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MicroRNA-125b (miR-125b) reduces myocardial infarct area and restrains myocardial ischemia reperfusion injury (I/R). In this study, we aimed to investigate the effect of bone marrow mesenchymal stem cell (BMSC)-derived exosomes carrying miR-125b on I/R rats. The myocardial I/R model in rats was constructed by ligation of the left anterior descending coronary artery (LAD). Rats were randomly divided into I/R and Sham group. Lv-cel-miR-67 (control) or Lv-miR-125b was transfected into BMSCs. Exosomes were extracted from transfected BMSCs, and separately named BMSC-Exo-67, BMSC-Exo-125b, and BMSC-Exo. MTT assay and flow cytometry were used to detect the viability and apoptosis of I/R myocardium cells, respectively. The expression of cell apoptosis proteins and the levels of inflammatory factors were examined by Western blot and ELISA assay, respectively. The target relationship between miR-125b and SIRT7 was predicted by using StarBase3.0, and was confirmed by using dual-luciferase reporter gene assay. qRT-PCR, immunohistochemistry staining, and Western blot were used to evaluate the expression of SIRT7 in myocardium tissues in I/R rats. BMSC-derived exosomes were successfully isolated and identified by TEM and positive expression of CD9 and CD63. The expression of miR-125b was down-regulated in I/R myocardium tissues and cells. BMSC-Exo-125b significantly up-regulated miR-125b in I/R myocardium cells. The intervention of BMSC-Exo-125b significantly increased the cell viability, decreased the apoptotic ratio, down-regulated Bax and caspase-3, up-regulated Bcl-2, and decreased the levels of IL-1β, IL-6, and TNF-α in I/R myocardium cells. SIRT7 was a target of miR-125b, and BMSC-Exo-125b significantly down-regulated SIRT7 in myocardium cells. In addition, the injection of BMSC-Exo-125b alleviated the pathological damages and down-regulated SIRT7 in myocardium tissues of I/R rats. BMSC-derived exosomes carrying miR-125b protected against myocardial I/R by targeting SIRT7.

Large-area single-crystal monolayers of two-dimensional (2D) materials such as graphene 1 – 3 , hexagonal boron nitride (hBN) 4 – 6 and transition metal dichalcogenides 7 , 8 have been grown. hBN is considered to be the ‘ideal’ dielectric for 2D-materials-based field-effect transistors (FETs), offering the potential for extending Moore’s law 9 , 10 . Although hBN thicker than a monolayer is more desirable as substrate for 2D semiconductors 11 , 12 , highly uniform and single-crystal multilayer hBN growth has yet to be demonstrated. Here we report the epitaxial growth of wafer-scale single-crystal trilayer hBN by a chemical vapour deposition (CVD) method. Uniformly aligned hBN islands are found to grow on single-crystal Ni (111) at early stage and finally to coalesce into a single-crystal film. Cross-sectional transmission electron microscopy (TEM) results show that a Ni 23 B 6 interlayer is formed (during cooling) between the single-crystal hBN film and Ni substrate by boron dissolution in Ni. There are epitaxial relationships between hBN and Ni 23 B 6 and between Ni 23 B 6 and Ni. We also find that the hBN film acts as a protective layer that remains intact during catalytic evolution of hydrogen, suggesting continuous single-crystal hBN. This hBN transferred onto the SiO 2 (300 nm)/Si wafer acts as a dielectric layer to reduce electron doping from the SiO 2 substrate in MoS 2 FETs. Our results demonstrate high-quality single-crystal  multilayered hBN over large areas, which should open up new pathways for making it a ubiquitous substrate for 2D semiconductors. Using a chemical vapour deposition method, it is possible to epitaxially grow wafer-scale single-crystal trilayers of hexagonal boron nitride—an important dielectric for 2D materials—on Ni (111) foils by boron dissolution.

To fully explore the regulation resources on both sides of the source and load under uncertain environment and collaboratively achieve the energy saving and emission reduction goals, a low-carbon economic optimization dispatch model combining demand response and carbon trading mechanism is proposed in this paper. Firstly, the economic principle of demand response (DR) is analyzed, as well as the demand response compensation model is constructed for shiftable loads and curtailable loads respectively. Second, we describe the source-load synergistic low-carbon effect. The source side further reduces carbon emissions by establishing a reward-punishment laddered carbon trading model. Accordingly, the optimization model is constructed with the objective of minimizing the sum of DR compensation cost, carbon trading cost and system operation cost. The triangular fuzzy method is used to deal with the uncertainty problem of new energy and load forecasting. Finally, the economic and low-carbon nature of this proposed model is verified by simulation and example analysis.

