Development of two novel on-site detection visualization methods for murine hepatitis virus based on the multienzyme isothermal rapid amplification.

Murine hepatitis virus (MHV) infection is one of the most prevalent types of mice infection in laboratory. MHV could cause death in mice and even interfere with the results in animal experiments. Herein, we developed two isothermal approaches based on the Multienzyme Isothermal Rapid Amplification (MIRA), for rapid detection of MHV in conserved M gene. We designed and screened several pairs of primers and probes and the isothermal fluorescence detector was applied for the exonuclease Ⅲ reverse transcription MIRA (exo-RT-MIRA) assay. To further simplify the workflow, the portable fluorescence visualization instrument, also as a palm-sized handheld system, was used for the naked-eye exo-RT-MIRA assay. The amplification temperature and time were optimized. The assay could be processed well at 42°C 20 min for the exo-RT-MIRA and the naked-eye exo-RT-MIRA assay. The limit of detection (LoD) of the exo-RT-MIRA assay was 43.4 copies/µL. The LoD of the naked-eye exo-RT-MIRA assay was 68.2 copies/µL. No nonspecific amplifications were observed in the two assays. A total of 107 specimens were examined by qPCR and two assays developed. The experimental results statistical analysis demonstrated that the exo-RT-MIRA assay with the qPCR yielded sufficient agreement with a kappa value of 1.000 (p<0.0001). The results also exhibited a good agreement (kappa value, 0.961) (p<0.0001) between the naked-eye exo-RT-MIRA assay and the qPCR assay. In our study, the exo-RT-MIRA assay and the naked-eye exo-RT-MIRA assay presented the possibility of new methods in MHV point-of-testing diagnosis.

The hepatotoxicity of hexafluoropropylene oxide trimer acid caused by apoptosis via endoplasmic reticulum-mitochondrial crosstalk.

As a ubiquitous pollutant in the environment, hexafluoropropylene oxide trimer acid (HFPO-TA) has been proven to have strong hepatotoxicity. However, the underlying mechanism is still unclear. Consequently, in vivo and in vitro models of HFPO-TA exposure were established to investigate the detrimental effects of HFPO-TA on the liver. In vivo, we discovered that HFPO-TA enhanced endoplasmic reticulum (ER)-mitochondrial association, caused mitochondrial oxidative damage, activated ER stress, and induced apoptosis in mouse livers. In vitro experiments confirmed that IP3R overexpression on ER structure increased mitochondrial calcium levels, which led to mitochondrial damage and mitochondria-dependent apoptosis in HepG2 cells exposed to HFPO-TA. Subsequently, damaged mitochondria released a large amount of mitochondrial ROS, which activated ER stress and ER stress-dependent apoptosis. In conclusion, this study demonstrates that HFPO-TA can induce apoptosis by regulating the crosstalk between ER and mitochondria, ultimately leading to liver damage. These findings reveal the significant hepatotoxicity of HFPO-TA and its potential mechanisms.

Aflatoxin B1-Induced Testosterone Biosynthesis Disorder via the ROS/AMPK Signaling Pathway in Male Mice.

The worldwide prevalence of Aflatoxin B1 (AFB1), which contaminates feedstock and food, is on the rise. AFB1 inhibits testosterone (T) biosynthesis, but the mechanism is not yet clear. By establishing in vivo and in vitro models, this study found the number of Leydig cells (LCs), T content, and the expression of T biosynthesis key enzymes were suppressed after AFB1 treatment. AFB1 exposure also increased reactive oxygen species (ROS) and promoted mitochondrial injury and mitochondrial pathway apoptosis. Moreover, the AMPK signaling pathway was activated, and using an AMPK inhibitor relieved apoptosis and the suppressed T biosynthesis key enzymes of LCs caused by AFB1 through regulating downstream p53 and Nur77. Additionally, adding ROS intervention could inhibit AMPK activation and alleviate the decreased T content caused by AFB1. In summary, AFB1 promotes the apoptosis of LCs and inhibits T biosynthesis key enzyme expression via activating the ROS/AMPK signaling pathway, which eventually leads to T synthesis disorder.

Atomic Imaging of Multi-Dimensional Ruddlesden-Popper Interfaces in Lead-Halide Perovskites.

