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Persistent luminescence (PersL) materials exhibit thermal-favored optical behavior, enabling their unique applications in security night vision signage, in vivo bioimaging, and optical anti-counterfeiting. Therefore, developing efficient and color-tunable PersL materials is significantly crucial in promoting advanced practical use. In this study, hexagonal Zr4+ -doped CsCdCl3 perovskite is synthesized via a hydrothermal reaction with a tunable photoluminescent (PL) behavior through heterovalent substitution. Moreover, the incorporation of Zr4+ ions result in an extra blue emission band, originating from the enhanced excitonic recombination in D3d octahedrons. Furthermore, the afterglow performances of the samples are dramatically improved, along with the noticeable temperature-dependent PersL as well as the thermo-luminescence with tunable color output. Detailed analysis reveals that the unique temperature-dependent PersL and thermo-luminescence color change are attributed to the presence of multiple luminous centers and abundant traps. Overall, this work facilitates the development of optical intelligence platforms and novel thermal distribution probes with the as-developed halides perovskite for its superior explored PersL characteristic.
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Low-temperature anticounterfeiting technologies play a crucial role in ensuring the authenticity and integrity of temperature-sensitive products such as vaccines, pharmaceuticals, and food items. In this work, a low-temperature anticounterfeiting route based on the differentiated photoluminescence (PL), PersL, and thermally stimulated luminescence (TSL) behaviors of metal halide perovskite, pure CsCdCl3, and CsCdCl3:10% Te4+ is proposed. The CsCdCl3 host exhibits pronounced color shifts, encompassing PL, PersL, and TSL behaviors, ranging from blue to yellow and orange as the temperature rises from 100 K to room temperature. This color change is attributed to a change in the luminous center (from the D3d octahedron to the C3v octahedron). Conversely, the addition of Te4+ as the luminescence center inhibits the matrix emission, maintains the characteristic orange emission of Te4+, and regulates the trap distribution of the matrix at low temperature and the TL luminescence intensity. This work highlights the significant promise of CsCdCl3:10% Te4+ and CsCdCl3 phosphors as innovative low-temperature anticounterfeiting technologies, especially for cold-chain vaccine safety monitoring.
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Two-dimensional (2D)-halide perovskites have been enriched over recent years to offer remarkable features from diverse chemical structures and environmental stability endowed with exciting functionalities in photoelectric detectors and phosphorescence systems. However, the low conversion efficiency of singlet to triplet in 2D hybrid halide perovskites reduces phosphorescence lifetimes. In this study, the long persistent luminescence of 2D all-inorganic perovskites with a self-assembled 2D interlayer galleries structure is investigated. The results show that the decay time of the long persistent luminescence increases from 450â s to 600â s, and the luminescence color changes from cyan to orange, and the thermal stability of photoluminescence enhances dramatically after replacing Cd2+ by appropriate Mn2+ ions in 2D Cs2 CdCl4 Ruddlesden-Popper phase perovskites. Furthermore, diversified anti-counterfeiting modes are fabricated to highlight the promising applications of Cs2 CdCl4 perovskite systems with tunable persistent luminescence in advanced anti-counterfeiting. Therefore, our studies provide a novel model for realizing tunable long persistent luminescence of perovskite with 2D self-assembled layered structure for advanced anti-counterfeiting.
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BACKGROUND: In the process of international communication in Chinese Wushu (ICCW), the government controls the orientation, scale, pace. However, the ICCW currently lacks a standardised government capacity structural system, and a detailed study of framework construction may be required to ensure the smooth development of the ICCW. OBJECTIVES: This study aims to clarify these elements and construct a framework for a governmental capacity system for ICCW. METHODS: For this purpose, an expert interview outline was designed, and in-depth interviews were conducted with 61 experts. Using grounded theory in the qualitative research method, NVivo 12 software was used to conduct a three-level coding analysis of the interview text for data processing and analysis. RESULTS: We extracted 58 opening codes and 11 tree nodes and categorised them into three core categories: supply side government capacity, environment-side government capacity, and demand-side government capacity, accounting for 62.36 %, 24.76 %, and 12.86 % of the total, respectively, which jointly constructed the framework structure system of the governmental capacity system for the ICCW. CONCLUSIONS: This study found that these three-dimensional government capacities have synergistic effects and that multiple measures work together. The government should ensure the supply side's direct promotion effect; the environmental side's indirect influencing effect; and the demand side's internal driving effect to promote ICCW. Meanwhile, a closed-loop systematic study of communication processes should be conducted in combination with communication organisations and individuals.
