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The interplay of topology, magnetism, and correlations gives rise to intriguing phases of matter. In this study, through state-of-the-art angle-resolved photoemission spectroscopy, density functional theory, and dynamical mean-field theory calculations, we visualize a fourfold degenerate Dirac nodal line at the boundary of the bulk Brillouin zone in the antiferromagnet YMn2Ge2. We further demonstrate that this gapless, antiferromagnetic Dirac nodal line is enforced by the combination of magnetism, space-time inversion symmetry, and nonsymmorphic lattice symmetry. The corresponding drumhead surface states traverse the whole surface Brillouin zone. YMn2Ge2 thus serves as a platform to exhibit the interplay of multiple degenerate nodal physics and antiferromagnetism. Interestingly, the magnetic nodal line displays a d-orbital dependent renormalization along its trajectory in momentum space, thereby manifesting Hund's coupling. Our findings offer insights into the effect of electronic correlations on magnetic Dirac nodal lines, leading to an antiferromagnetic Hund nodal line.
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In this study, Cu doped carbon dots (Cu-CDs) of uniform particle size and good water solubility was synthesized using Angelica Sinensis Radix as precursor materials through a one-step hydrothermal. The Lucigenin-(Cu-CDs) chemiluminescence sensor allows the simultaneous determination of o-toluenesulfonamide (TFA) and sulfamethoxazole (STZ) concentrations. Under optimal conditions, the sensor demonstrates the capability to detect TFA and STZ within the ranges of 50 µM-800 µM and 15 µM-120 µM, respectively. The limits of detection (LOD) for TFA and STZ are determined as 0.09 µM and 0.05 µM, respectively. While the limits of quantification (LOQ) are established at 0.3 µM and 0.17 µM, respectively. The feasibility of the method for determining TFA and STZ content in chicken samples was substantiated, demonstrating spiked recovery rates ranging from 97.5% to 102.3 % and 97.5%-99.8 %, respectively. The possible reaction mechanism was clarified based on chemiluminescence, UV-vis measurement and free radical analysis results. The newly established system is characterized by stability, convenience, and robust anti-interference capabilities, thus expanding the application of carbon dots and offering a promising strategy for the detection of TFA and STZ.
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INTRODUCTION: Heterogeneous tissue stiffening promotes tumor progression and resistance, and predicts a poor clinical outcome in patients with hepatocellular carcinoma (HCC). Ferroptosis, a congenital tumor suppressive mechanism, mediates the anticancer activity of various tumor suppressors, including immune checkpoint inhibitors, and its induction is currently considered a promising treatment strategy. However, the role of extracellular matrix (ECM) stiffness in regulating ferroptosis and ferroptosis-targeted resistance in HCC remains unclear. OBJECTIVES: This research aimed to explore how extracellular matrix stiffness affects ferroptosis and its treatment efficacy in HCC. METHODS: Ferroptosis analysis was confirmed via cell activity, intracellular ferrous irons, and mitochondrial pathology assays. Baseline PD-L2, SMYD3, and SLC7A11 (xCT) were evaluated in 67 sorafenib-treated patients with HCC (46 for non-responder and 21 for responder) from public data. The combined efficacy of shPD-L2, sorafenib, and anti-PD-1 antibody in HCC was investigated in vivo. RESULTS: Here, we revealed that matrix stiffness-induced PD-L2 functions as a suppressor of xCT-mediated ferroptosis to promote cancer growth and sorafenib resistance in patients with HCC. Mechanically, matrix stiffening induced the expression of PD-L2 by activating SMYD3/H3K4me3, which acts as an RNA binding protein to enhance the mRNA stability of FTL and elevate its protein level. Knockdown of PD-L2 significantly promoted xCT-mediated ferroptosis induced by RSL3 or sorafenib on stiff substrate via FTL, whereas its overexpression abolished these upward trends. Notably, PD-L2 deletion in combination with sorafenib and anti-PD-1 antibody significantly sensitized HCC cells and blunted cancer growth in vivo. Additionally, we found the ferroptosis- and immune checkpoint-related prognostic genes that combined PD-L2, SLC7A11 and SYMD3 well predict the clinical efficacy of sorafenib in patients with HCC. CONCLUSION: These findings expand our understanding of the mechanics-dependent PD-L2 role in ferroptosis, cancer progression and resistance, providing a basis for the clinical translation of PD-L2 as a therapeutic target or diagnostic biomarker.
