Browse Articles

Correction to “Elastomeric Micro‐Balloons for Remote Control of Cerebral Blood Flow and Real‐Time In vivo Imaging of Rodent Brain Response to Hypoperfusion”

Assessment of fire susceptibility in Wildland—Urban interfaces according to explainable artificial intelligence: a case study of Antalya province, Mediterranean region, Türkiye

Deficiency in circulating T cells in four core genotypes mice with <i>Sry</i> translocation

Abstract Sex differences exist in the immune responses to infections and in the prevalence and severity of autoimmune and allergic diseases. These sex differences may be caused by sex hormones and/or variable inactivation of X chromosome genes. The 4 core genotypes mice allow for distinction between the effects of sex hormones and chromosomes on physiology and disease pathology. In the FCG mouse model, the Sry gene is deleted from the Y chromosome and inserted into chromosome 3 as multiple copies of a transgene, allowing for phenotypic male and female mice with XX and XY chromosomes. We sought to investigate the role of sex hormones and chromosomes in respiratory syncytial virus infection and allergen-induced airway inflammation. However, in performing these studies, we found that the immune response in FCG males (XXM and XYM) was significantly blunted. XXF and XYF had 4-fold more CD3+CD4+ T cells and over 7-fold more CD3+CD8+ T cells compared to XXM and XYM in the lungs following stimulus. CD4+ and CD8+ T cells were also significantly decreased in XXM and XYM mice in the lungs, spleen, and peripheral blood at baseline with no effect on B cells, NK cells, or myeloid cells. Thymic T cell numbers were similar among groups, and bone marrow progenitors were unchanged between groups. Overall, the translocation of Sry to chromosome 3 resulted in dramatically decreased immune responses to RSV infection and allergen-challenge, indicating that FCG male mice do not mount appropriate immune responses to a respiratory virus infection.

Scalable Synthesis of 3D Hierarchical MoS ₂ as a Durable, High‐Charge‐Retention Friction Layer for the Facile Fabrication of High‐Power Triboelectric Nanogenerators

ABSTRACT Given the increasing demand for sustainable energy and self‐powered devices, energy‐harvesting technologies, such as triboelectric nanogenerators (TENGs), are drawing attention. To address the short charge retention in conventional polymer materials, 2D materials with high surface areas and intrinsic charge‐trapping capabilities, such as MoS 2 , are being utilized as friction layers in TENGs. However, their power generation is too low for practical applications owing to their atomically thin nature, limiting their use as fillers in polymer‐based systems. We report a 2D‐material‐based high‐power TENG using 3D hierarchical MoS 2 (3DH‐MoS 2 ) as a primary friction material. The 3DH‐MoS 2 is synthesized via low‐temperature metal–organic chemical vapor deposition, enabling the direct growth of a uniform, large‐area, 3D‐nanostructured friction layer on a polymer substrate without additional processes. This 3D nanostructure increases the amount of charge‐trapping sites and significantly enhances the durability of the device. The 4 × 4 cm 2 3DH‐MoS 2 ‐based TENG produces a maximum output voltage of 320.1 V and a power density of 0.841 mW cm −2 , proving it can effectively power light‐emitting diodes and a calculator, maintaining its performance over 10 000 cycles. In addition, the device can generate electricity from gas and water flow and human motion, highlighting the potential and versatility of 2D‐material‐based energy‐harvesting systems.

Geochemical assessment of metal and REE concentrations in a region with exploration of petroleum resources, Democratic Republic of the Congo

Identification of a regulatory allosteric site in Arid5a unveils a therapeutic axis for systemic inflammation

