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Fluorescent imaging and biosensing in the near‐infrared‐II (NIR‐II) window holds great promise for non‐invasive, radiation‐free, and rapid‐response clinical diagnosis. However, it's still challenging to develop bright NIR‐II fluorophores. In this study, we report a new strategy to enhance the brightness of NIR‐II aggregation‐induced emission (AIE) fluorophores through intramolecular electrostatic locking. By introducing sulfur atoms into the side chains of the thiophene bridge in TSEH molecule, the molecular motion of the conjugated backbone can be locked through intramolecular interactions between the sulfur and nitrogen atoms. This leads to enhanced NIR‐II fluorescent emission of TSEH in both solution and aggregation states. Notably, the encapsulated nanoparticles (NPs) of TSEH show enhanced brightness, which is 2.6‐fold higher than TEH NPs with alkyl side chains. The in vivo experiments reveal the feasibility of TSEH NPs in vascular and tumor imaging with a high signal‐to‐background ratio and precise resection for tiny tumors. In addition, polystyrene nanospheres encapsulated with TSEH are utilized for antigen detection in lateral flow assays, showing a signal‐to‐noise ratio 1.9‐fold higher than the TEH counterpart in detecting low‐concentration antigens. This work highlights the potential for developing bright NIR‐II fluorophores through intramolecular electrostatic locking and their potential applications in clinical diagnosis and biomedical research. [ABSTRACT FROM AUTHOR]

SUMMARY: Carotenoids are photosynthetic pigments and antioxidants that contribute to different plant colors. However, the involvement of TOPLESS (TPL/TPR)‐mediated histone deacetylation in the modulation of carotenoid biosynthesis through ethylene‐responsive element‐binding factor‐associated amphiphilic repression (EAR)‐containing transcription factors (TFs) in apple (Malus domestica Borkh.) is poorly understood. MdMYB44 is a transcriptional repressor that contains an EAR repression motif. In the present study, we used functional analyses and molecular assays to elucidate the molecular mechanisms through which MdMYB44‐MdTPR1‐mediated histone deacetylation influences carotenoid biosynthesis in apples. We identified two carotenoid biosynthetic genes, MdCCD4 and MdCYP97A3, that were confirmed to be involved in MdMYB44‐mediated carotenoid biosynthesis. MdMYB44 enhanced β‐branch carotenoid biosynthesis by repressing MdCCD4 expression, whereas MdMYB44 suppressed lutein level by repressing MdCYP97A3 expression. Moreover, MdMYB44 partially influences carotenoid biosynthesis by interacting with the co‐repressor TPR1 through the EAR motif to inhibit MdCCD4 and MdCYP97A3 expression via histone deacetylation. Our findings indicate that the MdTPR1‐MdMYB44 repressive cascade regulates carotenoid biosynthesis, providing profound insights into the molecular basis of histone deacetylation‐mediated carotenoid biosynthesis in plants. These results also provide evidence that the EAR‐harboring TF/TPL repressive complex plays a universal role in histone deacetylation‐mediated inhibition of gene expression in various plants. Significance Statement: MdMYB44 regulated carotenoid biosynthesis partially by interacting with co‐repressor TPR1 via EAR motif to inhibit MdCCD4 and MdCYP97A3 expression through histone deacetylation, providing evidence that the EAR‐harboring TF/TPL repressive complex has a universal role in histone deacetylation‐mediated gene expression inhibition in various plants. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the role of Nkx1‐2, a transcription factor with the NK homeobox domain, in the regulation of fat production. Methods: Gene expression was analyzed using quantitative real‐time polymerase chain reaction or transcriptome sequencing. CRISPR/Cas9 technology was employed to generate nkx1.2 knockout zebrafish and nkx1.2‐deleted 3T3‐L1 cells. Lipid droplet production in zebrafish larvae was visually quantified using Nile red staining, whereas lipid droplets in 3T3‐L1 cells were stained with Oil red O. The binding of Nkx1‐2 to the promoter was verified through an electrophoretic mobility shift assay experiment. Results: Nkx1‐2 plays crucial roles in the regulation of fat production in zebrafish. Knockout of nkx1.2 in zebrafish leads to weight loss, accompanied by significantly reduced lipid droplet production and decreased visceral and liver fat content. Furthermore, genes related to lipid biosynthesis are significantly downregulated. In 3T3‐L1 preadipocytes, Nkx1‐2 induces differentiation into mature adipocytes by binding to the cebpa promoter, thereby activating its transcription. Additionally, the expression of nkx1.2 is regulated by the p38 MAPK, JNK, or Smad2/3 signaling pathways in 3T3‐L1 cells. Conclusions: Our findings suggest that Nkx1‐2 functions as a positive regulator of fat production, playing a critical role in adipocyte differentiation and lipid biosynthesis. [ABSTRACT FROM AUTHOR]