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Subarachnoid hemorrhage (SAH) is one of the most severe type of cerebral strokes, which can cause multiple cellular changes in the brain leading to neuronal injury and neurological deficits. Specifically, SAH can impair adult neurogenesis in the hippocampal dentate gyrus, thus may affecting poststroke neurological and cognitive recovery. Here, we identified a non-canonical role of milk fat globule epidermal growth factor 8 (MFGE8) in rat brain after experimental SAH, involving a stimulation on adult hippocampal neurogenesis(AHN). Experimental SAH was induced in Sprague-Dawley rats via endovascular perforation, with the in vivo effect of MFGE8 evaluated via the application of recombinant human MFGE8 (rhMFGE8) along with pharmacological interventions, as determined by hemorrhagic grading, neurobehavioral test, and histological and biochemical analyses of neurogenesis related markers. Results: Levels of the endogenous hippocampal MFGE8 protein, integrin-ß3 and protein kinase B (p-Akt) were elevated in the SAH relative to control groups, while that of hippocalcin (HPCA) and cyclin D1 showed the opposite change. Intraventricular rhMGFE8 infusion reversed the decrease in doublecortin (DCX) immature neurons in the DG after SAH, along with improved the short/long term neurobehavioral scores. rhMGFE8 treatment elevated the levels of phosphatidylinositol 3-kinase (PI3K), p-Akt, mammalian target of rapamycin (mTOR), CyclinD1, HPCA and DCX in hippocampal lysates, but not that of integrin ß3 and Akt, at 24 hr after SAH. Treatment of integrin ß3 siRNA, the PI3K selective inhibitor ly294002 or Akt selective inhibitor MK2206 abolished the effects of rhMGFE8 after SAH. In conclusion, MFGE8 is upregulated in the hippocampus in adult rats with reduced granule cell genesis. rhMFGE8 administration can rescue this impaired adult neurogenesis and improve neurobehavioral recovery. Mechanistically, the effect of MFGE8 on hippocampal adult neurogenesis is mediated by the activation of integrin ß3/Akt pathway. These findings suggest that exogenous MFGE8 may be of potential therapeutic value in SAH management. Graphical abstract and proposed pathway of rhMFGE8 administration attenuate hippocampal injury by improving neurogenesis in SAH models. SAH caused hippocampal injury and neurogenesis interruption. Administered exogenous MFGE8, recombinant human MFGE8(rhMFGE8), could ameliorate hippocampal injury and improve neurological functions after SAH. Mechanistically, MFGE8 bind to the receptor integrin ß3, which activated the PI3K/Akt pathway to increase the mTOR expression, and further promote the expression of cyclin D1, HPCA and DCX. rhMFGE8 could attenuated hippocampal injury by improving neurogenesis after SAH, however, know down integrin ß3 or pharmacological inhibited PI3K/Akt by ly294002 or MK2206 reversed the neuro-protective effect of rhMFGE8.
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Suitable H2O and H adsorption on the surface of transition metal chalcogenide cocatalyst is highly required to achieve their excellent alkaline H2-evolution rate. However, the weak adsorption of H2O and H atoms on NiTe surface greatly hinders its alkaline H2-evolution efficiency. Herein, an electron-deficient modulation strategy is proposed to synchronously improve the adsorption of H2O and H atoms on NiTe surface, which can greatly improve the alkaline photocatalytic H2 evolution of TiO2. In this case, highly electronegative oxygen atoms are introduced into the NiTe cocatalysts to induce the formation of electron-deficient Niδ+ and Teδ+ sites in the ultra-small-sized NiO1-xTex nanodots (0.5-2 nm), which can be uniformly loaded onto the TiO2 surface to prepare the NiO1-xTex/TiO2 photocatalysts by a facile complexation-photodeposition strategy. The resulting NiO1-xTex/TiO2 (0.6:0.4) photocatalyst exhibits the optimal activity (2143.36 µmol g-1 h-1), surpassing the activity levels of TiO2 and NiTe/TiO2 samples by 42.3 and 1.8 times, respectively. The experimental and theoretical investigations have revealed that the presence of highly electronegative O atoms in the NiO1-xTex cocatalyst can redistribute the charges of Ni and Te atoms for the formation of electron-deficient Niδ+ and Teδ+ active sites, thereby synchronously enhancing the adsorption of H2O on Niδ+ sites and H on Teδ+ sites and promoting alkaline photocatalytic H2 evolution. The current research about the synchronous optimization of the H2O and H adsorption offers a significant approach to design high-performance H2-evolution materials.
