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Lightweight, miniaturized optical imaging systems are vastly anticipated in these fields of aerospace exploration, industrial vision, consumer electronics, and medical imaging. However, conventional optical techniques are intricate to downscale as refractive lenses mostly rely on phase accumulation. Metalens, composed of subwavelength nanostructures that locally control light waves, offers a disruptive path for small-scale imaging systems. Recent advances in the design and nanofabrication of dielectric metalenses have led to some high-performance practical optical systems. This review outlines the exciting developments in the aforementioned area whilst highlighting the challenges of using dielectric metalenses to replace conventional optics in miniature optical systems. After a brief introduction to the fundamental physics of dielectric metalenses, the progress and challenges in terms of the typical performances are introduced. The supplementary discussion on the common challenges hindering further development is also presented, including the limitations of the conventional design methods, difficulties in scaling up, and device integration. Furthermore, the potential approaches to address the existing challenges are also deliberated.This review outlines the exciting developments in high-performance dielectric metalenses whilst highlighting the challenges of using dielectric metalenses to replace conventional optics in miniature optical systems.

Income inequality has long been an important issue in development economics. Applying international data from 119 countries between 2004 and 2018, this study discusses the relationship between the accessibility of financial services and income inequality. Using the density of the bank branch network to represent the accessibility of financial services, we discover that income inequality is negatively related to the accessibility of financial services, especially in less developed countries and regions. In this nexus, the poverty ratio serves as an intermediary variable. The significance of the nexus is weaker in countries where fintech is more popularized, indicating the substitution effect between fintech and traditional banking services. Nevertheless, the substitution effect is limited, and bank branches will keep playing an important role in delivering financial services. For countries with inadequate banking services, bank branches should be increased to encourage residents to participate in the financial system, while it is no longer necessary to add a large number of branches in countries where fintech has been popularized. Faced with the trend of financial digitalization and the economic shock caused by the COVID-19 pandemic, banks should launch more online services and increase intelligent machines in the branches. By doing so, financial services are more resilient to social changes, so as to alleviate the inequality of income distribution in the long term.

Background Sepsis-associated encephalopathy (SAE) is characterized by diffuse brain dysfunction, long-term cognitive impairment, and increased morbidity and mortality. The current treatment for SAE is mainly symptomatic; the lack of specific treatment options and a poor understanding of the underlying mechanism of disease are responsible for poor patient outcomes. Fgr is a member of the Src family of tyrosine kinases and is involved in the innate immune response, hematologic cancer, diet-induced obesity, and hemorrhage-induced thalamic pain. This study investigated the protection provided by an Fgr kinase inhibitor in SAE and the underlying mechanism(s) of action. Methods A cecal ligation and puncture (CLP)-induced mouse sepsis model was established. Mice were treated with or without an Fgr inhibitor and a PGC-1α inhibitor/activator. An open field test, a novel object recognition test, and an elevated plus maze were used to assess neurobehavioral changes in the mice. Western blotting and immunofluorescence were used to measure protein expression, and mRNA levels were measured using quantitative PCR (qPCR). An enzyme-linked immunosorbent assay was performed to quantify inflammatory cytokines. Mitochondrial membrane potential and morphology were measured by JC-1, electron microscopy, and the MitoTracker Deep Red probe. Oxidative stress and mitochondrial dysfunction were analyzed. In addition, the regulatory effect of Fgr on sirtuin 1 (SIRT1) was assessed. Results CLP-induced sepsis increased the expression of Fgr in the hippocampal neurons. Pharmacological inhibition of Fgr attenuated CLP-induced neuroinflammation, the survival rate, cognitive and emotional dysfunction, oxidative stress, and mitochondrial dysfunction. Moreover, Fgr interacted with SIRT1 and reduced its activity and expression. In addition, activation of SIRT1/PGC-1α promoted the protective effects of the Fgr inhibitor on CLP-induced brain dysfunction, while inactivation of SIRT1/PGC-1α counteracted the benefits of the Fgr inhibitor. Conclusions To our knowledge, this is the first report of Fgr kinase inhibition markedly ameliorating SAE through activation of the SIRT1/PGC-1α pathway, and this may be a promising therapeutic target for SAE. Graphical Abstract