The hole transport layer (HTL) is an important component in organic solar cells (OSCs). As a commonly used HTL, poly(3,4‐ethylenedioxythiophene):poly(styrene‐sulfonate) (PEDOT:PSS) in OSCs generally exhibits relatively low conductivity, hindering device performance improvement. Herein, amine‐functionalized carbon dots (CDs‐N) are introduced as dopants of PEDOT:PSS, which can effectively enhance the HTL conductivity while maintaining a similar work function. The PEDOT:PSS+CDs‐N devices exhibit higher power conversion efficiencies due to the improved charge extraction ability. It is found that the larger conjugated backbones of CDs‐N and the amine functional groups interacting with PSS are keys for such optimization. This work illustrates the potential of CDs for the applications on interface layers in OSCs. [ABSTRACT FROM AUTHOR]

Zero‐dimensional nitrogen‐doped carbon dots (N‐CDs) have been proved effective when introduced into the polymerization system of aniline as the hard template to synthesis small‐sized, monodisperse and highly conductive N‐CDs/PANI (N‐CDs/PANI) nanocomposites, which were then added into acrylic (AC) resin to produce coatings with excellent corrosion resistance and antifouling performances in this paper. Compared with the PANI, the N‐CDs/PANI did show remarkably improved anticorrosion and antifouling properties. The protection efficiency of the AC resin coating was increased by 5 times and to 57.3% with the addition of the N‐CDs/PANI, which is higher than that of the AC resin coating, about 37.0%, with the addition of the PANI. In addition, the AC resin coating containing N‐CDs/PANI exhibited additional antifouling properties with an algae inhibition rate of about 24.6%, since the redox property of the carbon dots could destroy the photosynthesis of microorganisms such as Chlorella. Furthermore, because that the N‐CDs/PANI had better dispersibility than PANI and could be more uniformly dispersed in the AC resin, the adhesion of the N‐CDs/PANI‐AC coating was better than that of the PANI‐AC coating. [ABSTRACT FROM AUTHOR]

Tumor‐targeted photodynamic therapy (PDT) is desirable as it can achieve efficient killing of tumor cells with no or less harm to normal cells. Herein, a facile molecular engineering strategy is developed for photosensitizers (PSs) with aggregation induced emission (AIE) characteristics and responsive properties to the acidic tumor microenvironment (TME). By the marriage of pH‐sensitive sulfonamide moieties with AIE PSs, two near‐infrared AIE luminogens called DBP‐SPy and DBP‐SPh are designed and synthesized. Both luminogens can form negatively charged nanoaggregates in the aqueous medium at physiological pH. The DBP‐SPy nanoaggregates undergo surface charge conversion to become positive at pH close to the signature pH of TME, while DBP‐SPh nanoaggregates show no such property. The endowed response to acidic TME enables the enhanced cellular uptake of DBP‐SPy at pH = 6.8. By contrast, its cellular uptake is much sacrificed at pH 7.4. As a result, under white light irradiation, DBP‐SPy nanoaggregates demonstrate a considerable photodynamic therapeutic effect on cancer cells in vitro and excellent tumor growth inhibition in vivo. Hence, this study not only provides an acidic TME‐responsive AIE PS for precise PDT, but also inspires new design strategies for AIE‐based theragnostic systems with targeting characteristics. [ABSTRACT FROM AUTHOR]

