwide. Lateral roots (LRs) are important for water and nutrient acquisition, therefore understanding the genetic basis of natural variation in lateral root length (LRL) is of great agronomic relevance to improve salt tolerance in cultivated germplasms. Here, using a genome-wide association study, we showed that the genetic variation in ZmSULTR3;4, which encodes a plasma membrane-localized sulfate transporter, is associated with natural variation in maize LRL under salt stress. The transcript of ZmSULTR3;4 was found preferentially in the epidermal and vascular tissues of root and increased by salt stress, supporting its essential role in the LR formation under salt stress. Further candidate gene association analysis showed that DNA polymorphisms in the promoter region differentiate the expression of ZmSULTR3;4 among maize inbred lines that may contribute to the natural variation of LRL under salt stress. Nucleotide diversity and neutrality tests revealed that ZmSULTR3;4 has undergone selection during maize domestication and improvement. Overall, our results revealed a regulatory role of ZmSULTR3;4 in salt regulated LR growth and uncovered favorable alleles of ZmSULTR3;4, providing an important selection target for breeding salt-tolerant maize cultivar.

Inhibition of KLF6 reduces the inflammation and apoptosis of type II alveolar epithelial cells in acute lung injury.

BACKGROUND: The development of acute lung injury (ALI) into a severe stage leads to acute respiratory distress syndrome (ARDS). The morbidity and mortality of ALI and ARDS are very high. Objective: This study is aimed to explore the effect of Krüppel-like factor 6 (KLF6) on lipopolysaccharide (LPS)-induced type II alveolar epithelial cells in ALI by interacting with cysteine-rich angiogenic inducer 61 (CYR61). MATERIAL AND METHODS: ALI mice model and LPS-induced type II alveolar epithelial cells were conducted to simulate ALI in vivo and in vitro. The messenger RNA (mRNA) and protein expression of KLF6 in lung tissues were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. Pathological changes in lung tissues were observed by hematoxylin and eosin (H&E) staining. The viability and KLF6 expression of A549 cells treated with different concentrations of LPS were detected by cell counting kit-8 (CCK-8) assay, RT-qPCR, and Western blot analysis. After indicated treatment, the viability and apoptosis of A549 cells were analyzed by CCK-8 and TUNEL assays, and the inflammation factors of A549 cells were detected by Enzyme-linked-immunosorbent serologic assay, RT-qPCR, and Western blot analysis. The combination of KLF6 and CYR61 was determined by chromatin immunoprecipitation (ChIP)-PCR and dual-luciferase reporter assay. RESULTS: KLF6 expression was increased in lung tissues of ALI mice and LPS-induced A549 cells. Interference with KLF6 improved the viability, reduced the inflammatory damage, and promoted the apoptosis of LPS-induced A549 cells. In addition, KLF6 could bind to CYR61. Interference with KLF6 could decrease CYR61 expression in LPS-induced A549 cells. LPS also enhanced the TLR4/MYD88 signaling pathway, which was reversed by KLF6 interference. The above phenomena in LPS-induced A549 cells transfected with Si-KLF6 could be reversed by overexpression of CYR61. CONCLUSION: Inhibition of KLF6 promoted the viability and reduced the inflammation and apoptosis of LPS-induced A549 cells, which was reversed by CYR61.

EMI characteristics analysis and suppression technique of magnetic near-field coupling in power delivery adapter.

With the continuous improvement of the power density of the power delivery (PD) adapter, switching frequency increases and volume decreases. The EMI issues caused by magnetic near-field coupling effects have become bottlenecks in the PD adapter's EMI suppression. In this paper, the coupling characteristics of the magnetic field are deeply analyzed, and the equivalent circuit considering near-field coupling effects is derived. According to the electromagnetic field theory, the mathematical models of near-field coupling between transformer as well as power PCB circuits and the input plug are established. Based on this, the influence of the structure parameters of the input plug is studied. Finally, a new input plug loop structure is proposed, which can reduce the near-field coupling effects between the transformer as well as power PCB circuits and input plug. The experimental results verify the theoretical analysis to be correct and effective.

Abscisic acid-induced cytoplasmic translocation of constitutive photomorphogenic 1 enhances reactive oxygen species accumulation through the HY5-ABI5 pathway to modulate seed germination.