Surface-enhanced Raman scattering (SERS) technology has attracted more and more attention due to its high sensitivity, low water interference, and quick measurement. Constructing high-performance SERS substrates with high sensitivity, uniformity and reproducibility is of great importance to put the SERS technology into practical application. In this paper, we report a simple fabrication process to construct dense silver-coated PMMA nanoparticles-on-a-mirror SRES substrates. The electric field enhancement at the ultra-small metallic nanogap is further amplified by the silver mirror, which can achieve higher SERS intensity. The thickness of the PMMA layer was optimized so that the absorption peak can match the excitation wavelength, thus obtaining maximum SERS intensity. The optimized substrate possessed excellent SERS behavior for crystal violet (CV) molecules under 532 nm laser excitation, with a low detection limit of 10 − 13 M. Moreover, SERS analysis was quantitatively achieved in the broad linear concentrations. The fabricated substrate demonstrated excellent uniformity and reproducibility with a relative standard deviation (RSD) of 7.75% in peak intensities. The substrate also showed long-term stability, and it can be stored for 37 days with an acceptable SERS peak intensities. This proposed method will open up new possibilities to fabricate high-performance SERS sensors, which can be widely used for the practical application of chemical and biochemical sensing.

Metasurface solar absorber serves as a kind of important component for green energy devices to convert solar electromagnetic waves into thermal energy. In this work, we design a new solar light absorber configuration that incorporates the titanium nitride substrate, aluminum oxide layer, titanium nitride layer, and the topmost refractory nanostructures. The metasurface absorber based on this configuration can achieve an average spectral absorption of over 91% and a total solar radiation absorption of 91.5% at ultra-wide wavelengths of 300–2500 nm. It is discovered that the excellent performance of the proposed metasurface absorber is attributed to the synergistic effects of surface plasmonic effect and Fabry–Pérot (FP) cavity resonance by comprehensive analysis of the simulated field distributions. Furthermore, the effect of geometrical parameter of the proposed configuration on absorber performance is studied, indicating the proposed configuration possesses a large fabrication tolerance. Moreover, the proposed configuration is not sensitive to the polarization direction and the angle of incident light. It is also found that the use of other refractory metal materials and other shapes as the topmost absorbent nanostructures also have good results with this configuration. This work can offer a universal platform for constructing and guiding the design of refractory metasurface solar absorbers.

(1) Background: the epigenetic mechanisms underlying the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remain poorly understood; (2) Methods: to investigate this process, we conducted genome-wide DNA methylation sequencing to map the epigenetic changes during the AKI-CKD transition in a mouse model. By integrating DNA methylome and transcriptome analyses, we identified genes and signaling pathways regulated by DNA methylation throughout this progression; (3) Results: our analysis identified four candidate genes—Atp1a3, Ncf1, Lpl, and Slc27a2—that were regulated by DNA methylation and strongly correlated with kidney disease prognosis. Additionally, we found that the PPAR signaling pathways, among others, were implicated in this process. Treatment with DNA methyltransferase inhibitors mitigated fibrosis and improved lipid metabolism in the kidneys during AKI-CKD progression; (4) Conclusions: this study provides the first comprehensive epigenetic map of the AKI-CKD transition. Our findings offer new insights into the epigenetic regulation of kidney disease progression and highlight potential therapeutic targets to prevent the transition from AKI to CKD.

Interstitial fibrosis after acute kidney injury is an ongoing pathological process of chronic inflammatory injury and repair. Macrophages participate in renal inflammation, repair and fibrosis by continuously changing their phenotype and function. The tissue microenvironment of kidney injury induces changes in key metabolic enzymes, pathways and metabolites in macrophages, leading to phenotypic and functional conversions, but the detailed mechanisms are unclear. However, in the early phase of acute kidney injury, macrophages shift to a pro-inflammatory role relying on glycolysis and pentose phosphate pathways. The tissue microenvironment regulates the suppression of glycolysis-related genes and the up-regulation of oxidative phosphorylation and tricarboxylic acid cycle genes in macrophages, resulting in a gradual shift to an anti-inflammatory phenotype, which is involved in tissue repair and remodelling. In the late stage of injury, if macrophages continue to be overactive, they will be involved in renal fibrosis. The concomitant enhancement of nucleotide and amino acid metabolism, especially arginine and glutamine metabolism, is critical for the macrophage function and phenotypic transition during the above injury process. Macrophage metabolic reprogramming therefore provides new therapeutic targets for intervention in inflammatory injury and interstitial fibrosis in kidney disease.