Robotic materials, with coupled sensing, actuation, computation, and communication, have attracted increasing attention because they are able to not only tune their conventional passive mechanical property via geometrical transformation or material phase change but also become adaptive and even intelligent to suit varying environments. However, the mechanical behavior of most robotic materials is either reversible (elastic) or irreversible (plastic), but not transformable between them. Here, a robotic material whose behavior is transformable between elastic and plastic is developed, based upon an extended neutrally stable tensegrity structure. The transformation does not depend on conventional phase transition and is fast. By integrating with sensors, the elasticity‐plasticity transformable (EPT) material is able to self‐sense deformation and decides whether to undergo transformation or not. This work expands the capability of the mechanical property modulation of robotic materials. [ABSTRACT FROM AUTHOR]

The immunoproteasome is a specialized type of proteasome involved in MHC class I antigen presentation, antiviral adaptive immunity, autoimmunity, and is also part of a broader response to stress. Whether the immunoproteasome is regulated by DNA stress, however, is not known. We here demonstrate that mitochondrial DNA stress upregulates the immunoproteasome and MHC class I antigen presentation pathway via cGAS/STING/type I interferon signaling resulting in cell autonomous activation of CD8+ T cells. The cGAS/STING‐induced adaptive immune response is also observed in response to genomic DNA and is conserved in epithelial and mesenchymal cells of mice and men. In patients with idiopathic pulmonary fibrosis, chronic activation of the cGAS/STING‐induced adaptive immune response in aberrant lung epithelial cells concurs with CD8+ T‐cell activation in diseased lungs. Genetic depletion of the immunoproteasome and specific immunoproteasome inhibitors counteract DNA stress induced cytotoxic CD8+ T‐cell activation. Our data thus unravel cytoplasmic DNA sensing via the cGAS/STING pathway as an activator of the immunoproteasome and CD8+ T cells. This represents a novel potential pathomechanism for pulmonary fibrosis that opens new therapeutic perspectives. Synopsis: Immunoproteasomes are activated by interferons and involved in MHC class I‐mediated CD8+ T‐cell activation as part of antiviral immune responses. This study demonstrates that cytoplasmic DNA sensing by the cGAS/STING pathway induces immunoproteasome‐mediated activation of CD8+ T cells that may be involved in idiopathic pulmonary fibrosis. Sensing of intracellular mitochondrial and genomic DNA via the cGAS/STING pathway activates the immunoproteasome and MHC class I antigen presentation in human and murine epithelial cells and fibroblasts.cGAS/STING activation induces CD8+ T cell adaptive immune responses in a cell‐autonomous manner.Immunoproteasomes and CD8+ T cells are activated in lungs of patients with idiopathic pulmonary fibrosis. [ABSTRACT FROM AUTHOR]

The one‐stage detectors achieve a good trade‐off between performance and latency, owing to the plain architecture and divergent learning mechanism for classification and localization. However, the two sub‐tasks require features with various inherency with which to generate inconsistent detections, fettering detectors. In this study, the misalignment is deeply analyzed via kernel density estimation (KDE) for the first time. Moreover, to address the misalignment, a plug‐and‐play detection head, named Diff‐Head, is devised and embedded in one‐stage detectors. Concretely, the authors merge parallel branches into a semi‐parallel structure, establishing the correlation between classification and regression. In the regression branch, a feature difference module (FDM) gets rid of the features that favour classification by subtracting salient object features from the original feature map, and position encoding (PE) modules enhance the absolute position information. The flexibility and efficiency of the detection head are retained. Experiments on Pascal visual object classes (VOC) and MS COCO demonstrate that Diff‐Head is effective and achieves competitive performance with state‐of‐the‐art detectors. Meanwhile, the amount of parameters is reduced at least 30% and 83.0% average precision (AP) is achieved on Pascal VOC. The analyses of consistency and error show that Diff‐Head has better localization and the capability of mitigating the misalignment. [ABSTRACT FROM AUTHOR]

