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Layered transition metal oxides are widely considered as ideal cathode materials for SIBs. However, the existing P2 and O3 structures possess specific issues, which limit their practical applications. To address these issues, this work designed a novel intergrowth layered oxide cathode with P2 and O3 phases by implementing Cu and Ti into the structure with the formation of high-entropy cathode materials with superior performance for SIBs. The electrochemical test results show that the optimized high-entropy cathode with the P2/O3 intergrowth structure possesses a high initial discharge capacity of 157.85â mAh g-1 at 0.1â C, an excellent rate performance of 84.41â mAh g-1 at 10â C, and long-term stability with capacity retention of 83.25 % after 500 cycles at 5â C. Furthermore, the analysis results of ex situ XRD and inâ situ XRD indicate that the adverse phase transition of P2-O2 under high voltage is effectively suppressed. This work indicates that the integration of high-entropy strategy with the two-phase intergrowth structure can effectively stabilize the layered structure, suppress the slipping of transition metal layers, and improve electrochemical performance, which provides a new approach for designing high-performance and practical layered transition metal oxide cathode materials for advanced SIBs.
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In contrast to adult mammals, adult zebrafish can fully regenerate injured cardiac tissue, and this regeneration process requires an adequate and tightly controlled immune response. However, which components of the immune response are required during regeneration is unclear. Here, we report positive roles for the antigen presentation-adaptive immunity axis during zebrafish cardiac regeneration. We find that following the initial innate immune response, activated endocardial cells (EdCs), as well as immune cells, start expressing antigen presentation genes. We also observe that T helper cells, a.k.a. Cd4+ T cells, lie in close physical proximity to these antigen-presenting EdCs. We targeted Major Histocompatibility Complex (MHC) class II antigen presentation by generating cd74a; cd74b mutants, which display a defective immune response. In these mutants, Cd4+ T cells and activated EdCs fail to efficiently populate the injured tissue and EdC proliferation is significantly decreased. cd74a; cd74b mutants exhibit additional defects in cardiac regeneration including reduced cardiomyocyte dedifferentiation and proliferation. Notably, Cd74 also becomes activated in neonatal mouse EdCs following cardiac injury. Altogether, these findings point to positive roles for antigen presentation during cardiac regeneration, potentially involving interactions between activated EdCs, classical antigen-presenting cells, and Cd4+ T cells.
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Presentación de Antígeno , Lesiones Cardíacas , Antígenos de Histocompatibilidad Clase II , Regeneración , Pez Cebra , Animales , Regeneración/inmunología , Presentación de Antígeno/inmunología , Lesiones Cardíacas/inmunología , Antígenos de Histocompatibilidad Clase II/metabolismo , Antígenos de Histocompatibilidad Clase II/inmunología , Antígenos de Histocompatibilidad Clase II/genética , Ratones , Linfocitos T CD4-Positivos/inmunología , Miocitos Cardíacos/inmunología , Miocitos Cardíacos/metabolismo , Proteínas de Pez Cebra/genética , Proteínas de Pez Cebra/metabolismo , Antígenos de Diferenciación de Linfocitos B/metabolismo , Antígenos de Diferenciación de Linfocitos B/genética , Proliferación Celular , Inmunidad Innata , Corazón/fisiopatología , Corazón/fisiología , Mutación , Inmunidad Adaptativa , Animales Modificados GenéticamenteRESUMEN
This study aimed to investigate the predictive value of neutrophil-to-lymphocyte ratio (NLR) and Remnant Cholesterol (Remnant-C) in relation to cardiovascular events and all-cause mortality in the general population. A population-based study. We conducted a retrospective cohort study analyzing data from the National Health and Nutrition Examination Survey (NHANES) spanning the years of 2011-2018, with follow-up for mortality status until December 31, 2019. KaplanâMeier and Cox proportional hazards regression analyses were used to evaluate the associations between NLR, Remnant-C, and cardiovascular events as well as all-cause mortality. Overall, 9409 individuals with both complete blood count and blood lipids were included in the analysis. Baseline NLR and Remnant-C were calculated. During the follow-up (median, 59.3 months), 177 cardiovascular events and 561 all-cause mortality occurred. In fully adjusted model, people with NLR > 2.26 were significantly associated with higher risk of cardiovascular events (HR 2.14, 95% CI 1.30-3.52, P < 0.001) and all-cause mortality (HR 1.66, 95% CI 1.30-2.12, P < 0.001). NLR exhibited a positive correlation with Remnant-C (r = 0.04, P < 0.001). Elevated NLR levels shown stronger association with cardiovascular events (HR 1.21, 95% CI 1.14-2.28, P < 0.001) compared with Remnant-C (HR 1.02, 95% CI 1.00-1.04, P = 0.020). Our findings suggest that NLR and Remnant-C are potential predictive markers for cardiovascular events in the general population. We observed a correlation between NLR and Remnant-C, and high NLR levels demonstrate a stronger association with the prediction of cardiovascular events and all-cause mortality compared with Remnant-C.
