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Summary: In this paper, a multiphase digital control called digital integration constant on‐time (DICOT) control is proposed, which applies the concept of signal accumulation, solves the drawbacks of ripple‐based digital COT control that the switching frequency and transient performance are affected by the A/D sample delay and sampling noise. Besides, the multiphase interleaving approach of the proposed DICOT control is well‐suitable for digital control and no higher calculation frequency is required compared to single‐phase. In the aspect of the current balance, almost all existing researches work on analog COT current balance scheme and few works are investigating the resolution improvement of digital COT current balance. In this paper, the current balance model of multiphase COT control is derived and can be applied in the Buck system with an arbitrary number of phases, the delay‐line‐based high‐resolution COT current balance scheme is proposed to enhance the control resolution. Finally, the two‐phase DICOT control is tested on the multiphase Buck system, the transient performance is tested of 100 A load step with the slew rate of 1000 A/μs, and the voltage undershoot and overshoot are 20 and 36 mV, respectively. The current balance is tested and the errors are 0.01% and 0.11% at the light and heavy loads, respectively. [ABSTRACT FROM AUTHOR]

To solve the challenges of low recognition accuracy, slow speed, and weak generalization ability inherent in traditional methods for multi‐damage recognition of concrete bridges, this paper proposed an efficient lightweight damage recognition model, constructed by improving the you only look once v4 (YOLOv4) with MobileNetv3 and fused inverted residual blocks, named YOLOMF. First, a novel lightweight network named MobileNetv3 with fused inverted residual (MobileNetv3‐FusedIR) is constructed as the backbone network for YOLOMF. This is achieved by integrating the fused mobile inverted bottleneck convolution (Fused‐MBConv) into the shallow layers of MobileNetv3. Second, the standard convolution in YOLOv4 is replaced with the depthwise separable convolution, resulting in a reduction in the number of parameters and complexity of the model. Third, the effects of different activation functions on the damage recognition performance of YOLOMF are thoroughly investigated. Finally, to verify the effectiveness of the proposed method in complex environments, a data enhancement library named Imgaug is used to simulate concrete bridge damage images under challenging conditions such as motion blur, fog, rain, snow, noise, and color variations. The results indicate that the YOLOMF shows excellent multi‐damage recognition proficiency for concrete bridges across varying field‐of‐view sizes as well as complex environmental conditions. The detection speed of YOLOMF reaches 85f/s, facilitating effective real‐time multi‐damage detection for concrete bridges under complex environments. [ABSTRACT FROM AUTHOR]

Lanthanide ion contained metal–organic frameworks (MOFs) have garnered significant attention in the fields of solid‐state lighting and chemical sensing due to their porous structure and distinctive optical properties. However, they also present challenges because of the limited photoluminescence (PL) intensity resulting from the parity‐forbidden f–f transitions of lanthanide ions. Herein, the study reports a new heterometallic MOFs Ln3Li2L4 (Li‐Ln‐MOF, Ln = Y, Eu, Tb and Dy, L = deprotonated 1,3,5‐tris(4‐carboxyphenyl)benzene) with a Brunauer‐Emmett‐Teller (BET) surface area of 774.1 m2/g. The porous crystal structure of Li‐Ln‐MOF is characterized by three kinds of channels interpenetrating with each other. By employing ligand alternation and lanthanide ion alloying strategies, Li‐Y1‐xEux‐MOF1 crystal isostructural with Li‐Ln‐MOF is synthesized by using 2,4,6‐tris(4‐carboxyphenyl)‐1,3,5‐triazine (H3TATB) as ligand. The Li‐Y0.7Eu0.3‐MOF1 crystal excels in the comprehensive performance with a BET surface area of 858.8 m2 g−1 and a near‐unity PL quantum yield. The time density functional theory and natural transition orbitals calculations unravel that the outstanding optical properties Li‐Y0.7Eu0.3‐MOF1 originates from the charge transfer between TATB3− and Eu3+. Benefiting from the excellent comprehensive performance of Li‐Y1‐xEux‐MOF1, the study reveals their potentials as single‐composition white‐light emission and fluorescent sensing probe for the detection of nitrobenzene. [ABSTRACT FROM AUTHOR]

Background: Lysine methyltransferase 2D (KMT2D) mediates mono‐methylation of histone H3 lysine 4 (H3K4me1) in mammals. H3K4me1 mark is involved in establishing an active chromatin structure to promote gene transcription. However, the precise molecular mechanism underlying the KMT2D‐mediated H3K4me1 mark modulates gene expression in triple‐negative breast cancer (TNBC) progression is unresolved. Methods and Results: We recognized Y‐box‐binding protein 1 (YBX1) as a "reader" of the H3K4me1 mark, and a point mutation of YBX1 (E121A) disrupted this interaction. We found that KMT2D and YBX1 cooperatively promoted cell growth and metastasis of TNBC cells in vitro and in vivo. The expression levels of KMT2D and YBX1 were both upregulated in tumour tissues and correlated with poor prognosis for breast cancer patients. Combined analyses of ChIP‐seq and RNA‐seq data indicated that YBX1 was co‐localized with KMT2D‐mediated H3K4me1 in the promoter regions of c‐Myc and SENP1, thereby activating their expressions in TNBC cells. Moreover, we demonstrated that YBX1 activated the expressions of c‐Myc and SENP1 in a KMT2D‐dependent manner. Conclusion: Our results suggest that KMT2D‐mediated H3K4me1 recruits YBX1 to facilitate TNBC progression through epigenetic activation of c‐Myc and SENP1. These results together unveil a crucial interplay between histone mark and gene regulation in TNBC progression, thus providing novel insights into targeting the KMT2D‐H3K4me1‐YBX1 axis for TNBC treatment. Highlights: YBX1 is a KMT2D‐mediated H3K4me1‐binding effector protein and mutation of YBX1 (E121A) disrupts its binding to H3K4me1.KMT2D and YBX1 cooperatively promote TNBC proliferation and metastasis by activating c‐Myc and SENP1 expression in vitro and in vivo.YBX1 is colocalized with H3K4me1 in the c‐Myc and SENP1 promoter regions in TNBC cells and increased YBX1 expression predicts a poor prognosis in breast cancer patients. [ABSTRACT FROM AUTHOR]