Ruddlesden-Popper (RP) interface with defined stacking structure will fundamentally influence the optoelectronic performances of lead-halide perovskite (LHP) materials and devices. However, it remains challenging to observe the atomic local structures in LHPs, especially for multi-dimensional RP interface hidden inside the nanocrystal. In this work, the advantages of two imaging modes in scanning transmission electron microscopy (STEM), including high-angle annular dark field (HAADF) and integrated differential phase contrast (iDPC) STEM, are successfully combined to study the bulk and local structures of inorganic and organic/inorganic hybrid LHP nanocrystals. Then, the multi-dimensional RP interfaces in these LHPs are atomically resolved with clear gap and blurred transition region, respectively. In particular, the complex interface by the RP stacking in 3D directions can be analyzed in 2D projected image. Finally, the phase transition, ion missing, and electronic structures related to this interface are investigated. These results provide real-space evidence for observing and analyzing atomic multi-dimensional RP interfaces, which may help to better understand the structure-property relation of LHPs, especially their complex local structures.

Atomic Imaging of the Pb Precipitation in Lead-Halide Perovskites.

The lead iodide (PbI2 ) in lead-halide perovskite (LHP) is both a positive additive for material properties and a site for the formation of device defects. Therefore, atomic-level detection of PbI2 and its derived Pb structures are crucial for understanding the performance and stability of the LHP material. In this work, the atomic imaging of the LHP, PbI2 , and Pb lattices is achieved using low-dose integrated differential phase contrast (iDPC) scanning transmission electron microscopy (STEM). Combining it with the traditional high-angle annular dark field (HAADF)-STEM, the Pb precipitation in different LHPs (CsPbI3 , CsPbBr3, and FAPbI3 ) and under different conditions (light, air, and heat) can be investigated in real space. Then, the features of Pb precipitation (positions and sizes) are visually revealed under different conditions and the stabilities of different LHPs. Meanwhile, the pathway of Pb precipitation is directly imaged and confirmed by the iDPC-STEM during an in situ heating process, supporting the detailed mechanism of Pb precipitation. These results provide the visual evidence for analyzing atomic Pb precipitation in LHPs, which helps better understand the structure-property relation induced by Pb impurity.

Fast Organic Cation Exchange in Colloidal Perovskite Quantum Dots toward Functional Optoelectronic Applications.

Colloidal quantum dots with lower surface ligand density are desired for preparing the active layer for photovoltaic, lighting, and other potential optoelectronic applications. In emerging perovskite quantum dots (PQDs), the diffusion of cations is thought to have a high energy barrier, relative to that of halide anions. Herein, we investigate the fast cross cation exchange approach in colloidal lead triiodide PQDs containing methylammonium (MA+) and formamidinium (FA+) organic cations, which exhibits a significantly lower exchange barrier than inorganic cesium (Cs+)-FA+ and Cs+-MA+ systems. First-principles calculations further suggest that the fast internal cation diffusion arises due to a lowering in structural distortions and the consequent decline in attractive cation-cation and cation-anion interactions in the presence of organic cation vacancies in mixed MA+-FA+ PQDs. Combining both experimental and theoretical evidence, we propose a vacancy-assisted exchange model to understand the impact of structural features and intermolecular interaction in PQDs with fewer surface ligands. Finally, for a realistic outcome, the as-prepared mixed-cation PQDs display better photostability and can be directly applied for one-step coated photovoltaic and photodetector devices, achieving a high photovoltaic efficiency of 15.05% using MA0.5FA0.5PbI3 PQDs and more precisely tunable detective spectral response from visible to near-infrared regions.

Fabrication of a PCN/BiOBr 2D hybrid with improved photocatalytic performance of 2,4-dichorophenol degradation.