Immune-inflammatory dysregulation characterizes acute kidney injury (AKI) throughout its early progression and chronic evolution. Neutrophils and the neutrophil extracellular traps (NETs) they release play multiple roles in this process. Recent research indicates that NETs, characterized by their unique “DNA-histone-granule proteins (e.g., neutrophil elastase [NE], myeloperoxidase [MPO], proteinase 3 [PR3], and cathepsin G).” structure, have become a pivotal research focus in neutrophil biology, while their formation is intricately linked to signals within the tissue microenvironment. This review traces neutrophil dynamics from bone marrow development and recruitment to the kidney, culminating in suicidal or vital NETosis. It specifically compares neutrophil extracellular trap (NET) mechanisms in sterile versus infectious AKI. Besides, it details how non-specific NET components, while aiding pathogen and necrotic tissue clearance, simultaneously damage renal tubular epithelial and endothelial cells, amplifying inflammatory cascades. Furthermore, the review comprehensively summarizes therapeutic strategies targeting NETs for AKI, including inhibition of NET formation/release, blockade of specific NET components, and promotion of NET clearance. These studies offer new perspectives on the spatiotemporal-specific roles of NETs in AKI, laying a solid theoretical groundwork for advancing their exploration in AKI subtyping and precision therapy.

Pancreatic cancer (PC) is highly lethal because of its immunosuppressive tumor microenvironment and resistance to immunotherapy. This study explored the role of NAT10-mediated N4-acetylcytidine (ac4C) RNA modification in pancreatic cancer progression and immune evasion. NAT10 (N-acetyltransferase 10) is overexpressed in pancreatic cancer tissues and correlates with poor prognosis. Mechanistically, NAT10 stabilizes ETS2 mRNA through ac4C acetylation, forming a positive feedback loop that upregulates NAT10 and PD-L1, thereby suppressing CD8 + T cell infiltration and promoting immune evasion. In addition, NAT10 stabilizes KRT8 mRNA via ac4C acetylation, which drives cancer cell proliferation and metastasis. Single-cell RNA sequencing analysis revealed enhanced interactions between pancreatic cancer epithelial cells with high NAT10 and KRT8 expression, and T cells, thereby providing new insights into the immune microenvironment. In vivo, NAT10 knockdown significantly inhibited tumor growth, enhanced CD8 + T cell infiltration, and reduced lung metastasis. Notably, combination therapy with an NAT10 inhibitor and anti-PD-L1 antibody demonstrated superior antitumor efficacy compared to monotherapy. In conclusion, NAT10 promotes pancreatic cancer progression and immune evasion by regulating the ETS2-PD-L1 axis and stabilizing KRT8 mRNA, highlighting its potential as a therapeutic target for overcoming immunotherapy resistance. Highlights NAT10 Promotes Pancreatic Cancer Immune Suppression via ac4C-Mediated Regulation of the ETS2-PD-L1 Axis and KRT8. NAT10-ETS2 Positive Feedback Loop Amplifies Malignant Progression and Immune Suppression. Combination Therapy Targeting NAT10 and PD-L1 is More Effective Than Monotherapy.

Exposure to ultraviolet radiation induces photodamage towards cellular macromolecules that can progress to photoaging and photocarcinogenesis. The topical administration of compounds that maintain the redox balance in cells presents an alternative approach to combat skin oxidative damage. Cerium oxide nanoparticles (CNPs) can act as antioxidants due to their enzyme-like activity. In addition, a recent study from our group has demonstrated the photoprotective potential of tannic acid (TA). Therefore, this work aimed to synthesize CNPs associated with TA (CNP-TA) and investigate its photoprotective activity in L929 fibroblasts exposed to UVB radiation. CNP conjugation with TA was confirmed by UV–Vis spectra and X-ray photoelectron spectroscopy. Bare CNPs and CNP-TA exhibited particle sizes of ~5 and ~10 nm, superoxide dismutase activity of 3724 and 2021 unit/mg, and a zeta potential of 23 and −19 mV, respectively. CNP-TA showed lower cytotoxicity than free TA and the capacity to reduce the oxidative stress caused by UVB; supported by the scavenging of reactive oxygen species, the prevention of endogenous antioxidant system depletion, and the reduction in oxidative damage in lipids and DNA. Additionally, CNP-TA improved cell proliferation and decreased TGF-β, metalloproteinase-1, and cyclooxygenase-2. Based on these results, CNP-TA shows therapeutic potential for protection against photodamage, decreasing molecular markers of photoaging and UVB-induced inflammation.