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Enfermedades Cardiovasculares , Neutrófilos , Adulto , Humanos , Encuestas Nutricionales , Estudios Retrospectivos , Linfocitos , Enfermedades Cardiovasculares/epidemiología , PronósticoRESUMEN
Nonstoichiometric compounds are widely used in contemporary energy technologies due to their high surface polarity, tailored electronic structure, high electrical conductivity, and other enhanced properties. However, the preparation of such nonstoichiometric compounds can be complicated and, in some cases, uncontrollable and dangerous. Here, we report a "one-pot" strategy for synthesizing N-doped porous graphitic carbon that is hybridized with nonstoichiometric scandium oxide (denoted as ScO0.95@N-PGC) and show that the composite significantly promotes sulfur cathode kinetics in lithium-sulfur (Li-S) batteries. The synthesis of the ScO0.95@N-PGC composite entails heating a porous dry gel that consists of a C source (glucose), a N source (dicyandiamide), and a Sc source (Sc(NO3)3·H2O). Thermally decomposing the dicyandiamide creates a highly reductive atmosphere that simultaneously affords the hypoxic state of the ScO0.95 and dopes the carbon matrix with nitrogen. Density functional theory reveals the presence of oxygen vacancies that enable the ScO0.95 crystals to function as excellent electrical conductors, exhibit enhanced adsorption toward polysulfides, and accelerate the cathode reactions by lowering the corresponding activation energies. Moreover, Li-S cells prepared from the ScO0.95@N-PGC composite display a high specific capacity (1046 mA h g-1 at 0.5 C), an outstanding cycling stability (641 mA h g-1 after 1000 charge-discharge cycles at 0.5 C, a capacity decay of 0.038% per cycle), and a particularly outstanding rate capability (438 mA h g-1 at 8 C). The methodology described establishes a sustainable approach for synthesizing nonstoichiometric compounds while broadening their potential utility in a broad range of energy technologies.
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OBJECTIVES: Epicardial adipose tissue (EAT) is closely adjacent to the coronary arteries and myocardium, its role as an endocrine organ to affect the pathophysiological processes of the coronary arteries and myocardium has been increasingly recognized. However, the specific gene expression profiles of EAT in coronary artery disease (CAD) has not been well characterized. Our aim was to investigate the role of EAT in CAD at the gene level. METHODS: Here, we compared the histological and gene expression difference of EAT between CAD and non-CAD. We investigated the gene expression profiles in the EAT of patients with CAD through the high-throughput RNA sequencing. We performed bioinformatics analysis such as functional enrichment analysis and protein-protein interaction network construction to obtain and verify the hub differentially expressed genes (DEGs) in the EAT of CAD. RESULTS: Our results showed that the size of epicardial adipocytes in the CAD group was larger than in the control group. Our findings on the EAT gene expression profiles of CAD showed a total of 747 DEGs (fold change >2, p value <0.05). The enrichment analysis of DEGs showed that more pro-inflammatory and immunological genes and pathways were involved in CAD. Ten hub DEGs (GNG3, MCHR1, BDKRB1, MCHR2, CXCL8, CXCR5, CCR8, CCL4L1, TAS2R10, and TAS2R41) were identified. CONCLUSION: Epicardial adipose tissue in CAD shows unique gene expression profiles and may act as key regulators in the CAD pathological process.
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The V4+/V3+ (3.4 V) redox couple has been well-documented in cathode material Na3V2(PO4)3 for sodium-ion batteries. Recently, partial cation substitution at the vanadium site of Na3V2(PO4)3 has been actively explored to access the V5+/V4+ redox couple to achieve high energy density. However, the V5+/V4+ redox couple in partially substituted Na3V2(PO4)3 has a voltage far below its theoretical voltage in Na3V2(PO4)3, and the access of the V5+/V4+ redox reaction is very limited. In this work, we compare the extraction/insertion behavior of sodium ions from/into two isostructural compounds of Na3VGa(PO4)3 and Na3VAl(PO4)3, found that, by DFT calculations, the lower potential of the V5+/V4+ redox couple in Na3VM(PO4)3 (M = Ga or Al) than that in Na3V2(PO4)3 is because of the extraction/insertion of sodium ions through the V5+/V4+ redox reaction at different crystallographic sites, that is, sodium ions extracting from the Na(2) site in Na3VM(PO4)3 while from the Na(1) site in Na3V2(PO4)3, and further evidenced that the full access of the V5+/V4+ redox reaction is restrained by the excessive diffusion activation energy in Na3VM(PO4)3.