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Aim: Atopic dermatitis (AD) often accompanies skin infections, and bacterial skin infections often cause persistent and worsening symptoms. In this study, we explored the key changes in the microbiota of AD patients, as well as the effects of different ages and the severity of rash on changes in the microbiota. Patients and Methods: A total of 95 AD patients and 77 healthy volunteers were recruited. The AD patients were divided into three groups based age and three groups according to the EASI score. Microorganisms collected from the skin were analyzed through 16S rRNA gene sequencing, revealing species diversity via α and ß diversity analyses. Species compositions were compared at the phylum and genus levels. The significance of skin microbiota at the genus level was assessed using the random forest algorithm. Finally, the impact of relationships between different microbial communities on the microbial community composition and the pathogenesis of AD was explored using Pearson correlation coefficients. Results: The species diversity of the skin microbiota in the AD group significantly decreased. Compared with that in the healthy volunteers (HV) group, the bacterial diversity in the two groups of samples significantly differed. Staphylococcus dominated the bacterial communities, and as AD symptoms gradually worsened, the abundance of Staphylococcus gradually increased. Among all bacterial genera with a relative abundance greater than 1%, Staphylococcus showed a negative correlation with other genera, and showed significant consistency in specimens from different age groups. Conclusion: Changes in the abundance of Staphylococcus in the skin bacterial colonies are the main cause of AD. Brevundimonas, Paracoccus, Corynebacterium, and Veillonella may serve as characteristic biomarkers for AD. These results indicate that altering the microbiota composition of the skin may aid in the treatment of AD.
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BACKGROUND: The canine influenza virus (CIV) outbreak has garnered considerable attention as it poses a significant threat to dog health. During the H3N2 CIV evolution in beagles, the virus formed a new clade after 2019 and gradually became more adaptable to other mammals. Therefore, successfully elucidating the biological characteristics and constructing a canine influenza infection model is required for CIV characterization. METHODS: We performed genetic analyses to examine the biological characteristics and infection dynamics of CIV. RESULTS: The genotype of our H3N2 CIV strain (from 2019 in Shanghai) belonged to the 5.1 clade, which is now prevalent in China. Using MDCK cells, we investigated viral cytopathic effects. Virus size and morphology were observed using transmission electron microscopy. Beagles were also infected with 104, 105, and 106 50% egg-infectious doses (EID50). When compared with the other groups, the 106 EID50 group showed the most obvious clinical symptoms, the highest virus titers, and typical lung pathological changes. Our results suggested that the other two treatments caused mild clinical manifestations and pathological changes. Subsequently, CIV distribution in the 106 EID50 group was detected by hematoxylin and eosin (H&E) and immunofluorescence (IF) staining, which indicated that CIV primarily infected the lungs. CONCLUSIONS: The framework established in this study will guide further CIV prevention strategies.
