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Hydrogenated metal borides have attracted much attention due to their potential high-temperature superconductivity. Here, we propose a new strategy for hydrogen intercalation tuning the stability and superconductivity of the boron honeycomb sublattice, and predict an unprecedented layered compound Na2B2H, which hosts excellent superconductivity. Strikingly, the superconducting transition temperature (Tc) of Na2B2H reaches 42 K at ambient pressure. The Tc value can be further increase to 63 K under 5% biaxial tensile strain. The excellent superconductivity originates from the strong electron-phonon coupling between the σ-bonding bands near the Fermi level and the B-B stretching optical E′ modes. The interstitial electron localization and crystal orbitals of the H-intercalated Na ion layer well match the boron honeycomb lattice and act as a chemical template to stabilize the B layer. Furthermore, the introduction of hydrogen tuned the Fermi level, and the coupling vibration of Na and H ions effectively enhanced the dynamic stability of the structure. Na2B2H represents a new family of layered high-temperature superconductors, and the strategy of stabilizing the honeycomb boron sublattice via chemical template hosts great potential for application to more layered compounds. [ABSTRACT FROM AUTHOR]

Abstract:Quantitative evaluations are of great importance in network security decision-making.In recent years,moving target defense (MTD) has appeared to be a promising defense approach that blocks asymmetrical advantage of attackers and favors the defender-notwithstanding,it has a limited deployment due to its uncertain efficiency and effectiveness in defense.In that case,quantitative metrics and evaluations of MTD are essential to prove its capability and impulse its further research.This article presents a comprehensive survey on state-of-the-art quantitative evaluations.First,taxonomy of MTD techniques is stated according to the software stack model.Then,a concrete review and comparison on existing quantitative evaluations of MTD is presented.Finally,notice-worthy open issues regarding this topic are proposed along with the conclusions of previous studies.

Existing studies suggest that biochar application can reduce soil nitrous oxide (N2O) emissions, mainly based on short‐term results. However, it remains unclear what the effects (i.e., legacy effects) and underlying mechanisms are on N2O emissions after many years of a single application of biochar. Here, we collected intact soil columns from plots without and with biochar application in a subtropical tea plantation 7 years ago for an incubation experiment. We used the N2O isotopocule analysis combined with ammonia oxidizer‐specific inhibitors and molecular biology approaches to investigate how the legacy effect of biochar affected soil N2O emissions. Results showed that the soil in the presence of biochar had lower N2O emissions than the control albeit statistically insignificant. The legacy effect of biochar in decreasing N2O emissions may be attributed to the reduced effectiveness of the soil substrate, nitrification and denitrification activities, and the promotion of the further reduction of N2O. The legacy effect of biochar reduced the relative contribution of nitrifier denitrification/bacterial denitrification, nitrification‐related N2O production, and the relative abundance of several microorganisms involved in the nitrogen cycle. Our global meta‐analysis also showed that the reduction of N2O by biochar increased with increasing application rate but diminished and possibly even reversed with increasing experimental time. In conclusion, our findings suggest that the abatement capacity of biochar on soil N2O emissions may weaken over time after biochar application, but this remains under further investigation. [ABSTRACT FROM AUTHOR]

Misuse and overuse of antibiotics have contributed to the rise of antimicrobial resistance as one of the top public health threats. Antibiotics and antibiotic resistance genes (ARGs) are prevalent in agricultural soils due to the widespread application of livestock and organic wastes. However, information about the occurrence, distribution, and risk of antibiotics and ARGs in agricultural soils is lacking for many scenarios. In this study, based on 2225 observations from 135 independent studies, we summarized the concentration or abundance of antibiotics or ARGs under different fertilizer sources and land-use patterns, analyzed the contributions of key environmental factors to the occurrence of antibiotics and ARGs in agricultural soils, and highlighted the potential ecological risk of typical antibiotics and the relationship between ARGs and mobile genetic elements (MGEs). Our results showed that cattle manure, chicken manure, swine manure, and sewage sludge were the primary pollution sources of antibiotics and ARGs in agricultural soils, and sulfonamides, tetracyclines, fluoroquinolones, and their corresponding ARGs were the main pollution types. Land-use type, soil, and climatic factors affected antibiotics concentration and ARG abundances. MGEs play a vital role in promoting the dissemination of ARGs, especially the sul1 gene is closely related to intI1. In conclusion, our findings and future research exploring these topics will contribute to better management of antibiotic and ARG contamination in agricultural soils and their risk to human health. [ABSTRACT FROM AUTHOR]