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Epicardial adipose tissue (EAT) contributes to the pathophysiological process of coronary artery disease (CAD). The expression profiles of long non-coding RNAs (lncRNA) in EAT of patients with CAD have not been well characterized. We conducted high-throughput RNA sequencing to analyze the expression profiles of lncRNA in EAT of patients with CAD compared to patients without CAD. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were executed to investigate the principal functions of the significantly dysregulated mRNAs. We confirmed a dysregulated intergenic lncRNA (lincRNA) (LINC00968) by real-time quantitative PCR (RT-qPCR). Subsequently, we constructed a ceRNA network associated with LINC00968, which included 49 mRNAs. Compared with the control group, lncRNAs and genes of EAT in CAD were characterized as metabolic active and pro-inflammatory profiles. The sequencing analysis detected 2539 known and 1719 novel lncRNAs. Then, we depicted both lncRNA and gene signatures of EAT in CAD, featuring dysregulation of genes involved in metabolism, nuclear receptor transcriptional activity, antigen presentation, chemokine signaling, and inflammation. Finally, we identified a ceRNA network as candidate modulator in EAT and its potential role in CAD. We showed the expression profiles of specific EAT lncRNA and mRNA in CAD, and a selected non-coding associated ceRNA regulatory network, which taken together, may contribute to a better understanding of CAD mechanism and provide potential therapeutic targets.Trial registration Chinese Clinical Trial Registry, No. ChiCTR1900024782.
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Tejido Adiposo/metabolismo , Enfermedad de la Arteria Coronaria/genética , ARN Largo no Codificante/genética , Tejido Adiposo/fisiología , Anciano , Ácidos Nucleicos Libres de Células/análisis , Ácidos Nucleicos Libres de Células/genética , China , Biología Computacional/métodos , Manejo de Datos/métodos , Femenino , Expresión Génica/genética , Perfilación de la Expresión Génica/métodos , Ontología de Genes , Redes Reguladoras de Genes/genética , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Pericardio/metabolismo , Pericardio/fisiología , ARN Largo no Codificante/metabolismo , ARN Mensajero/genética , Transcriptoma/genéticaRESUMEN
BACKGROUNDS: The epidemic of coronavirus disease 2019 (COVID-19) is spreading across the world. As the first country who suffered from the outbreak, China has been taking strict and effective measures to contain the epidemic and treat the disease under the instruction of updating guidance. AIMS: To compare the changes and updates in China's clinical guidance for COVID-19. METHODS: We explored China's experience in dealing with the epidemic by longitudinal comparison of China's clinical guidance for COVID-19. RESULTS: As of March 4, there are 7 editions of the guidance. With the increasing understanding of COVID-19, changes have been made in aetiology, epidemiology, pathology, clinical features, diagnostic criteria, clinical classification, and treatment. CONCLUSIONS: We have made a summary of the changes and updates in China's clinical guidance for COVID-19, which mirrors the deepening understanding of the disease over the course of fighting it, hoping to help clinicians worldwide.
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COVID-19 , Epidemias , China/epidemiología , Brotes de Enfermedades , Humanos , SARS-CoV-2RESUMEN
Sodium-ion batteries (SIBs) have grabbed worldwide attention as an alternative to lithium-ion batteries on account of the abundance and accessibility of the sodium element in nature. For the sake of meeting the requirements for various applications containing grid-scale energy storage system, electric vehicles, and so forth, a stable and high-voltage cathode is decisive to enhance the energy and power density of SIBs. In this research, sodium super ionic conductor structured Na3V1.5-xCr0.5+x(PO4)3 with different V/Cr ratios to balance the V3+/V4+ and V4+/V5+ redox couples was investigated as the potential cathode for SIBs. Among these candidates, Na3V1.3Cr0.7(PO4)3 manifested high energy density together with good cycling performance and rate capability. Combining the structural analysis and density functional theory calculation, the underlying mechanism of V3+ substitution by Cr3+ was uncovered, accounting for the improvement of electrochemical performance.
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Atrial fibrillation (AF) is the most common arrhythmia with diverse etiology that remarkably relates to high morbidity and mortality. With the advancements in intensive clinical and basic research, the understanding of electrophysiological and pathophysiological mechanism, as well as treatment of AF have made huge progress. However, many unresolved issues remain, including the core mechanisms and key intervention targets. Big data approach has produced new insights into the improvement of the situation. A large amount of data have been accumulated in the field of AF research, thus using the big data to achieve prevention and precise treatment of AF may be the direction of future development. In this review, we will discuss the current understanding of big data and explore the potential applications of big data in AF research, including predictive models of disease processes, disease heterogeneity, drug safety and development, precision medicine, and the potential source for big data acquisition. Grapical abstract.