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Enfermedades de los Perros , Genotipo , Subtipo H3N2 del Virus de la Influenza A , Infecciones por Orthomyxoviridae , Animales , Perros , Subtipo H3N2 del Virus de la Influenza A/genética , Infecciones por Orthomyxoviridae/virología , Infecciones por Orthomyxoviridae/patología , Enfermedades de los Perros/virología , Células de Riñón Canino Madin Darby , China/epidemiología , Pulmón/virología , Pulmón/patología , Filogenia , Carga Viral , Modelos Animales de EnfermedadRESUMEN
Background: Lung squamous cell carcinoma (LUSC) ranks among the carcinomas with the highest incidence and dismal survival rates, suffering from a lack of effective therapeutic strategies. Consequently, biomarkers facilitating early diagnosis of LUSC could significantly enhance patient survival. This study aims to identify novel biomarkers for LUSC. Methods: Utilizing the TCGA, GTEx, and CGGA databases, we focused on the gene encoding Family with Sequence Similarity 20, Member A (FAM20A) across various cancers. We then corroborated these bioinformatic predictions with clinical samples. A range of analytical tools, including Kaplan-Meier, MethSurv database, Wilcoxon rank-sum, Kruskal-Wallis tests, Gene Set Enrichment Analysis, and TIMER database, were employed to assess the diagnostic and prognostic value of FAM20A in LUSC. These tools also helped evaluate immune cell infiltration, immune checkpoint genes, DNA repair-related genes, DNA methylation, and tumor-related pathways. Results: FAM20A expression was found to be significantly reduced in LUSC, correlating with lower survival rates. It exhibited a negative correlation with key proteins in DNA repair signaling pathways, potentially contributing to LUSC's radiotherapy resistance. Additionally, FAM20A showed a positive correlation with immune checkpoints like CTLA-4, indicating potential heightened sensitivity to immunotherapies targeting these checkpoints. Conclusion: FAM20A emerges as a promising diagnostic and prognostic biomarker for LUSC, offering potential clinical applications.
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Biomarcadores de Tumor , Carcinoma de Células Escamosas , Neoplasias Pulmonares , Humanos , Biomarcadores de Tumor/genética , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/mortalidad , Neoplasias Pulmonares/inmunología , Carcinoma de Células Escamosas/diagnóstico , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/inmunología , Pronóstico , Regulación Neoplásica de la Expresión Génica , Biología Computacional/métodos , Bases de Datos Genéticas , Proteínas que Contienen Bromodominio , Proteínas del Tejido Nervioso , Factores de Transcripción , Antígenos NuclearesRESUMEN
[This corrects the article DOI: 10.3389/fmicb.2022.1001750.].
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A nematic phase breaks the point-group symmetry of the crystal lattice and is known to emerge in correlated materials. Here we report the observation of an intra-unit-cell nematic order and associated Fermi surface deformation in the kagome metal ScV6Sn6. Using scanning tunnelling microscopy and scanning tunnelling spectroscopy, we reveal a stripe-like nematic order breaking the crystal rotational symmetry within the kagome lattice itself. Moreover, we identify a set of Van Hove singularities adhering to the kagome-layer electrons, which appear along one direction of the Brillouin zone and are annihilated along other high-symmetry directions, revealing rotational symmetry breaking. Via detailed spectroscopic maps, we further observe an elliptical deformation of the Fermi surface, which provides direct evidence for an electronically mediated nematic order. Our work not only bridges the gap between electronic nematicity and kagome physics but also sheds light on the potential mechanism for realizing symmetry-broken phases in correlated electron systems.
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Gastric cancer (GC) is one of the most common clinical malignant tumors worldwide, with high morbidity and mortality. Presently, the overall response rate to immunotherapy is low, and current methods for predicting the prognosis of GC are not optimal. Therefore, novel biomarkers with accuracy, efficiency, stability, performance ratio, and wide clinical application are needed. Based on public data sets, the chemotherapy cohort and immunotherapy cohort from Sun Yat-sen University Cancer Center, a series of bioinformatics analyses, such as differential expression analysis, survival analysis, drug sensitivity prediction, enrichment analysis, tumor immune dysfunction and exclusion analysis, single-sample gene set enrichment analysis, stemness index calculation, and immune cell infiltration analysis, were performed for screening and preliminary exploration. Immunohistochemical staining and in vitro experiments were performed for further verification. Overexpression of COX7A1 promoted the resistance of GC cells to Oxaliplatin. COX7A1 may induce immune escape by regulating the number of fibroblasts and their cellular communication with immune cells. In summary, measuring the expression levels of COX7A1 in the clinic may be useful in predicting the prognosis of GC patients, the degree of chemotherapy resistance, and the efficacy of immunotherapy.