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Podocytes are particularly sensitive to lipid accumulation, which has recently emerged as a crucial pathological process in the progression of proteinuric kidney diseases like diabetic kidney disease and focal segmental glomerulosclerosis. However, the underlying mechanism remains unclear. Here, podocytes predominantly expressed protein dedicator of cytokinesis 5 (Dock5) is screened to be critically related to podocyte lipid lipotoxicity. Its expression is reduced in both proteinuric kidney disease patients and mouse models. Podocyte-specific deficiency of Dock5 exacerbated podocyte injury and glomeruli pathology in proteinuric kidney disease, which is mainly through modulating fatty acid uptake by the liver X receptor α (LXRα)/scavenger receptor class B (CD36) signaling pathway. Specifically, Dock5 deficiency enhanced CD36-mediated fatty acid uptake of podocytes via upregulating LXRα in an m6 A-dependent way. Moreover, the rescue of Dock5 expression ameliorated podocyte injury and proteinuric kidney disease. Thus, the findings suggest that Dock5 deficiency is a critical contributor to podocyte lipotoxicity and may serve as a promising therapeutic target in proteinuric kidney diseases.
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Enfermedades Renales , Podocitos , Ratones , Animales , Humanos , Podocitos/metabolismo , Podocitos/patología , Metabolismo de los Lípidos , Enfermedades Renales/metabolismo , Enfermedades Renales/patología , Ácidos Grasos/metabolismo , Lípidos , Factores de Intercambio de Guanina Nucleótido/metabolismoRESUMEN
Non-healing diabetic wounds and ulcer complications, with persistent cell dysfunction and obstructed cellular processes, are leading causes of disability and death in patients with diabetes. Currently, there is a lack of guideline-recommended hypoglycemic drugs in clinical practice, likely due to limited research and unclear mechanisms. In this study, it is demonstrated that liraglutide significantly accelerates wound closure in diabetic mouse models (db/db mice and streptozotocin-induced mice) by improving re-epithelialization, collagen deposition, and extracellular matrix remodeling, and enhancing the proliferation, migration, and adhesion functions of keratinocytes. However, these effects of improved healing by liraglutide are abrogated in dedicator of cytokinesis 5 (Dock5) keratinocyte-specific knockout mice. Mechanistically, liraglutide induces cellular function through stabilization of unconventional myosin 1c (Myo1c). Liraglutide directly binds to Myo1c at arginine 93, enhancing the Myo1c/Dock5 interaction by targeting Dock5 promoter and thus promoting the proliferation, migration, and adhesion of keratinocytes. Therefore, this study provides insights into liraglutide biology and suggests it may be an effective treatment for diabetic patients with wound-healing pathologies.
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Metabolic diseases such as obesity and diabetes induce lipotoxic cardiomyopathy, which is characterized by myocardial lipid accumulation, dysfunction, hypertrophy, fibrosis and mitochondrial dysfunction. Here, we identify that mitochondrial glycerol 3-phosphate dehydrogenase (mGPDH) is a pivotal regulator of cardiac fatty acid metabolism and function in the setting of lipotoxic cardiomyopathy. Cardiomyocyte-specific deletion of mGPDH promotes high-fat diet induced cardiac dysfunction, pathological hypertrophy, myocardial fibrosis, and lipid accumulation. Mechanically, mGPDH deficiency inhibits the expression of desuccinylase SIRT5, and in turn, the hypersuccinylates majority of enzymes in the fatty acid oxidation (FAO) cycle and promotes the degradation of these enzymes. Moreover, manipulating SIRT5 abolishes the effects of mGPDH ablation or overexpression on cardiac function. Finally, restoration of mGPDH improves lipid accumulation and cardiomyopathy in both diet-induced and genetic obese mouse models. Thus, our study indicates that targeting mGPDH could be a promising strategy for lipotoxic cardiomyopathy in the context of obesity and diabetes.