Seed germination is a physiological process regulated by multiple factors. Abscisic acid (ABA) can inhibit seed germination to improve seedling survival under conditions of abiotic stress, and this process is often regulated by light signals. Constitutive photomorphogenic 1 (COP1) is an upstream core repressor of light signals and is involved in several ABA responses. Here, we demonstrate that COP1 is a negative regulator of the ABA-mediated inhibition of seed germination. Disruption of COP1 enhanced Arabidopsis seed sensitivity to ABA and increased reactive oxygen species (ROS) levels. In seeds, ABA induced the translocation of COP1 to the cytoplasm, resulting in enhanced ABA-induced ROS levels. Genetic evidence indicated that HY5 and ABI5 act downstream of COP1 in the ABA-mediated inhibition of seed germination. ABA-induced COP1 cytoplasmic localization increased HY5 and ABI5 protein levels in the nucleus, leading to increased expression of ABI5 target genes and ROS levels in seeds. Together, our results reveal that ABA-induced cytoplasmic translocation of COP1 activates the HY5-ABI5 pathway to promote the expression of ABA-responsive genes and the accumulation of ROS during ABA-mediated inhibition of seed germination. These findings enhance the role of COP1 in the ABA signal transduction pathway.

COP1 promotes ABA-induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases.

Plant stomata play a crucial role in leaf function, controlling water transpiration in response to environmental stresses and modulating the gas exchange necessary for photosynthesis. The phytohormone abscisic acid (ABA) promotes stomatal closure and inhibits light-induced stomatal opening. The Arabidopsis thaliana E3 ubiquitin ligase COP1 functions in ABA-mediated stomatal closure. However, the underlying molecular mechanisms are still not fully understood. Yeast two-hybrid assays were used to identify ABA signaling components that interact with COP1, and biochemical, molecular and genetic studies were carried out to elucidate the regulatory role of COP1 in ABA signaling. The cop1 mutants are hyposensitive to ABA-triggered stomatal closure under light and dark conditions. COP1 interacts with and ubiquitinates the Arabidopsis clade A type 2C phosphatases (PP2Cs) ABI/HAB group and AHG3, thus triggering their degradation. Abscisic acid enhances the COP1-mediated degradation of these PP2Cs. Mutations in ABI1 and AHG3 partly rescue the cop1 stomatal phenotype and the phosphorylation level of OST1, a crucial SnRK2-type kinase in ABA signaling. Our data indicate that COP1 is part of a novel signaling pathway promoting ABA-mediated stomatal closure by regulating the stability of a subset of the Clade A PP2Cs. These findings provide novel insights into the interplay between ABA and the light signaling component in the modulation of stomatal movement.

CRISPR/Cas9 edited HSFA6a and HSFA6b of Arabidopsis thaliana offers ABA and osmotic stress insensitivity by modulation of ROS homeostasis.

The role of Heat Shock Transcription Factor 6 (HSFA6a & HSFA6b) in response to abiotic stresses such as ABA, drought, salinity, drought, and osmotic stress is individually well established. Unfortunately, the functional redundancy between the HSFA6a and HSFA6b as well as the consequences of simultaneous editing of both in response to aforementioned stresses remains elusive. Therefore, this study was designed with the aim of addressing whether there is any functional redundancy between HSFA6a and HSFA6b as well as to decipher their role in abiotic stresses tolerance in Arabidopsis thaliana, by using the CRISPR-Cas9. We have generated the single (hsfa6a and hsfa6b) as well as double mutants (hsfa6a/hsfa6b-1 and hsfa6a/hsfa6b-2) of HSFA6a and HSFA6b with higher frequencies of deletion, insertion, and substitution. The phenotypic characterization of generated double and single mutants under abiotic stresses such as ABA, mannitol, and NaCl identified double mutants more tolerant to subjected abiotic stresses than those of their single mutants. It warrants mentioning that we have identified that HSFA6a and HSFA6b also involved in other major ABA responses, including ABA-inhibited seed germination, stomatal movement, and water loss. In addition to the above, the simultaneous editing of HSFA6a and HSFA6b lead to a reduced ROS accumulation, accompanied by increased expression of much abiotic stress and ABA-responsive genes, including involved in regulation of ROS level. In conclusion, these results suggest that HSFA6a and HSFA6b may offer abiotic stress tolerance by regulating the ROS homeostasis in plants.

Trehalose-6-phosphate phosphatase E modulates ABA-controlled root growth and stomatal movement in Arabidopsis.

Trehalose plays important roles in plant growth and stress responses and is synthesized from trehalose-6-phosphate by trehalose-6-phosphate phosphatase (TPP). Here, we show that trehalose and abscisic acid (ABA) have synergistic effects on root growth and stomatal closure. The Arabidopsis thaliana genome contains ten genes encoding TPPs and the expression level of one, TPPE, and trehalose contents increased in response to ABA. In the presence of ABA, the ABA-responsive transcription factor ABA RESPONSE ELEMENT BINDING FACTOR2 (ABF2) directly binds to the TPPE promoter to activate its expression. Genetic analysis revealed that TPPE acts downstream of ABF2, which is supported by the findings that TPPE expression and trehalose content are reduced in the abf2 mutant and that a mutation in TPPE abolished the ABA-sensitive root elongation phenotype of 35S:ABF2 plants. Reactive oxygen species (ROS) accumulation in response to ABA failed to occur in tppe mutant plants, suggesting that TPPE is involved in ABA-controlled root elongation and stomatal movement by inducing ROS accumulation. This study uncovers a new branch of the ABA signaling pathway and provides a molecular basis for the role of trehalose in plant responses to abiotic stress.