Abstract Adenine-thymine (AT)-rich interactive domain-containing protein 5a (Arid5a) is an RNA-binding protein (RBP) that post-transcriptionally stabilizes mRNAs encoding proinflammatory mediators, including Interleukin-6 (IL-6), thereby amplifying inflammation. However, structural basis and regulatory mechanisms of Arid5a function remain poorly defined. In this study, we identified and characterized a conserved allosteric site within the ARID domain that regulates Arid5a-mediated mRNA stabilization. Using integrative in silico modeling and in vitro assays, 2 picolinamide-based inhibitors, NFP1 and NFP2, were designed to specifically engage the allosteric site constituent residues. Mutational and functional analyses revealed Tyr88 and Val91 as key regulatory elements within the allosteric site, essential for transmitting conformational regulation upon ligand engagement. Pharmacological inhibition of the allosteric site disrupted Arid5a interaction with target RNA stem-loop structure, reduced stability of Il6 mRNA, and attenuated inflammatory responses in Lipopolysaccharide (LPS)-stimulated macrophages. Furthermore, Arid5a inhibitors reduced the stability of other target mRNAs, including Signal transducer and activator of transcription 3 (Stat3) and OX40, in polarized T helper 17 (Th17) cells. In a murine model of LPS-induced septic shock, treatment with NFP1 or NFP2 significantly improved survival, reduced clinical severity, and mitigated tissue damage in vital organs. These findings identify a new mechanism regulating Arid5a activity and present Arid5a allosteric inhibition as a promising therapeutic strategy for managing systemic inflammation including sepsis.

Nanoscale Adhesive Architecture Coordinates With Matrix Stiffness to Regulate Stem Cell Aging via Focal Adhesion‐Mediated Chromatin Remodeling and FOXO1 Activation

ABSTRACT Stem cell aging critically limits the efficacy of regenerative biomaterials, yet how mechanical cues within the microenvironment modulate this process remains insufficiently understood. Here, we reveal that the nanoscale spacing of adhesive ligands imposes stiffness‐dependent effects on mesenchymal stem cell (MSC) senescence. Wider spacing (distance 150 nm) accelerates aging on stiff hydrogels (50 kPa) but mitigates it on soft hydrogels (5 kPa), relative to dense spacing (distance 30 nm). Using a molecular clutch‐based theoretical model, we demonstrate that ligand spacing and matrix stiffness cooperatively regulate cell behaviors through focal adhesion assembly. Enhanced focal adhesion formation amplifies stress fiber‐generated traction forces and nuclear envelope tension, leading to increased chromatin accessibility and transcriptional activation of FOXO1, a central regulator of cellular senescence. These mechanistic insights are further validated in vivo. Collectively, these findings delineate a mechanotransduction mechanism through which nanoscale adhesive architecture and matrix stiffness cooperatively govern stem cell aging.

Swappable and non-swappable homorepeats in orthologous proteins reflect distinct patterns of evolutionary flexibility

Abstract Proteins frequently contain runs of a single repeated amino acid, known as homorepeats or polyX regions. While their presence across orthologous proteins is an indicator of their functional importance, less is understood about whether different types of homorepeats can occupy the same position in related proteins: a concept we term “swappability”. Here we study homorepeat overlaps in orthologs from 695 species, tracking swappable and non-swappable cases to analyze their evolution and functional implications. We obtained 17,415,904 orthologous protein pairs from OrthoMCL, analyzed their homorepeats and aligned each orthologous pair to detect overlaps between these regions. Among more than 8.7 million orthologous pairs, we detected 99,386 non-swappable (same amino acid type) and 5,018 swappable (different amino acid type) overlapping homorepeats. Swappable cases tended to be longer and enriched in acidic residues, whereas non-swappable showed lineage-specific variation. Based on their prevalence in our data, we focused on D/E and A/S overlapping homorepeat pairs. PolyD and polyE were frequently found as swappable, maintaining their functional roles primarily linked to ribosomal biogenesis. PolyA and polyS, by contrast, show divergent enrichment patterns in their non-swappable forms, pointing to distinct functional specializations. This work illustrates the balance between positional conservation and sequence flexibility in homorepeat evolution.