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Studies have implicated necroptosis mechanisms in orthopaedic-related diseases, since necroptosis is a unique regulatory cell death pattern. However, the role of Necroptosis-related genes in rheumatoid arthritis (RA) has not been well described. We downloaded RA-related data information and Necroptosis-related genes from the Gene Expression Omnibus (GEO), Kyoto Gene and Genome Encyclopedia (KEGG) database, and Genome Enrichment Analysis (GSEA), respectively. We identified 113 genes associated with RA-related necroptosis, which was closely associated with the cytokine-mediated signaling pathway, necroptosis and programmed necrosis. Subsequently, FAS, MAPK8 and TNFSF10 were identified as key genes among 48 Necroptosis-associated differential genes by three machine learning algorithms (LASSO, RF and SVM-RFE), and the key genes had good diagnostic power in distinguishing RA patients from healthy controls. According to functional enrichment analysis, these genes may regulate multiple pathways, such as B-cell receptor signaling, T-cell receptor signaling pathways, chemokine signaling pathways and cytokine-cytokine receptor interactions, and play corresponding roles in RA. Furthermore, we predicted 48 targeted drugs against key genes and 31 chemical structural formulae based on targeted drug prediction. Moreover, key genes were associated with complex regulatory relationships in the ceRNA network. According to CIBERSORT analysis, FAS, MAPK8 and TNFSF10 may be associated with changes in the immune microenvironment of RA patients. Our study developed a diagnostic validity and provided insight to the mechanisms of RA. Further studies will be required to test its diagnostic value for RA before it can be implemented in clinical practice.
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Artritis Reumatoide , Enfermedades Musculoesqueléticas , Humanos , Apoptosis , Algoritmos , Artritis Reumatoide/tratamiento farmacológico , Artritis Reumatoide/genética , Biología Computacional , Citocinas , Perfilación de la Expresión GénicaRESUMEN
BACKGROUND: Diabetic cardiomyopathy (DbCM) is defined as the existence of abnormal myocardial structure and functions in the absence of other cardiac diseases, such as coronary artery disease, hypertension, and significant valvular disease, in individuals with diabetes. Although abundant epidemic evidence demonstrates that diabetes is independently associated with the risk of developing heart failure, DbCM is not normally diagnosed in clinical practices due to its exclusive diagnosis, and no diagnostic biomarker was applied in a clinical test. METHODS: To detect the concentrations of serum Annexin A2 in non-diabetic subjects, type 2 diabetic (T2DM) patients with or without DbCM, and analyzed its relationship to parameters of cardiac functions, glucose, lipid metabolism, and renal functions. 266 eligible participants were included and were divided into 3 groups including non-diabetic subjects (NGR), T2DM patients without DbCM (T2DM group), and the DbCM group. Echocardiography, coronary computed tomography angiography, electrocardiogram, blood pressure, thyroid function, and clinical and other biochemical parameters were measured in all participants. RESULTS: Serum Annexin A2 concentrations were higher in DbCM (P < 0.05) and T2DM (P < 0.05) groups compared with the NGR group, especially in DbCM patients. Correlation analysis showed that serum Annexin A2 levels were negatively associated with left ventricular (LV) ejection fraction (EF), LV fractional shortening (FS), the ratio of early (E-wave) and late (A-wave) LV diastolic filling velocities (E/A ratio), and estimated glomerular filtration rate (eGFR), and were positively correlated with age, blood urea nitrogen (BUN) and creatinine (Cr) (all P < 0.05). Multiple logistical regression analyses revealed that serum in both the second and the third tertiles of Annexin A2 concentration were significantly associated with DbCM. E/A ratio is the independent factor for Annexin A2 concentration when adjusted for LV FS%, BUN, and Cr. CONCLUSIONS: Circulating Annexin A2 concentrations might be induced in DbCM patients and were negatively associated with cardiac systolic and diastolic functions, which suggested it might be a predictor of early diagnosis in DbCM and might be a potential therapeutic target for DbCM.