Photocatalysis has received much attention as an environmentally friendly route to manage the emerging organic pollution problems. Herein, BiOBr nanosheets have been synthesized by a hydrothermal method, and then PCN/BiOBr hybrids are designed via a facile wet chemical method. The as-prepared PCN/BiOBr hybrids are characterized by X-ray diffraction (XRD), UV-vis diffuse reflectance spectra (UV-vis DRS), X-ray photoelectron spectroscopy (XPS) and scanning electron microscopy (SEM). The PCN/BiOBr composite exhibits remarkable improved activity in the degradation of 2,4-dichlorophenol (2,4-DCP) as compared to the pristine BiOBr. Based on the ·OH amount-related fluorescence spectra fluorescence and the photoelectrochemistry (PEC) tests, it is confirmed that the enhanced photocatalytic performance of PCN/BiOBr is attributed to the promoted charge separation. Moreover, by means of the radical-trapping experiments it is demonstrated that the formed ·O2- species, as the electron-modulated direct products, are the primary active species during the photocatalytic degradation of 2,4-DCP. This work would provide a feasible design strategy to fabricate high-activity photocatalysts for 2,4-DCP degradation.

High-Throughput Deposition of Recyclable SnO2 Electrodes toward Efficient Perovskite Solar Cells.

Chemical bath deposited (CBD) SnO2 is one of the most prevailing electron transport layers for realizing high-efficiency perovskite solar cells (PSCs) so far. However, the state-of-the-art CBD SnO2 process is time-consuming, contradictory to its prospect in industrialization. Herein, a simplified yet efficient method is developed for the fast deposition of SnO2 electrodes by incorporating a concentrated Sn source stabilized by the ethanol ligand with antimony (Sb) doping. The higher concentration of Sn source promotes the deposition rate, and Sb doping improves the hole-blocking capability of the CBD SnO2 layer so that its target thickness can be reduced to further save the deposition time. As a result, the deposition time can be appreciably reduced from 3-4 h to only 5 min while maintaining 95% of the maximum efficiency, indicating the power of the method toward high-throughput production of efficient PSCs. Additionally, the CBD SnO2 substrates are recyclable after removing the upper layers of complete PSCs, and the refurbished PSCs can maintain ≈98% of their initial efficiency after three recycling-and-fabrication processes.

In situ imaging of the atomic phase transition dynamics in metal halide perovskites.

Phase transition dynamics are an important concern in the wide applications of metal halide perovskites, which fundamentally determine the optoelectronic properties and stabilities of perovskite materials and devices. However, a more in-depth understanding of such a phase transition process with real atomic resolution is still limited by the immature low-dose electron microscopy and in situ imaging studies to date. Here, we apply an emergent low-dose imaging technique to identify different phase structures (α, ß and γ) in CsPbI3 nanocrystals during an in-situ heating process. The rotation angles of PbI6 octahedrons can be measured in these images to quantitatively describe the thermal-induced phase distribution and phase transition. Then, the dynamics of such a phase transition are studied at a macro time scale by continuously imaging the phase distribution in a single nanocrystal. The structural evolution process of CsPbI3 nanocrystals at the particle level, including the changes in morphology and composition, is also visualized with increasing temperature. These results provide atomic insights into the transition dynamics of perovskite phases, indicating a long-time transition process with obvious intermediate states and spatial distribution that should be generally considered in the further study of structure-property relations and device performance.

Recent advances and promise of MXene-based composites as electrode materials for sodium-ion and potassium-ion batteries.

With the increasing demand for sustainable energy and concerns about the scarcity of lithium resources, sodium and potassium ion batteries have emerged as promising alternative energy storage technologies. MXene, as a novel two-dimensional material, possesses exceptional electrical conductivity, high surface area, and tunable structural features that make it an ideal candidate for high-performance electrode materials. However, its limited theoretical capacity hinders its widespread application. To overcome this limitation, MXene has been combined with other materials through synergistic effects between different components to enhance the overall electrochemical performance and expand its application in sodium/potassium ion batteries. Recently, substantial advancements have been realized in the exploration of MXene-based composites as energy storage materials, encompassing their synthesis, design, and the comprehension of charge storage mechanisms. This paper aims to propose a comprehensive summary of the latest developments in MXene-based composites as electrode materials for sodium ion batteries and potassium ion batteries, with a particular emphasis on the enhanced physicochemical properties resulting from composite formation. Moreover, the challenges faced by MXene materials in sodium ion batteries and potassium ion batteries are thoroughly discussed, and future research directions to further advance this field are proposed.

Hexafluoropropylene oxide trimer acid exposure triggers necroptosis and inflammation through the Wnt/ß-catenin/NF-κB axis in the liver.