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Fibrilación Atrial , Macrodatos , Minería de Datos , Aprendizaje Automático , Animales , Fibrilación Atrial/diagnóstico , Fibrilación Atrial/fisiopatología , Fibrilación Atrial/terapia , Exactitud de los Datos , HumanosRESUMEN
BACKGROUND: Coronary artery disease (CAD) is a common disease with high cost and mortality. Here, we studied the differentially expressed genes (DEGs) between epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) from patients with CAD to explore the possible pathways and mechanisms through which EAT participates in the CAD pathological process. METHODS: Microarray data for EAT and SAT were obtained from the Gene Expression Omnibus database, including three separate expression datasets: GSE24425, GSE64554 and GSE120774. The DEGs between EAT samples and SAT control samples were screened out using the limma package in the R language. Next, we conducted bioinformatic analysis of gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways to discover the enriched gene sets and pathways associated with DEGs. Simultaneously, gene set enrichment analysis was carried out to discover enriched gene functions and pathways from all expression data rather than DEGs. The PPI network was constructed to reveal the possible protein interactions consistent with CAD. Mcode and Cytohubba in Cytoscape revealed the possible key CAD genes. In the next step, the corresponding predicted microRNAs (miRNAs) were analysed using miRNA Data Integration Portal. RT-PCR was used to validate the bioinformatic results. RESULTS: The three datasets had a total of 89 DEGs (FC log2 > 1 and P value < 0.05). By comparing EAT and SAT, ten common key genes (HOXA5, HOXB5, HOXC6, HOXC8, HOXB7, COL1A1, CCND1, CCL2, HP and TWIST1) were identified. In enrichment analysis, pro-inflammatory and immunological genes and pathways were up-regulated. This could help elucidate the molecular expression mechanism underlying the involvement of EAT in CAD development. Several miRNAs were predicted to regulate these DEGs. In particular, hsa-miR-196a-5p and hsa-miR-196b-5p may be more reliably associated with CAD. Finally, RT-PCR validated the significant difference of OXA5, HOXC6, HOXC8, HOXB7, COL1A1, CCL2 between EAT and SAT (P value < 0.05). CONCLUSIONS: Between EAT and SAT in CAD patients, a total of 89 DEGs, and 10 key genes, including HOXA5, HOXB5, HOXC6, HOXC8, HOXB7, COL1A1, CCND1, CCL2, HP and TWIST1, and miRNAs hsa-miR-196a-5p and hsa-miR-196b-5p were predicted to play essential roles in CAD pathogenesis. Pro-inflammatory and immunological pathways could act as key EAT regulators by participating in the CAD pathological process.
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The roles of nitric oxide (NO), endothelium-derived hyperpolarizing factors (EDHF), and calcium-activated K+ (KCa) channels in diabetes-associated endothelial dysfunction of small renal arteries are not clear. The present study investigated acetylcholine (ACh)-induced vasorelaxation of renal arcuate arteries from obese Zucker (OZ) rats at different diabetes durations, and the relative contribution of NO, EDHF, and KCa channels to the endothelial dysfunction. OZ rats of 7 weeks (prediabetic stage), 12 weeks (early diabetic stage), and 20 weeks (late diabetic stage), and time-matched lean control rats, were studied. Segments of arcuate arteries (130 to 180 µm) were isolated, cannulated and pressurized. Vascular endothelial functions were tested using ACh-induced vasodilation. Our experiments demonstrated: (1) ACh-elicited vasodilation was impaired in OZ rats of 20 weeks, but not in rats of 7 and 12 weeks; (2) inhibition of NO or EDHF (contributed by epoxyeicosatrienoic acids [EETs]) production significantly decreased ACh-induced vasodilation in both lean and OZ rats of 20 weeks. The reduction of ACh-induced vasodilation by inhibition of NO or EDHF formation was less in OZ rats, as compared to lean rats; and (3) inhibition of KCa channels markedly reduced ACh-induced vasodilation in lean control rats, but not in OZ rats of 20 weeks. Our observations indicated that endothelium-dependent vasodilation in renal arcuate arteries is impaired in diabetes mellitus; NO and EDHF, mainly EETs, dominate the ACh-induced vasodilation in renal arcuate arteries; the contribution of NO and EETs is impaired in diabetic rats; KCa channels are involved in ACh-induced vasodilation; and the activity of KCa channels is downregulated in diabetes mellitus.