Myocardial ischemia reperfusion (I/R) injury is a complex process with intense inflammatory response and cardiomyocyte apoptosis. As a decoy receptor of IL-1β, Interleukin-1 receptor type 2 (IL-1R2) inhibits IL-1β signaling. However, its role in I/R injury remains unknown. Here we found that the serum levels of IL-1R2 were significantly increased in patients with acute myocardial infarction (AMI) following interventional therapy. Similarly, after myocardial I/R surgery, IL-1R2 expression was significantly increased in heart of wild-type mice. In addition, IL-1R2-deficient mice heart showed enlarged infarct size, increased cardiomyocyte apoptosis together with reduced cardiac systolic function. Following exposure to hypoxia and reoxygenation (H/R), neonatal rat ventricular myocytes (NRVM) significantly increased IL-1R2 expression relying on NF-κB activation. Consistently, IL-1R2-deficient mice increased immune cells infiltrating into heart after surgery, which was relevant with cardiac damage. Additionally, IL-1R2 overexpression in cardiomyocyte protected cardiomyocyte against apoptosis through reducing the IL-17RA expression both in vivo and in vitro. Our results indicate that IL-1R2 protects cardiomyocytes from apoptosis, which provides a therapeutic approach to turn down myocardial I/R injury.

Myocardial infarction (MI), a consequence of coronary artery occlusion, triggers the degradation of ferritin, resulting in elevated levels of free iron in the heart and thereby inducing ferroptosis. Targeting myocardial ferroptosis through the chelation of excess iron has therapeutic potential for MI treatment. However, iron chelation in post ischemic injury areas using conventional iron‐specific chelators is hindered by ineffective myocardial intracellular chelation, rapid clearance, and high systemic toxicity. A chitosan‐desferrioxamine nanosponge (CDNS) is designed by co‐crosslinking chitosan and deferoxamine through noncovalent gelation to address these challenges. This architecture facilitates direct iron chelation regardless of deferoxamine (DFO) release due to its sponge‐like porous hydrogel structure. Upon cellular internalization, CDNS can effectively chelate cellular iron and facilitate the efflux of captured iron, thereby inhibiting ferroptosis and associated oxidative stress and lipid peroxidation. In MI mouse models, myocardial injection of CDNS promotes sustainable retention and the suppression of ferroptosis in the infarcted heart. This intervention improves cardiac function and alleviates adverse cardiac remodeling post‐MI, leading to decreased oxidative stress and the promotion of angiogenesis due to ferroptosis inhibition by CDNS in the infarcted heart. This study reveals a nanosponge‐based nanomedicine targeting myocardial ferroptosis with efficient iron chelation and efflux, offering a promising MI treatment. This work addresses the challenges of prevalent iron chelation strategies in myocardial infarction (MI) treatment and proposes a novel therapeutic approach using chitosan–deferoxamine nanosponge (CDNS). This CDNS facilitates efficient iron chelation, promotes iron efflux, and exhibits significant benefits in MI mouse models. This article highlights the potential of this nanomaterial‐driven iron chelation therapy for MI treatment.

Background Deoxycholic acid (DCA), a gut microbiota-derived secondary metabolite, exhibits broad-spectrum antimicrobial activity, particularly against Clostridium perfringens ( C. perfringens ). However, its specific antibacterial mechanism remains unclear. Objective To investigate the antibacterial activity and mechanism of DCA against C. perfringens , this study employed in vitro experiments combined with transcriptomic analysis to explore the inhibitory effects and underlying mechanism of DCA on C. perfringens . Result The results indicate that DCA can effectively inhibit the formation of C. perfringens biofilms, disrupt their cell walls, increase cell membrane permeability, and cause nucleic acid leakage. Transcriptome analysis revealed that DCA can up-regulating the oxidative phosphorylation pathway in C. perfringens and down-regulating antioxidant activity, peroxidase activity, and oxidoreductase activity, suggesting its potential antibacterial mechanism. This study provides insights into the antimicrobial activity of DCA and its mechanisms, laying a theoretical foundation for its development as a novel antimicrobial agent or feed additive.

Graphite films with large grain sizes have been reportedly obtained by using metal as catalysts, but the obtained graphite is mostly heavily wrinkled, thus containing defects that degrade its properties. We report the synthesis of mirror-like and large-grained graphite films with only a few nano kinks and controllable dimensions, achieved by using flat Ni-Mo alloy melts of the same lateral dimensions as the metal foils used to make this alloy melt. The graphite film exhibited few nano kinks and a mirror-like appearance because the deliberate evaporation of much of the Ni produced a porous substrate, which in turn dramatically weakened the substrate-graphite film interaction before cooling. The mirror-like graphite appears to be 100% AB-stacked with millimeter-sized grains that are much larger than the multi-micron grain size of highly oriented pyrolytic graphite and rivaled in size only by a small percentage of natural graphite. Our graphite films have an electrical conductivity of 2.25 × 10 4 S cm −1 at 300 K. Tensile loading of macroscale samples showed an average Young’s modulus of 969 ± 69 GPa and average fracture strength of 1.29 ± 0.203 GPa, and Frequency Domain Thermoreflectance revealed an average in-plane thermal conductivity of 2034.4 ± 68 W m −1 ·K −1 . Graphite films often have defects due to metal catalysts. Here, authors synthesized mirror-like, large-grained graphite films with minimal defects using Ni-Mo alloy melts, achieving high electrical and thermal conductivity and strong mechanical properties.