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Antineoplásicos , Resistencia a Antineoplásicos , Inmunoterapia , Oxaliplatino , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/tratamiento farmacológico , Neoplasias Gástricas/genética , Neoplasias Gástricas/inmunología , Neoplasias Gástricas/terapia , Oxaliplatino/uso terapéutico , Oxaliplatino/farmacología , Resistencia a Antineoplásicos/genética , Inmunoterapia/métodos , Antineoplásicos/uso terapéutico , Antineoplásicos/farmacología , Línea Celular Tumoral , Biomarcadores de Tumor/metabolismo , Biomarcadores de Tumor/genética , Masculino , Femenino , Pronóstico , Persona de Mediana EdadRESUMEN
In 2016, a distinct branch of H3N2 canine influenza virus (CIV) emerged, which has mutations related to mammalian adaptation and has replaced previously prevalent strains. This branch poses a risk of zoonotic infection. To prevent and control H3N2 CIV, an H3N2 virus-like particle (VLP) vaccine based on the insect cell baculovirus expression system has been developed in the study. The H3N2 VLP vaccine induced high titers of hemagglutination inhibition (HI) antibodies in nasal and muscular immunized beagle dogs. Meanwhile, the VLP vaccine provided effective protection against homologous virus challenge comparable to inactivated H3N2 canine influenza virus. In addition, the intranasal H3N2 VLP vaccine induced significantly higher Th1, Th2, and Th17 immune responses, respectively (p,0.05). Importantly, intramuscular injection of VLP and inactivated H3N2 virus has complete protective effects against homologous H3N2 virus attacks. Nasal immunization with H3N2 VLP can partially protect beagles from H3N2 influenza. IMPORTANCE: A new antigenically and genetically distinct canine influenza virus (CIV) H3N2 clade possessing mutations associated with mammalian adaptation emerged in 2016 and substituted previously circulating strains. This clade poses a risk for zoonotic infection. In our study, intramuscular injection of the H3N2 virus-like particle (VLP) vaccine and inactivated H3N2 CIV confer completely sterilizing protection against homologous H3N2 canine influenza virus challenge. Our results provide further support for the possibility of developing VLP vaccines that can reliably induce immunity in animal species.
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Perovskite quantum dots (QDs) have shown attractive prospects in the field of visible photocatalysis, especially in the synthesis of high value-added chemicals. However, under aerobic conditions, the stable operation of QD catalysts has been limited by the reactive oxygen species (ROS) generated by photoexcitation, especially superoxide species O2â -. Here, we propose a strategy of Ce3+ doping in perovskite QDs to guide superoxide species for photocatalytic oxidation reactions. In C(sp3)-H bond oxidation of hydrocarbons, superoxide species were rapidly generated and efficiently utilized on the surface of perovskite QDs, which achieves the stable operation of the catalytic system and obtains a high product conversion rate (15.3â mmol/g/h for benzaldehydes). The mechanism studies show that the strong Ce-oxygen affinity accelerates the relaxation process of photoinduced exciton transfer to superoxide species and inhibits the radiative recombination pathway. This work provides a new idea of utilizing oxygen species on perovskite surface and broadens the design strategy of high-performance QD photocatalysts.
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Cucumber plants are highly susceptible to the hemibiotroph oomycete Phytophthora melonis. However, the mechanism of resistance to cucumber blight remains poorly understood. Here, we demonstrated that cucumber plants with impairment in the biosynthesis of brassinosteroids (BRs) or gibberellins (GAs) were more susceptible to P. melonis. By contrast, increasing levels of endogenous BRs or exogenously application of 24-epibrassinolide enhanced the resistance of cucumber plants against P. melonis. Furthermore, we found that both knockout and overexpression of the BR biosynthesis gene CYP85A1 reduced the endogenous GA3 content compared with that of wild-type plants under the condition of inoculation with P. melonis, and the enhancement of disease resistance conferred by BR was inhibited in plants with silencing of the GA biosynthetic gene GA20ox1 or KAO. Together, these findings suggest that GA homeostasis is an essential factor mediating BRs-induced disease resistance. Moreover, BZR6, a key regulator of BR signaling, was found to physically interact with GA20ox1, thereby suppressing its transcription. Silencing of BZR6 promoted endogenous GA biosynthesis and compromised GA-mediated resistance. These findings reveal multifaceted crosstalk between BR and GA in response to pathogen infection, which can provide a new approach for genetically controlling P. melonis damage in cucumber production.