The pathological retinal angiogenesis often causes blindness. Current anti‐angiogenic therapy for proliferative retinopathy targets the vascular endothelial growth factor (VEGF), but many patients do not radically benefit from this therapy. Herein, we report that circulating prostaglandin (PG) F2α metabolites were increased in type 2 diabetic patients with proliferative retinopathy, and the PGF2α receptor (Ptgfr) was upregulated in retinal endothelial cells (ECs) from a mouse model of oxygen‐induced retinopathy (OIR). Further, disruption of the PTGFR receptor in ECs attenuated OIR in mice. PGF2α promoted the proliferation and tube formation of human retinal microvascular endothelial cells (HRMECs) via the release of ELR+ CXC chemokines, such as CXCL8 and CXCL2. Mechanistically, the PGF2α/PTGFR axis potentiated ELR+ CXC chemokine expression in HRMECs through the Gq/CAMK2G/p38/ELK‐1/FOS pathway. Upregulated FOS‐mediated ELR+ CXC chemokine expression was observed in retinal ECs from PDR patients. Moreover, treatment with PTGFR inhibitor lessened the development of OIR in mice in a CXCR2‐dependent manner. Therefore, inhibition of PTGFR may represent a new avenue for the treatment of retinal neovascularization, particularly in PDR. Synopsis: The pathological retinal angiogenesis often causes blindness. Here we showed that PGF2α/PTGFR axis promotes to oxygen‐induced retinopathy (OIR) in mice, and PTGFR receptor may represent a novel therapeutic target for pathological retinal neovascularization, particularly for proliferative diabetic retinopathy (PDR). PGF2α/PTGFR signaling is upregulated in retina tissues from OIR mice and patients with PDR.PTGFR deletion specifically in endothelial cells markedly attenuates OIR in mice.PGF2α promotes proliferation and cord formation of human retinal microvascular endothelial cells (HRMECs) via release of ELR+ CXC chemokines.PGF2α/PTGFR axis potentiates ELR+ CXC chemokine expression in HRMECs through the Gq/CAMK2G/p38/ELK‐1/FOS pathway. [ABSTRACT FROM AUTHOR]

Brown adipose tissue (BAT) functions as a thermogenic organ and is negatively associated with cardiometabolic diseases. N6‐methyladenosine (m6A) modulation regulates the fate of stem cells. Here, we show that the prostaglandin E2 (PGE2)–E‐prostanoid receptor 3 (EP3) axis was activated during mouse interscapular BAT development. Disruption of EP3 impaired the browning process during adipocyte differentiation from pre‐adipocytes. Brown adipocyte‐specific depletion of EP3 compromised interscapular BAT formation and aggravated high‐fat diet‐induced obesity and insulin resistance in vivo. Mechanistically, activation of EP3 stabilized the Zfp410 mRNA via WTAP‐mediated m6A modification, while knockdown of Zfp410 abolished the EP3‐induced enhancement of brown adipogenesis. EP3 prevented ubiquitin‐mediated degradation of WTAP by eliminating PKA‐mediated ERK1/2 inhibition during brown adipocyte differentiation. Ablation of WTAP in brown adipocytes abrogated the protective effect of EP3 overexpression in high‐fat diet‐fed mice. Inhibition of EP3 also retarded human embryonic stem cell differentiation into mature brown adipocytes by reducing the WTAP levels. Thus, a conserved PGE2‐EP3 axis promotes BAT development by stabilizing WTAP/Zfp410 signaling in a PKA/ERK1/2‐dependent manner. Synopsis: Development of brown adipose tissue (BAT) is tightly regulated by transcriptional and epigenetic reprogramming, but its upstream regulation remains poorly understood. Here, prostaglandin receptor signalling is shown to be a key promoter of brown adipogenesis enhancing expression of thermogenic gene programs. The PGE2/EP3 axis is activated during the development of interscapular BAT in mice.BAT‐specific depletion of EP3 results in adipocyte whitening and aggravated diet‐induced obesity.Loss of EP3 accelerates ubiquitin‐mediated degradation of N6‐methyladenosine methyltransferase WTAP, decreasing m6A‐dependent mRNA stability of brown gene transcription factor Zfp410.EP3 receptor‐mediated control of brown adipogenesis is conserved in human embryonic stem cell differentiation. [ABSTRACT FROM AUTHOR]