Hexafluoropropylene oxide trimer acid (HFPO-TA), an emerging alternative to perfluorooctanoic acid (PFOA), has recently been identified as a significant environmental pollutant. Nevertheless, there is a scarcity of studies regarding the hepatotoxic effects of HFPO-TA. Here, we investigated the types and potential mechanisms of liver damage caused by HFPO-TA. Initially, we validated that the introduction of HFPO-TA resulted in the Wnt/ß-catenin signaling (W/ß signaling) activation, as well as the induction of necroptosis and inflammation, both in the liver of mice and in HepG2 cells. Subsequently, we established that the W/ß signaling mediated the necroptosis and inflammation observed in the liver and HepG2 cells exposed to HFPO-TA. Finally, we demonstrated that the phosphorylated form of NF-κB p65 (p-NF-κB p65) played a role in mediating the necroptosis and inflammation, and its activity could be regulated by the W/ß signaling pathway in the liver of mice and HepG2 cells exposed to HFPO-TA. In conclusion, our investigation elucidates the role of HFPO-TA in inducing necroptosis and inflammation in the liver, which is facilitated through the activation of the W/ß/NF-κB axis.

Parkin-mediated mitophagy protects against aluminum trichloride-induced hippocampal apoptosis in mice via the mtROS-NLRP3 pathway.

Aluminum is a neurotoxic food contaminant. Aluminum trichloride (AlCl3) causes hippocampal mitochondrial damage, leading to hippocampal injury. Damaged mitochondria can release mitochondrial reactive oxygen species (mtROS) and activate nucleotide-binding oligomerization domain-like receptor-containing 3 (NLRP3) inflammasomes and apoptosis. E3 ubiquitin ligase PARK2 (Parkin)-mediated mitophagy can attenuate mitochondrial damage. However, the role of mitophagy in AlCl3-induced mice hippocampal damage and its regulatory mechanism remain elusive. First, C57BL/6 N mice were treated with 0, 44.825, 89.65, and 179.3 mg/kg body weight AlCl3 drinking water for 90 d. Apoptosis, NLRP3-inflammasome activation and mitochondrial damage were increased in AlCl3-induced hippocampal damage. In addition, Parkin-mediated mitophagy peaked in the middle-dose group and was slightly attenuated in the high-dose group. Subsequently, we used wild-type and Parkin knockout (Parkin-/-) mice to investigate the AlCl3-induced hippocampal damage. The results showed that Parkin-/- inhibited mitophagy, and aggravated AlCl3-induced mitochondrial damage, NLRP3-inflammasome activation, apoptosis and hippocampal damage. Finally, we administered MitoQ (mtROS inhibitor) and MCC950 (NLRP3 inhibitor) to AlCl3-treated Parkin-/- mice to investigate the mechanism of Parkin-mediated mitophagy. The results showed that inhibition of mtROS and NLRP3 attenuated hippocampal NLRP3-inflammasome activation, apoptosis, and damage in AlCl3-treated Parkin-/- mice. These findings indicate that Parkin-mediated mitophagy protects against AlCl3-induced hippocampal apoptosis in mice via the mtROS-NLRP3 pathway.

Controllable Colloidal Synthesis of MAPbI3 Perovskite Nanocrystals for Dual-Mode Optoelectronic Applications.

This study demonstrates an acetate ligand (AcO-)-assisted strategy for the controllable and tunable synthesis of colloidal methylammonium lead iodide (MAPbI3) perovskite nanocrystals (PNCs) for efficient photovoltaic and photodetector devices. The size of colloidal MAPbI3 PNCs can be tuned from 9 to 20 nm by changing the AcO-/MA ratio in the reaction precursor. In situ observations and detailed characterization results show that the incorporation of the AcO- ligand alters the formation of PbI6 octahedral cages, which controls PNC growth. A well-optimized AcO-/MA ratio affords MAPbI3 PNCs with a low defect density, a long carrier lifetime, and unique solid-state isotropic properties, which can be used to fabricate solution-processed dual-mode photovoltaic and photodetector devices with a conversion efficiency of 13.34% and a detectivity of 2 × 1011 Jones, respectively. This study provides an avenue to further the precisely controllable synthesis of hybrid PNCs for multifunctional optoelectronic applications.