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Brasinoesteroides , Cucumis sativus , Resistencia a la Enfermedad , Giberelinas , Phytophthora , Enfermedades de las Plantas , Phytophthora/fisiología , Brasinoesteroides/metabolismo , Cucumis sativus/microbiología , Cucumis sativus/genética , Cucumis sativus/metabolismo , Cucumis sativus/parasitología , Resistencia a la Enfermedad/genética , Enfermedades de las Plantas/microbiología , Enfermedades de las Plantas/parasitología , Enfermedades de las Plantas/inmunología , Giberelinas/metabolismo , Regulación de la Expresión Génica de las Plantas , Proteínas de Plantas/metabolismo , Proteínas de Plantas/genética , Reguladores del Crecimiento de las Plantas/metabolismo , Transducción de SeñalRESUMEN
Flocking control of autonomous underwater vehicles (AUVs) has been regarded as the basis of many sophisticated marine coordination missions. However, there is still a research gap on the flocking of AUVs in weak communication and complex marine environment. This article attempts to fill up the above research gap from graph theory and intelligent learning perspectives. We first employ the bearing rigidity graph to describe the topology relationships of AUVs, through which an iterative gradient decent-based localization estimator is provided to obtain the position information. In order to improve the localization accuracy and energy efficiency, a min-weighted bearing rigidity graph generation strategy is developed. Along with this, we adopt the semi-supervised broad learning system (BLS) to design the model-free flocking controllers for AUVs in obstacle environment. The innovations of this article are summarized as follows: 1) the min-weighted bearing rigidity-based localization strategy can balance the localization accuracy and communication consumption as compared to the neighboring rule-based solutions and 2) the semi-supervised broad learning-based flocking controller can decrease the training time and solve the label limit over the supervised learning-based controllers. Finally, simulation and experimental studies are provided to verify the effectiveness.
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In this study, the copper-nickel (Cu-Ni) bimetallic electrocatalysts for electrochemical CO2 reduction reaction(CO2RR) are fabricated by taking the finely designed poly(ionic liquids) (PIL) containing abundant Salen and imidazolium chelating sites as the surficial layer, wherein Cu-Ni, PIL-Cu and PIL-Ni interaction can be readily regulated by different synthetic scheme. As a proof of concept, Cu@Salen-PIL@Ni(NO3)2 and Cu@Salen-PIL(Ni) hybrids differ significantly in the types and distribution of Ni species and Cu species at the surface, thereby delivering distinct Cu-Ni cooperation fashion for the CO2RR. Remarkably, Cu@Salen-PIL@Ni(NO3)2 provides a C2+ faradaic efficiency (FEC2+) of 80.9% with partial current density (jC 2+) of 262.9 mA cm-2 at -0.80 V (versus reversible hydrogen electrode, RHE) in 1 m KOH in a flow cell, while Cu@Salen-PIL(Ni) delivers the optimal FEC2+ of 63.8% at jC2+ of 146.7 mA cm-2 at -0.78 V. Mechanistic studies indicates that the presence of Cu-Ni interfaces in Cu@Salen-PIL@Ni(NO3)2 accounts for the preserve of high-valence Cu(I) species under CO2RR conditions. It results in a high activity of both CO2-to-CO conversion and C-C coupling while inhibition of the competitive HER.
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One rare stephacidin-asperochratide hybrid, stephaochratidin A (1), was isolated from the deep-sea-derived Aspergillus ochraceus MCCC 3A00521. The relative structure of 1 was determined by comprehensive analyses of its 1D and 2D NMR data as well as HRESIMS data. And the absolute configuration was unambiguously assigned by ECD calculations and the X-ray single-crystal diffraction analysis. Plausible biosynthetic pathway of 1 was proposed. Stephaochratidin A (1) exhibited significant ferroptosis inhibitory activity with the EC50 value of 15.4 µM by downregulating HMOX-1 expression and lipid peroxidation.