The extensive utilization of fluorine industrial products has brought abundant fluorine pollution. The fluorine removal is important. In this study, CaO, as a novel coprecipitator, was conducted to synthesize Ca‐Fe‐SO4 layered double hydroxide (CF) via co‐precipitation of FeSO4. Ca‐Fe mixed metal oxide adsorbent (CCF) was fabricated by calcinating CF for efficient fluoride adsorption. The results showed that CCF adsorbent had an excellent adsorption performance for fluoride. It was attributed to two reasons as follows: On one hand, Ca had a strong affinity for fluoride, improving the adsorption capacity of adsorbent for fluoride. On the other hand, Fe had a strong magnetism, which could promote the recovery of the adsorbed material. The adsorption capacity of CCF for fluorine was analyzed by batch adsorption experiments, the adsorption capacity was 160.66 mg/g at temperature of 298 K and pH of 7. Moreover, the adsorption process of fluorine and the actual adsorption process were in accordance with Langmuir model and the pseudo‐second‐order kinetic model, respectively. According to the analysis of pHzpc, FITR and XPS, the main adsorption mechanisms of CCF for fluoride in water were complexation and electrostatic interactions. Therefore, this study suggested that CaO can be a novel coprecipitator to prepare a new efficient fluorine adsorbent for the treatment of industrial wastewater. [ABSTRACT FROM AUTHOR]

Summary: Our previous study using transposon mutagenesis indicated that disruption of the putative response regulator gene orrA impacted antibiotic production in Streptomyces coelicolor. In this study, the role of OrrA was further characterized by comparing the phenotypes and transcriptomic profiles of the wild‐type S. coelicolor strain M145 and ΔorrA, a strain with an inactivated orrA gene. Chromatin immunoprecipitation using a strain expressing OrrA fused with FLAG showed that OrrA binds the promoter of wblA, whose expression was downregulated in ΔorrA. The interaction of OrrA with the wblA promoter was further validated by a pull‐down assay. Similar to ΔorrA, the deletion mutant of wblA (ΔwblA) was defective in development, and developmental genes were expressed at similar levels in ΔorrA and ΔwblA. Although both OrrA and WblA downregulated actinorhodin and undecylprodigiosin, their roles in regulation of the calcium‐dependent antibiotic and yellow‐pigmented type I polyketide differed. sco1375, a gene of unknown function, was identified as another OrrA target, and overexpression of either sco1375 or wblA in ΔorrA partially restored the wild‐type phenotype, indicating that these genes mediate some of the effects of OrrA. This study revealed targets of OrrA and provided more insights into the role of the orphan response regulator OrrA in Streptomyces. [ABSTRACT FROM AUTHOR]

Li‐ion hybrid supercapacitors (LHSCs) are intensely studied due to their favorable power densities. However, combined higher energy density materials, particularly anodes, are desirably sought. Herein, a defect‐dominating structure protocol is reported. Specifically, two visible structural defects, i.e., crystal vacancy and lattice distortion have been introduced in situ in ultrafine niobium nitride (NbN) monocrystals that are integrated into a carbon (C) framework. Highly reversible Li‐ion storage capacities up to 540 mAh g−1 are demonstrated in such a NbN@C composite anode, together with excellent rate capability and cycling stability. An extra vacancy‐induced capacity contribution of the defective NbN component is evidenced by first‐principles density functional theory (DFT) simulations in contrast to perfect modeling. Coupling with an activated carbon (AC) cathode, the NbN@C//AC cell can deliver balanced energy and power densities of 53.8 Wh kg−1 and 7818 W kg−1 at 4 A g−1, and retain a desired energy density of 56.1 Wh kg−1 after 10 000 cycles at 1 A g−1. Findings from this study, particularly the demonstrated defects‐induced extra capacity of pseudocapacitive materials, may inspire new structural material designs of LHSCs. [ABSTRACT FROM AUTHOR]