Beyond Light: Insights Into the Role of Constitutively Photomorphogenic1 in Plant Hormonal Signaling.

Light is an important environmental factor with profound effects in plant growth and development. Constitutively photomorphogenic1 (COP1) is a vital component of the light signaling pathway as a negative regulator of photomorphogenesis. Although the role of COP1 in light signaling has been firmly established for some time, recent studies have proven that COP1 is also a crucial part of multiple plant hormonal regulatory pathways. In this article, we review the available evidence involving COP1 in hormone signaling, its molecular mechanisms, and its contribution to the complicated regulatory network linking light and plant hormone signaling.

Mechanism of synergy of BH3 mimetics and paclitaxel in chronic myeloid leukemia cells: Mcl-1 inhibition.

Paclitaxel is an alternative chemotherapeutic agent for chronic myelogenous leukemia (CML) when primary or secondary resistance of tyrosine kinase inhibitors (TKI) is emerging, because paclitaxel could bypass the apoptotic deficiencies linked to p53 and fas ligand pathways in CML. However, high levels of Bcl-2 family proteins in CML could resist paclitaxel-induced apoptosis. Herein, we utilized two BH3 mimetics ABT-737 and S1 to study the potential of BH3 mimetics in combination with paclitaxel in treatment of CML cells and illustrated the mechanism by which BH3 mimetics synergize with paclitaxel. As a single agent, S1 could induce apoptosis in CML-derived cell line K562, whereas ABT-737 was largely ineffective. However, both of the two agents could efficiently synergize with paclitaxel through intrinsic apoptosis pathway. By using Bcl-2 siRNA, Bcl-XL siRNA or Mcl-1 siRNA, we found although each of the three members exhibited activities to block paclitaxel-induced apoptosis, Mcl-1 was the determinant for the synergistic effect between paclitaxel and ABT-737 or S1. Furthermore, paclitaxel/ABT737 synergized to drastically upregulate Bim to displace Bak from Mcl-1, whereas S1 directly binds Mcl-1 to release both Bim and Bak. As such, ABT-737 and S1 sensitized CML to paclitaxel by Mcl-1 inhibition, indirect inhibition through Bim antagonizing Mcl-1, or direct inhibition through binding to Mcl-1 itself. Finally, activation of JNK/Bim pathway was identified as the apical mechanism for ABT-737/paclitaxel synergism. Together, our results demonstrated potent synergy between BH3 mimetics and paclitaxel in the killing of CML cells and revealed an important role for Mcl-1 in mediating synergism by these agents.

Design and application of a rigid quinazolone scaffold based on two-face Bim α-helix mimicking.

Based on our previous discovery of an anthraquinone scaffold mimicking two faces of Bim α-helix, we derived a quinazolone scaffold through structure simplification and optimization. It was inferred that a rigid bicyclic ring was necessary and efficient to maintain the two-faced binding mode. A novel dual inhibitor 6c [6,7,8-trihydroxy-3-(2-hydroxy-5-methylbenzyl)-2-phenylquinazolin-4(3H)-one] was obtained based on this scaffold. 6c exhibited dual binding activity with K(i) values of 0.123 µM for Mcl-1 and 0.179 µM for Bcl-2.

Prevention of chemotherapy-induced alopecia in rodent models.

Alopecia (hair loss) is experienced by thousands of cancer patients every year. Substantial-to-severe alopecia is induced by anthracyclines (e.g., adriamycin), taxanes (e.g., taxol), alkylating compounds (e.g., cyclophosphamide), and the topisomerase inhibitor etoposide, agents that are widely used in the treatment of leukemias and breast, lung, ovarian, and bladder cancers. Currently, no treatment appears to be generally effective in reliably preventing this secondary effect of chemotherapy. We observed in experiments using different rodent models that localized administration of heat or subcutaneous/intradermal injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin induced a stress protein response in hair follicles and effectively prevented alopecia from adriamycin, cyclophosphamide, taxol, and etoposide. Model tumor therapy experiments support the presumption that such localized hair-saving treatment does not negatively affect chemotherapy efficacy.

Extraction of nonlinear hysteretic properties of seismically isolated bridges from quick - release field tests

A time domian system identification method is used to identify the hysteretic properties of lead-rubber bearings installed in seismically isolated bridge systems. The longitudinal or transverse motion of the superstructure is idealized as a single degree of freedom (SDOF) system, where the total damping effect has been divided two parts.