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Aspergillus ochraceus , Ferroptosis , Ferroptosis/efectos de los fármacos , Estructura Molecular , Aspergillus ochraceus/química , Humanos , Peroxidación de Lípido/efectos de los fármacosRESUMEN
In this study, we identified FOXP3 as a transcription factor for lncRNA SNHG1, which exerts a significant protective role against cardiomyocyte hypertrophy. Through DNA-pull down experiments and ChIP analysis, we confirmed that FOXP3 could bind to the promoter of SNHG1. Luciferase reporter and RT-qPCR experiments validated that FOXP3 overexpression promoted SNHG1 expression in cardiomyocytes. Furthermore, in a model of cardiomyocyte hypertrophy, FOXP3 expression was upregulated, particularly in cardiomyocytes. Functional assays demonstrated that FOXP3 overexpression inhibited cardiomyocyte hypertrophy, while FOXP3 knockdown held the opposite effect. Additionally, we revealed that lncRNA SNHG1 acted as a sponge for miR-182, miR-326, and miR-3918, thereby stabilizing FOXP3 mRNA in cardiomyocytes. The protective role of SNHG1 against cardiomyocyte hypertrophy was found to depend on the presence of FOXP3, forming a positive FOXP3/SNHG1 feedback axis. Moreover, we unveiled this positive FOXP3/SNHG1 feedback axis suppressed cardiomyocyte hypertrophy by negatively regulating Parkin-mediated mitophagy. These findings provide novel insights into the molecular mechanisms underlying cardiomyocyte hypertrophy and offer potential therapeutic targets for related interventions.
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Factores de Transcripción Forkhead , MicroARNs , Mitofagia , Miocitos Cardíacos , ARN Largo no Codificante , Ubiquitina-Proteína Ligasas , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Factores de Transcripción Forkhead/metabolismo , Factores de Transcripción Forkhead/genética , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Ubiquitina-Proteína Ligasas/metabolismo , Ubiquitina-Proteína Ligasas/genética , Animales , MicroARNs/genética , MicroARNs/metabolismo , Cardiomegalia/metabolismo , Cardiomegalia/genética , Ratas , Humanos , Ratas Sprague-Dawley , Células CultivadasRESUMEN
Despite much research in the field of island biogeography, mechanisms regulating insular diversity remain elusive. Here, we aim to explore mechanisms underlying plant species-area relationships in two tropical archipelagoes in the South China Sea. We found positive plant species-area relationships for both coral and continental archipelagoes. However, our results showed that different mechanisms contributed to similar plant species-area relationships between the two archipelagoes. For coral islands, soil nutrients and spatial distance among communities played major roles in shaping plant community structure and species diversity. By contrast, the direct effect of island area, and to a lesser extent, soil nutrients determined plant species richness on continental islands. Intriguingly, increasing soil nutrients availability (N, P, K) had opposite effects on plant diversity between the two archipelagoes. In summary, the habitat quality effect and dispersal limitation are important for regulating plant diversity on coral islands, whereas the passive sampling effect, and to a lesser extent, the habitat quality effect are important for regulating plant diversity on continental islands. More generally, our findings indicate that island plant species-area relationships are outcomes of the interplay of both niche and neutral processes, but the driving mechanisms behind these relationships depends on the type of islands.
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Combatting climate change depends on demand-side mitigation strategies related to food, which is in turn contingent on explicit estimation and management of dish-level emissions. Here, on the basis of a bottom-up integrated emissions framework, we first estimate the greenhouse gas emissions of 540 dishes from 36 cuisines using data from over 800,488 restaurants in China's provincial capital cities. By mining residents' dietary preferences, we then design various dietary change strategies to explicitly link food emissions to the Paris Agreement pledges. The results show that China's food system greenhouse gas emissions were approximately 4.64 GtCO2eq in 2020, accounting for 37% of total emissions, with average per-dish emissions of 8.44 kgCO2eq. Current emission patterns of food consumption in China may not be consistent with the attainment of the 1.5 °C and 2 °C climate targets, but transitioning towards low-emission cuisines and dishes could change that by reducing emissions by 38-69%.