Improving polarizability is an important strategy for designing high‐performance mid‐infrared (mid‐IR) nonlinear optical (NLO) materials. The substitution of equivalent or aliovalent atoms can manipulate the polarizability by adjusting the symmetry of the polyhedron. Herein, the Li+ and Cd2+ are introduced into the Cu3PS4 as the equivalent and aliovalent dopants for the Cu site. As a result, Li+ can significantly improve the bandgap (Eg) of LixCu3−xPS4 from 2.38 to 2.88 eV, leading to a higher laser‐induced damage threshold (LIDT) of 4.9 times than AgGaS2 (AGS) with a comparable second harmonic generation (SHG) response of AGS (26−45 µm). Interestingly, Cd2+ can improve the SHG response and enlarge the Eg simultaneously. As a result, Cd0.4Cu2.2PS4 has a large SHG response of 10 × AGS at 2050 nm (26−45 µm) and a LIDT of 2.6 × AGS. Theoretical calculations reveal that lattice vacancies induced by Cd2+ significantly boost polarizability compared to LixCu3−xPS4 with no vacancy, leading to a strong NLO response. [ABSTRACT FROM AUTHOR]

As a class of emerging photoluminescent materials, hybrid halide crystals have drawn research attention for their potential application in the fields of light‐emitting, security, and waveguide. Nevertheless, hybrid halide crystals containing antimony with long‐term stability and tunable light emission are still increasingly in demand. In this work, serial new hybrid halide crystals (BZA)2ZnCl4·2H2O:xSb3+ (x = 0–0.2, x represents the reaction ratio) and (BZA)2SbCl5 are synthesized (BZA = 2,4‐diamino‐6‐phenyl‐1,3,5‐triazine). In (BZA)2ZnCl4·2H2O:xSb3+ crystals, Sb3+ cations replace partial Zn2+ cations to form [SbCl4]− tetrahedron. Red light emission caused by the substitution of Sb3+ for Zn2+ enhances as the doping rate increases, resulting in the tunable emission from light blue to pink and finally to dark red. There are two kinds of Sb3+ in (BZA)2SbCl5 crystal. Sb(1) has a sixfold coordination with Cl to form a [Sb(1)Cl5]∞ 1D zigzag chain. Sb(2) atom adopts a fivefold coordination with Cl and is separated from each other by BZA+ cations. (BZA)2SbCl5 crystal shows bright orange‐yellow light emission with a photoluminescence quantum yield of 45%. Moreover, the organic–inorganic hybrid metal halide crystals containing antimony have excellent long‐term stability, with phase and luminescence keeping nearly unchanged after more than six months in ambient air. [ABSTRACT FROM AUTHOR]

Aims: Excessive influx of manganese (Mn) into the brain across the blood–brain barrier induces neurodegeneration. CYP1B1 is involved in the metabolism of arachidonic acid (AA) that affects vascular homeostasis. We aimed to investigate the effect of brain CYP1B1 on Mn‐induced neurotoxicity. Method: Brain Mn concentrations and α‐synuclein accumulation were measured in wild‐type and CYP1B1 knockout mice treated with MnCl2 (30 mg/kg) and biotin (0.2 g/kg) for 21 continuous days. Tight junctions and oxidative stress were analyzed in hCMEC/D3 and SH‐SY5Y cells after the treatment with MnCl2 (200 μM) and CYP1B1‐derived AA metabolites (HETEs and EETs). Results: Mn exposure inhibited brain CYP1B1, and CYP1B1 deficiency increased brain Mn concentrations and accelerated α‐synuclein deposition in the striatum. CYP1B1 deficiency disrupted the integrity of the blood–brain barrier (BBB) and increased the ratio of 3, 4‐dihydroxyphenylacetic acid (DOPAC) to dopamine in the striatum. HETEs attenuated Mn‐induced inhibition of tight junctions by activating PPARγ in endothelial cells. Additionally, EETs attenuated Mn‐induced up‐regulation of the KLF/MAO‐B axis and down‐regulation of NRF2 in neuronal cells. Biotin up‐regulated brain CYP1B1 and reduced Mn‐induced neurotoxicity in mice. Conclusions: Brain CYP1B1 plays a critical role in both cerebrovascular and dopamine homeostasis, which might serve as a novel therapeutic target for the prevention of Mn‐induced neurotoxicity. [ABSTRACT FROM AUTHOR]