The CXCL10/CXCR3 axis drives actin remodeling to recruit CD4+ T cells to gut epithelium during transmissible gastroenteritis virus infection

Abstract The immune system initially protects hosts against viral pathogens, with chemokines guiding immune cell movement. However, their expression patterns and immune cell recruitment mechanisms during transmissible gastroenteritis virus (TGEV) infection are still not fully understood. Here, we identified a distinct chemokine expression profile in intestinal epithelial cells following TGEV infection. Among these, CXCL10 selectively induced the chemotaxis of CD4+ CXCR3+ T cells, while only modestly recruiting CD8+ CXCR3+ (Tc1) T cells and showing minimal involvement in B cell recruitment, thereby shaping the intestinal immune microenvironment to promote TGEV infection. CXCL10 can also upregulate the expression of its receptor CXCR3, thereby further potentiating the migration of CD4+ T cells to the infected region. During this process, CXCL10 activated the CXCR3-Rho GTPase-cofilin signaling axis, driving actin cytoskeletal remodeling. Through this process, CD4+ T cells are channeled from the lamina propria to the infected intestinal lining, facilitating their functional responses. Collectively, these findings reveal a novel mechanism underlying Th1 cell trafficking during TGEV infection and suggest objectives for therapeutic vaccine creation and disease management.

Reducing Solvent Selectivity via Solid Additive‐Assisted Strategy Enables Organic Solar Cells With Approaching 21% Efficiency

ABSTRACT Currently, high‐performance organic solar cells (OSCs) are predominantly fabricated using chloroform (CF) to achieve an optimal active‐layer morphology. However, its rapid film formation results in a narrow processing window and severely limits industrial scalability. Therefore, reducing solvent selectivity during active‐layer processing is essential to facilitate scalable OSC manufacturing. Herein, this critical issue is finely addressed by a solid‐additive‐assisted strategy, in which 2,6‐dimethylnaphthalene (2,6‐DMN) is incorporated to modulate the film formation dynamic and molecular aggregation in different processing solvents. It is revealed that 2,6‐DMN enables stage‐specific control over the film formation process. Its mechanism involves suppressing acceptor aggregation during spin‐coating and then promoting ordered acceptor self‐assembly during annealing. This two‐stage modulation simplifies donor–acceptor interactions, mitigates excessive aggregation caused by slow solvent drying, and thereby prevents large‐scale phase separation. As a result, 2,6‐DMN induces a highly uniform and favorable active‐layer morphology across various processing solvents, thereby alleviating performance variations in devices caused by solvent effect. Consequently, the 2,6‐DMN‐based PM6:D18:L8‐BO‐X ternary device processed from o ‐xylene achieves a remarkable efficiency of 20.86%, setting a record for non‐halogenated solvent‐processed OSCs. This work provides a practical and efficient solid‐additive‐assisted strategy to mitigate the solvent selectivity in OSCs, demonstrating significant potential for achieving high‐performance OSCs with enhanced processing compatibility.

Genomic and structural analysis of dacB variants associated with cephalosporin resistance in Pseudomonas aeruginosa

Sorting nexin 5 deficiency impairs MHC class II antigen presentation and inflammatory responses during tuberculosis

Abstract Tuberculosis (TB) remains one of the leading causes of death from a single infectious agent worldwide, yet the host pathways that regulate antigen presentation and lung inflammation during Mycobacterium tuberculosis (Mtb) infection are incompletely defined. Sorting nexin 5 (SNX5) is a protein implicated in endosomal trafficking, antigen processing, and antiviral host defense, but its contribution to antibacterial immunity is unknown. Here, we show that SNX5-deficient mice exhibit increased mortality following low-dose aerosol Mtb infection despite unchanged pulmonary bacterial burden compared with wild-type mice. Snx5−/− mice developed exacerbated lung inflammation without major alterations in immune cell recruitment. In macrophages, Snx5 did not affect phagocytosis, vacuolar maturation, intracellular bacterial control, or global transcriptional responses to Mtb but was required for efficient major histocompatibility complex (MHC) class II antigen presentation. Snx5 deficiency was associated with reduced endolysosomal proteolysis and impaired MHC class II antigen presentation in vitro, resulting in reduced activation of antigen-specific CD4+ T cells without altering surface MHC class II abundance or costimulatory molecule expression. Together, these findings identify SNX5 as a regulator of MHC class II antigen presentation that influences inflammatory outcomes during pulmonary Mtb infection.