A green chemical precipitation route was used to yield a hydrated basic sulfate precursor upon calcination at 1000°C into a series of (Y,Gd)2O2SO4:Dy particles. The phosphors exhibited characteristic Dy3+ emissions from 4F9/2→6HJ (J = 15/2, 13/2, 11/2) transitions under ultraviolet light excitation; the quenching concentration of Dy3+ was determined to be 2.5 at.%. Substitution of Gd3+ for Y3+ led to an additional strong sharp band at ~277 nm (8S7/2→6IJ transition of Gd3+) in the photoluminescence excitation spectra, upon which the (Gd0.975Dy0.025)2O2SO4 phosphor achieved a ~2.8‐fold higher photoluminescence intensity via an effective energy transfer from Gd3+ to Dy3+ compared with the 354 nm excitation of Dy3+. Both the photoluminescence and photoluminescence excitation intensities of (Y,Gd)2O2SO4:Dy phosphors increased with rising Gd3+ concentration and calcination temperature in the range 750–1000°C. A higher Gd3+ concentration slightly prolonged the effective fluorescence lifetime. [ABSTRACT FROM AUTHOR]

Summary: Phosphate metabolism is known to be regulated by the PhoPR regulatory system in Streptomyces and some other bacteria. In this study, we report that MtrA also regulates phosphate metabolism in Streptomyces. Our data showed that, in Streptomyces coelicolor, MtrA regulates not only phosphate metabolism genes such as phoA but also phoP under different phosphate conditions, including growth on rich complex media without added inorganic phosphate and on defined media with low or high concentrations of inorganic phosphate. Cross‐regulation was also observed among mtrA, phoP and glnR under these conditions. We demonstrated both in vitro and in vivo binding of MtrA to the promoter regions of genes associated with phosphate metabolism and to the intergenic region between phoR and phoU, indicating that these phosphate metabolism genes are targets of MtrA. We further showed that MtrA in S. lividans and S. venezuelae has detectable regulatory effects on expression of phosphate metabolism genes. Additionally, the MtrA homologue from Corynebacterium glutamicum bound predicted MtrA sites of multiple phosphate metabolism genes, implying its potential for regulating phosphate metabolism in this species. Overall, our findings support MtrA as a major regulator for phosphate metabolism in Streptomyces and also potentially in other actinobacteria. [ABSTRACT FROM AUTHOR]

Triple‐negative breast cancer (TNBC) is a highly aggressive and metastatic malignancy with poor treatment outcomes. The interaction between the tumor microenvironment (TME) and breast cancer stem cells (BCSCs) plays an important role in the development of TNBC. Owing to their ability of self‐renewal and multidirectional differentiation, BCSCs maintain tumor growth, drive metastatic colonization, and facilitate the development of drug resistance. TME is the main factor regulating the phenotype and metastasis of BCSCs. Immune cells, cancer‐related fibroblasts (CAFs), cytokines, mesenchymal cells, endothelial cells, and extracellular matrix within the TME form a complex communication network, exert highly selective pressure on the tumor, and provide a conducive environment for the formation of BCSC niches. Tumor growth and metastasis can be controlled by targeting the TME to eliminate BCSC niches or targeting BCSCs to modify the TME. These approaches may improve the treatment outcomes and possess great application potential in clinical settings. In this review, we summarized the relationship between BCSCs and the progression and drug resistance of TNBC, especially focusing on the interaction between BCSCs and TME. In addition, we discussed therapeutic strategies that target the TME to inhibit or eliminate BCSCs, providing valuable insights into the clinical treatment of TNBC. [ABSTRACT FROM AUTHOR]