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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]

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]

Calcium/calmodulin‐dependent protein kinase (CAMKs) can control a wide range of cancer‐related functions in multiple tumour types. Herein, we explore the expressions and clinical significances of calcium/calmodulin‐dependent protein kinase 1 (CAMK1) in pancreatic cancer (PC). The expression of CAMK1 in PC was analysed by Gene Expression Profiling Interactive Analysis 2 (GEPIA 2) database and the Oncomine database. For further validation, the protein level of CAMK1 in PC tissues was also detected in the Human Protein Atlas (HPA) database and the tissue microarray (TMA)‐based immunohistochemistry (IHC). GEPIA 2 and Kaplan‐Meier Plotter (KM Plotter) databases were used to explore the prognostic significances of CAMK1 in overall survival (OS) and disease‐free survival (DFS) of PC at mRNA level. The relationship between CAMK1 expression and the clinicopathological characteristics of PC was further explored. Additionally, the Search Tool for the Retrieval of Interacting Genes (STRING) database was used to analyse protein‐protein interactions (PPI). We found CAMK1 was highly expressed in PC both in bioinformatics analyses and TMA‐IHC results. The prognostic analyses from the public databases also showed consistent results with follow‐up data. The PPI network suggested that CALM1, CALM3, CREB1, CALM2, SYN1, NOS3, ATF1, GAPDH, PPM1F and FBXL12 were important significant genes associated with CAMK1. Our finding revealed CAMK1 has prognostic value in PC patients, suggesting that CAMK1 may has a distinct role in PC patients and can be used as a candidate marker for investigating clinical prognosis of PC. [ABSTRACT FROM AUTHOR]

In this work, chromium coating conducted by magnetron sputtering was introduced to braze SiC ceramics using inactive AgCu filler metal. The results showed that reliable metallurgical bonding of SiC ceramics was obtained at 900°C for 10 minutes. SEM, XRD, and TEM were used to identify the reaction phase in the joint, and the typical interfacial microstructure was SiC/mixed CrSi2 + Cr23C6 layer/CrSi2/Ag(s,s)+Cu(s,s)/CrSi2/mixed CrSi2 + Cr23C6 layer/SiC. The shear strength of SiC joint using chromium coating brazed with inactive AgCu filler metal was 29.6 MPa and the joint fractured at the SiC substrate entirely after shear test. The proposed active element coating method provides a feasible way to achieve the brazing of ceramics. [ABSTRACT FROM AUTHOR]

Non‐tuberculous mycobacteria (NTM), also known as an environmental and atypical mycobacteria, can cause the chronic pulmonary infectious diseases. Macrophages have been suggested as the main host cell to initiate the innate immune responses to NTM infection. However, the molecular mechanism to regulate the antimicrobial immune responses to NTM is still largely unknown. Current study showed that the NTM clinical groups, Mycobacterium abscessus and Mycobacterium smegmatis, significantly induced the M1 macrophage polarization with the characteristic production of nitric oxide (NO) and marker gene expression of iNOS, IFNγ, TNF‐α, IL1‐β and IL‐6. Interestingly, a non‐histone nuclear protein, HMGN2 (high‐mobility group N2), was found to be spontaneously induced during NTM‐activated M1 macrophage polarization. Functional studies revealed that HMGN2 deficiency in NTM‐infected macrophage promotes the expression of M1 markers and the production of NO via the enhanced activation of NF‐κB and MAPK signalling. Further studies exhibited that HMGN2 knock‐down also enhanced IFNγ‐induced M1 macrophage polarization. Finally, we observed that silencing HMGN2 affected the survival of NTM in macrophage, which might largely relevant to enhanced macrophage polarization into M1 phenotype under the NTM infection. Collectively, current studies thus suggested a novel function of HMGN2 in regulating the anti‐non‐tuberculous mycobacteria innate immunity of macrophage. [ABSTRACT FROM AUTHOR]

High‐optical‐quality ternary [(Y1‐xGdx)0.99Dy0.01]2O3 (x = 0 and 0.4) ceramics were successfully fabricated by vacuum sintering with in‐line transmittances of 71.4%‐75.1% at 574 nm, the wavelength of Dy3+ emission (the 4F9/2 → 6H13/2 transition). Substitution of Gd3+ for Y3+ significantly affected the photoluminescent and scintillant properties of the ceramics. Gd3+ addition effectively increased lattice parameters and theoretical densities of the ceramic samples; this contributed to enhanced X‐ray absorption coefficients. Both [(Y1‐xGdx)0.99Dy0.01]2O3 (x = 0 and 0.4) ceramics displayed typical Dy3+ emissions from 4F9/2 → 6HJ (J = 15/2, 13/2, 11/2) transitions under UV and X‐ray irradiations. By incorporating Gd3+ into the lattice, a stronger excitation peak of Gd3+ due to internal f‐f transitions relative to Dy3+ was observed at 276 nm; subsequent ceramics obtained a sharper PL intensity and a warmer hue via effective energy transfer from Gd3+ to Dy3+. Using a Gd3+ dopant generally reduces the total photoluminescence/photoluminescence excitation intensities and light output; it also delays the lifetime and afterglow of the transparent ceramics. [ABSTRACT FROM AUTHOR]

Summary: In Streptomyces, GlnR is an activator protein that activates nitrogen‐assimilation genes under nitrogen‐limiting conditions. However, less is known regarding the regulation of these genes under nitrogen‐rich conditions. We determined that the developmental regulator MtrA represses nitrogen‐assimilation genes in nitrogen‐rich media and that it competes with GlnR for binding to GlnR boxes. The GlnR boxes upstream of multiple nitrogen genes, such as amtB, were confirmed as MtrA binding sites in vitro by electrophoretic mobility shift assays and in vivo by ChIP‐qPCR analysis. Transcriptional analysis indicated that, on nutrient‐rich medium, MtrA profoundly repressed expression of nitrogen‐associated genes, indicating opposing roles for MtrA and GlnR in the control of nitrogen metabolism. Using in vitro and in vivo analysis, we also showed that glnR is itself a direct target of MtrA and that MtrA represses glnR transcription. We further demonstrated functional conservation of MtrA homologues in the recognition of GlnR boxes upstream of nitrogen genes from different actinobacterial species. As mtrA and glnR are widespread among actinomycetes, this mechanism of potential competitive control over nitrogen metabolism genes may be common in this group, adding a major new layer of complexity to the known regulatory network for nitrogen metabolism in Streptomyces and related species. [ABSTRACT FROM AUTHOR]