Homogenizing Vertical Strain Distribution Enables High‐Performance Tin‐Based Perovskite Solar Cells With Thicker Absorber via Two‐Step Deposition

ABSTRACT Owing to typically restricted active layer thickness (∼200 nm), solution‐processed tin‐based perovskite solar cells (TPVSCs) suffer from incomplete photon‐to‐electron conversion, which fundamentally limits power conversion efficiency (PCE). Unfortunately, we uncover for the first time that increasing the active layer thickness induces detrimental vertical lattice strain gradient and faster crystallization rate, which exacerbate defect formation and ultimately cause a severe mismatch between electron diffusion length and absorber thickness in the tin‐based perovskite device. To address this, we innovatively introduce reductive 4,4′‐thiobisbenzenethiol (TBBT), whose ‐SH groups can form bidentate coordination with Sn 2+ ions. This interaction can relax Sn‐I bonds, which is beneficial for lattice homogeneity. Concurrently, it retards crystallization kinetics, thus achieving an electron diffusion length commensurate with active layer thickness. Ultimately, the excellent PCEs of 15.02% (certified 14.78%) for rigid devices and 12.43% for flexible devices at 0.04 cm 2 , and 13.37% for rigid devices at 1.00 cm 2 are achieved. Notably, the unencapsulated rigid device retains T 95 of 3500 h shelf storage and T 90 of 684 h under MPP tracking. Meanwhile, the flexible device maintains 85% of its initial PCE after 4000 bending cycles. These results demonstrate that our strategy yields synergistic gains in both efficiency and stability.

Retraction Note: Synthesis, antimicrobial, anti-inflammatory, antioxidant and cytotoxicity of new pyrimidine and pyrimidopyrimidine derivatives

Immunotherapy of malignant melanoma using T cell–activating microbeads

Abstract Metastatic disease is the prime cause of death from many malignancies. Due to the multiple different lesions and the increased aggressiveness of the cancer cells, metastatic disease is often difficult to treat. Here, the introduction of immune checkpoint blockers (ICBs) has greatly helped to improve patients’ prognosis by harnessing antitumor immunity, particularly anticancer T cells in multiple human cancers. Despite the success of ICBs in, for example, metastatic melanoma 2 major challenges remain in the field: therapy-limiting toxicities induced by systemic ICB administration and lack of a life-prolonging response in a substantial number of patients. Therefore, highly potent local immunotherapeutic approaches might offer a solution and enhance treatment of metastatic disease. Here, we describe antibody-functionalized paramagnetic microbeads as a means to fill this void. These microbeads are readily engulfed by the vast majority of human cancer cell line cells studied inducing direct cytotoxicity (first hit). Focusing on malignant melanoma, we further observed that loading the microbeads with a conventional anti-CD28 monoclonal antibody (bead-bound conventional anti-CD28 monoclonal antibody, BBC-28) not only efficiently induced proliferation and cytokine release by human T cells expressing CD28, but also enhanced killing of melanoma cells by melanoma-reactive T cells (second hit). Thus, we provide proof-of-concept data that BBC-28, after local application into, for example, skin metastases, may also induce a combination of direct toxicity and enhanced anticancer immunity, leading to efficient treatment of metastatic disease.

In‐Material Self‐Adaptive Dynamic Encoding in FeO _x Optomemory Device for Real‐Time Analog Signal Processing

ABSTRACT In‐sensor vision computing system as an emerging edge computing platform shows great potential to process dynamic information. However, it still requires an electric to reset weight, largely limiting its capability in processing complex signals. Here we propose FeO x optomemory that can automatically convert its states from negative photoconductance memory (NPM) to positive photoconductance memory (PPM). The formation of neutral oxygen vacancy ( V o ) from both the photogenerated electron‐based iron reduction process (Fe 3+ to Fe 2+ ) and the photoelectron trapping by charged oxygen vacancy ( V o x+ ) builds the NPM effect under low light dosage illumination. The decrease in V o by the photogenerated hole‐based iron oxidization process (Fe 2+ to Fe 3+ ) and the increase in V o x+ by Joule‐heating assisted photoelectron detrapping from V o sites causes the automatic conversion from the NPM to the PPM when the light illumination exceeds the threshold dosage (0.72 µJ/µm 2 ). Such self‐adaptive conversion from NPM and PPM enables the FeO x optomemory to execute fully optical computing. The NPM effect provides rich echo states for dynamic feature encoding while the PPM initializes the encoded states, thus building a self‐adaptive reservoir computing (RC) system, yielding a recognition accuracy of 97.93%. This work provides an emerging in‐material encoding mechanism for in‐sensor edge computing system.