Dibutyl phthalate induces liver fibrosis via p38MAPK/NF-κB/NLRP3-mediated pyroptosis.

Dibutyl phthalate (DBP) is one of the most employed plasticizers pervading the environment. DBP is a newly identified global organic pollutant that can activate NLRP3 inflammasomes and induce inflammatory liver injury. However, its hepatotoxicity remains poorly understood. The objective of this investigation was to investigate the probable pathways underlying DBP-induced liver injury. First, C57BL/6N mice were orally administered DBP at 10 and 50 mg/kg B.W. doses for 28 days. The observed results indicated a significant increase in liver collagen deposition and upregulated protein expression of fibrosis markers in mice. In addition, the p38MAPK/NF-κB signaling pathway and pyroptosis-related protein expression were upregulated. To establish a correlation between these changes, we conducted a conditioned medium co-culture of human hepatocellular carcinoma (HepG2) and human hepatic stellate (LX-2) cells. We performed inhibitor interventions to validate the mechanism of DBP-induced liver fibrosis in vitro. After treatment with p38MAPK (SB203580), NF-κB (PDTC), and NLRP3 (MCC950) inhibitors, the activation of LX-2 cells, the p38MAPK/NF-κB signaling pathway and pyroptosis due to DBP were alleviated. Therefore, DBP exposure leads to NLRP3-mediated pyroptosis of hepatocytes via the p38MAPK/NF-κB signaling pathway, activating LX-2 cells and causing liver fibrosis. Our findings offer a conceptual framework to understand the pathological underpinnings of DBP-induced liver injury while proposing novel ideas to prevent and treat DBP hepatotoxicity. Thus, targeting p38MAPK, NF-κB, and NLRP3 may prevent DBP-induced liver fibrosis.

Dual-Interface Modulation with Covalent Organic Framework Enables Efficient and Durable Perovskite Solar Cells.

Dual-interface modulation including buried interface as well as the top surface has recently been proven to be crucial for obtaining high photovoltaic performance in lead halide perovskite solar cells (PSCs). Herein, for the first time, the strategy of using functional covalent organic frameworks (COFs), namely HS-COFs for dual-interface modulation, is reported to further understand its intrinsic mechanisms in optimizing the bottom and top surfaces. Specifically, the buried HS-COFs layer can enhance the resistance against ultraviolet radiation, and more importantly, release the tensile strain, which is beneficial for enhancing device stability and improving the order of perovskite crystal growth. Furthermore, the detailed characterization results reveal that the HS-COFs on the top surface can effectively passivate the surface defects and suppress non-radiation recombination, as well as optimize the crystallization and growth of the perovskite film. Benefiting from the synergistic effects, the dual-interface modified devices deliver champion efficiencies of 24.26% and 21.30% for 0.0725 cm2 and 1 cm2 -sized devices, respectively. Moreover, they retain 88% and 84% of their initial efficiencies after aging for 2000 h under the ambient conditions (25 °C, relative humidity: 35-45%) and a nitrogen atmosphere with heating at 65 °C, respectively.

Necroptosis and NLPR3 inflammasome activation mediated by ROS/JNK pathway participate in AlCl3-induced kidney damage.

Aluminum (Al) is a common environmental pollutant that can induce kidney damage. However, the mechanism is not clear. In the present study, to explored the exact mechanism of AlCl3-induced nephrotoxicity, C57BL/6 N male mice and HK-2 cells were used as experimental subjects. Our results showed that Al induced reactive oxygen species (ROS) overproduction, c-Jun N-terminal kinase (JNK) signaling activation, RIPK3-dependent necroptosis, NLRP3 inflammasome activation, and kidney damage. In addition, inhibiting JNK signaling could downregulate the protein expressions of necroptosis and NLRP3 inflammasome, thereby alleviating kidney damage. Meanwhile, clearing ROS effectively inhibited JNK signaling activation, which in turn inhibited necroptosis and NLRP3 inflammasome activation, ultimately alleviating kidney damage. In conclusion, these findings suggest that necroptosis and NLPR3 inflammasome activation mediated by ROS/JNK pathway participate in AlCl3-induced kidney damage.