PurposeTo evaluate the potential association between the lowering of low-density lipoprotein cholesterol (LDL-C) with contemporary lipid-lowering medicines and cognitive function.MethodsRandomized controlled trials (RCTs) in databases including PubMed, Embase, and the Web of Science and all databases in the Cochrane Library and ClinicalTrials.gov were collected from inception to January 1, 2020. The cognitive function of patients receiving proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, statins and ezetimibe was evaluated using meta-analysis.ResultsA total of 2910 studies were obtained from databases and other sources. Thirty-three studies were selected by screening, including 11 studies on alirocumab, 9 studies on evolocumab, 11 studies on statins and 2 studies on ezetimibe. In our study, a total of 128,691 patients with no cognitive impairment were divided into an intervention group (66,330 patients) and a control group (62,361 patients). The data were subjected to a random-effects model or a fixed-effects model for meta-analysis. The contemporary lipid-lowering medicines significantly reduced LDL-C in terms of both percentage (WMD: −45.06%, 95% CI −50.12% to −40.00%, P < 0.001) and absolute value (WMD: −64.01 mg/dL, 95% CI −72.25 to −55.78, P < 0.001). Compared with the control group, patients receiving treatment with contemporary lipid-lowering medicines did not show a significant difference in the rate of neurocognitive disorder (RR: 1.02, 95% CI 0.90 to 1.16, I2 = 0.0%, p = 0.696). Subgroup analysis was performed according to the intervention and LDL-C stratification. The result of this subgroup analysis was consistent with the main findings. Regarding global cognitive performance, no difference in major cognition was found among the pooled data (SMD: 0.02, 95% CI −0.01 to 0.04, P = 0.002), except for psychomotor speed (SMD: 0.09, 95% CI 0.02 to 0.16, P = 0.0024).ConclusionsContemporary lipid-lowering medicines were not associated with cognitive impairment in RCTs. A low LDL-C level did not influence the incidence of cognitive disorder or global cognitive performance.

The widespread use of per- and polyfluoroalkyl substances (PFASs) with different physico–chemical properties poses a great threat to the environment and human health. Simultaneous detection of different classes of PFASs is a difficult task, especially for rapid analysis of polluted water samples in environmental forensic cases. In this study, a simple sample preparation ultrahigh-performance liquid chromatography coupled with quadrupole Orbitrap high-resolution mass spectrometry was established for the detection of PFASs in a wide range of water matrices. By optimizing the conditions of pretreatment and the parameters of the instrument, the developed method provided good linearity of calibration standards (R2 > 0.99), and demonstrated excellent MLOQ (0.008–1.2 µg/L), with spiked recoveries ranging from 57.7% to 151% for 47 targets in surface water samples, and from 45.7 to 165% for 46 targets in ground and waste water samples, respectively. This method required an injection volume of 3 µL and an analysis time of only 18 min per sample. The validation method was successfully applied to the analysis of 20 environmental water samples, in which 15 target substances with different concentrations were detected, with total concentrations of 0.082 to 262.455 μg/L. The method is simple and exclusive, and can rapidly confirm the occurrence of PFASs in different water samples, providing a convenient and fast high-throughput analysis, which is especially suitable for the application in the environmental forensic investigation of PFASs pollution.

The precise recognition of urban fringes is vital to monitor urban sprawl and map urban management planning. The spatial clustering method is a prevalent way to identify urban fringes due to its objectivity and convenience. However, previous studies had problems with ignoring spatial heterogeneity, which could overestimate or underestimate the recognition results. Nighttime light can reflect the transitional urban–rural regions’ regional spatial characteristics and can be used to identify urban fringes. Accordingly, a new model has been established for urban fringe identification by combining spatial continuous wavelet transform (SCWT) and dual spatial clustering. Then, Nanjing City, China, as a case study, is employed to validate the model through the NPP/VIIRS nighttime light data. The identification of mutated points across the urban–rural gradient is conducted by utilizing the SCWT. By using dual spatial clustering in the urban fringe identification, it transmits the mutation points’ spatial patterns to the homogeneous spatially neighboring clusters effectively, which measures the similarity between mutation points regarding spatial and attribute domains. A comparison of the identified results by various spatial clustering approaches revealed that our method could be more suitable for the impacts of mutation points’ local spatial patterns on different density values over the whole density surface, thus leading to more accurate spatial boundaries featured by differentiating actual differences of mutation points between adjacent clusters.