Predicting leprosy reactions: a machine learning framework incorporating clinical, demographic, and healthcare system factors in China

IL-17–driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis

Abstract Idiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease targeting muscle and extramuscular organs, but the molecular mechanisms driving IIM pathogenesis remain largely undefined. Muscle fibroblasts are central to orchestrating inflammation in myositis. Here, we investigated muscle fibroblast dynamics using a single-cell RNA sequencing approach in an established murine model of anti-histidyl–tRNA synthetase (HRS, also known as Jo-1)-induced myositis. In fibroblasts, there was a robust activation of an IL-17 gene signature during disease. Among the induced genes was Nfkbiz, which encodes IκBζ, a noncanonical NF-κB transcriptional coactivator known to be key for pathologic IL-17 signaling in a variety of autoimmune settings. In muscle fibroblasts, IκBζ was potently activated by IL-17 in vitro and was essential for IL-17 signaling responsiveness. Surprisingly, however, the IL-17–IκBζ signaling axis was dispensable for the histopathological phenotype in HRS-induced myositis. Thus, despite a prominent IL-17 transcriptional signature, IL-17 and IκBζ are not required for autoantibody production or tissue inflammation in this model system.

Electrocatalyst/Semiconductor Interfaces in Photoelectrocatalysts: Mechanistic Analysis of the Impact of Nanoparticle Electrocatalyst Coverage on Performance

ABSTRACT Interfaces between metal nanoparticle electrocatalysts (np‐EC) and semiconductors (SC) play a key role in photovoltage generation in photoelectrochemical np‐EC/SC water splitting systems. In this contribution, we investigate how the coverage of np‐EC on SC influences the performance of photoelectrodes. We focus on a case study of np‐Ni/n‐Si photoelectrocatalysts for the oxygen evolution reaction (OER). By systematically varying Ni coverage, we show that np‐EC coverage not only impacts light absorption and electrocatalytic activity but also governs the chemical evolution of the EC/SC interface under operating conditions by dictating the terminal thickness of interfacial insulating SiO x layers that form during system operation. We demonstrate that this evolution of the interfacial SiO x ultimately governs the system performance. We shed light on the underlying processes that govern the rate of growth for these interfacial oxide layers and describe how catalyst coverage impacts these processes. These findings highlight reaction environment‐induced changes to the EC/SC interface as a critical parameter that affects the performance of photoelectrochemical systems.

NanoBiT screening identifies the azaoxafluorene VT11 as potent tau interaction inhibitor

Abstract Tauopathies are neurodegenerative disorders characterized by accumulating misfolded, insoluble tau protein aggregates in neurons or glial cells. In this study, we screened the Spectrum Collection and other compound libraries for inhibitors of tau self-interaction using a structural complementation reporter system ( NanoLuciferase Binary Technology ). Resulting candidates were tested in dose-response assays and evaluated for cell toxicity and microtubule destabilization. Further, a seed-induced tau interaction biosensor assay and a cell-free tau Real-Time Quaking-Induced Conversion assay have been established to study their effects on the kinetics of tau interaction and aggregation, respectively. The substances ritanserin, 3-methoxycatechol, gambogic amide, azaoxafluorenes VT11, and NS 185 and thieno[2,3-d][1.3]oxazine B6/55 showed a concentration-dependent tau self-interaction inhibition without relevant cell toxicity or microtubule destabilization. Ritanserin, VT11, NS 185 and B6/55 blocked tau interaction in the seed-induced tau interaction biosensor assay. Finally, the cell-free tau RT-QuIC assay displayed highest inhibitory potential for VT11. Thus, the azaoxafluorene VT11 seems to be a promising candidate for further investigations as tau interaction inhibitor to address a pivotal pathological process in Alzheimer’s disease and other tauopathies.