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Impact of layer count and thickness on spin wave modes in multilayer synthetic antiferromagnets
Abstract In this study, the spin-wave spectrum in multilayer synthetic antiferromagnets is calculated. The analysis focuses on the effects of varying both the thicknesses and the number of ferromagnetic layers within these structures. The results reveal that a non-reciprocal spin-wave dispersion occurs in structures with an even number of layers, while a reciprocal dispersion of two counterpropagating waves is observed for systems with an odd number of layers. As the number of layers and their thickness increase, the study identifies the distinctive presence of bulk and surface modes, with the latter being strongly affected by dynamic dipolar interactions. In multilayers with an even number of layers, such surface modes exhibit nonreciprocal behavior, maintaining their surface character only in one propagation direction. Conversely, in odd-layer systems, the symmetric counterpropagating surface modes have similar properties. Additionally, the bulk modes for both even and odd numbers of layers converge towards similar dynamic behavior as the thickness and number of layers increase. As the thickness of the ferromagnetic layers increases, the surface modes in multilayers with an odd number of layers remain localized at either the top or bottom, depending on the sign of the wave vector. In contrast, for the even case, the surface modes appear in both the top and bottom ferromagnetic layers when the layers are thin or ultrathin. However, as the ferromagnetic layer thickness increases, these modes gradually become predominantly localized at either the top or bottom of the multilayer. Finally, the study explores the application of an external magnetic field, demonstrating that surface chiral modes are absent in the saturated state, resulting in a reciprocal spin-wave dispersion. This establishes a magnetic field-mediated control over non-reciprocal localized surface modes.
Phonon-mediated high-temperature superconductivity in clathrate superhydride ThCeH18 under pressure
Obstructive Sleep Apnea and Dentistry: A Detailed Review of Current Perspectives and Clinical Impact
Major effects on oral and systemic health resulting from the challenging sleep-associated respiratory disorder known as obstructive sleep apnea are related to: Research revealing similar anatomical and functional areas between dentistry and sleep medicine underscores the increasing relevance of the dental practitioner in OSA treatment. Combining insights from multiple patient backgrounds, this overview presents the current knowledge on the objectives of dentistry in the screening, diagnosis, and treatment of obstructive sleep apnea. Together with craniofacial risk factors and intraoral symptoms observed in dental examinations, the pathogenesis and typical clinical characteristics of OSA are discussed in the review. Oral appliance treatment is being closely examined in conjunction with continuous positive airway pressure therapy, with an emphasis on design modifications, clinical efficacy, and long-term outcomes. Utilizing maxillomandibular advancement and interceptive orthodontics, this research explores orthodontic and surgical treatment options. These methods demonstrate the extent to which structural dental alterations increase airway patency. The paper addresses current challenges to effective use, including constraints in the area of practice, patient adherence issues, and instructional gaps. Ultimately, it advances research on digital technologies, outcome monitoring, and interprofessional training projects. By orienting dental practitioners as cooperative participants in OSA treatment, this research highlights the importance of developing integrated clinical pathways and strengthening training frameworks to facilitate evidence-based practice in dental sleep medicine.
Ena/VASP-EVH1 inhibition prevents chemotaxis and metastasis by blocking the EVH1–WAVE2 interaction
Cancer therapy would benefit from suppressing cancer cell motility in the process of metastasis. Such directed cell migration relies on the propulsive force established by the filamentous actin network within lamellipodia. Proteins of the Ena/VASP family and the WAVE regulatory complex orchestrate lamellar protrusions and therefore provide promising targets for pharmacological interventions. Here, we report a cross-talk between Ena/VASP proteins and WAVE2 that is important for cancer cell extravasation. Mutating the EVH1 domain recognition motif in WAVE2 abrogates chemotaxis of triple-negative MDA-MB-231 breast cancer cells and reduces their extravasation in a zebrafish model. In pilot experiments, orthotopic implantation of these cells into mice led to a reduction in macrometastasis, resulting in prolonged survival. Similarly, intervention by an Ena/VASP-EVH1 inhibitor also reduced metastasis in vivo. Our results suggest that pharmacological interference with the Ena/VASP–WAVE2 interaction may thus reduce metastasis.
Gears in chemical reaction networks for optimizing energy transduction efficiency
Abstract Similarly to gear systems in vehicles, most chemical reaction networks (CRNs) involved in energy transduction have at their disposal multiple transduction pathways, each characterized by distinct efficiencies. We conceptualize these pathways as ‘chemical gears’ and demonstrate their role in refining the second law of thermodynamics. This allows us to determine the optimal efficiency of a CRN, and the gear enabling it, solely based on its topology and operating conditions, defined by the chemical potentials of its input and output species. By suitably tuning reaction kinetics, a CRN can be engineered to self-regulate its gear settings, maintaining optimal efficiency under varying external conditions. We demonstrate this principle in a biological context with a CRN where enzymes function as gear shifters, autonomously adapting the system to achieve near-optimal efficiency across changing environments. Additionally, we analyze the gear system of an artificial molecular motor, identifying numerous counterproductive gears and providing insights into its transduction capabilities and optimization.
Highly stable two-level current fluctuation in complex oxide heterostructures
Recyclable self-secreting autonomous healing dielectrics for millisecond water quality sensing
Automatic pain classification in older patients with hip fracture based on multimodal information fusion
Portland cement concrete with addition of CAC cement for precast elements: case study
Wide-angle all-optical filtering via defective distributed Bragg reflectors
Integrated two-photon and optoacoustic microscopy for functional neuroimaging
Improved IEC performance via emotional stimuli-aware captioning
Genetic prediction of immune cells, inflammatory proteins, and metabolite-mediated association between gut microbiota and COPD: a Mendelian randomization study
Association between visceral adiposity index and hyperuricemia and gout among US adults: a cross-sectional analysis of NHANES 2007–2018
Genome-wide association analysis and gene mining of flavonoids in Xanthoceras sorbifolia
Abstract Xanthoceras sorbifolia is a unique woody oilseed tree in China, and its leaves are rich in flavonoids, which are involved in plant growth, development and defense. However, the mining of flavonoid synthesis-related genes in Xanthoceras sorbifolia leaves is lacking. In this study, 226 leaves of Xanthoceras sorbifolia from eight provinces in the key distribution areas were measured for flavonoid content, and the differences in flavonoid content of Xanthoceras sorbifolia were analysed to screen out excellent seed sources and six excellent single plants with higher flavonoid content. Genome-wide association analysis (GWAS) was used to identify genes controlling the synthesis of flavonoids, and 62 significant Single nucleotide polymorphism (SNP) sites were identified, which were closely associated with 8 traits, and a total of 11 genes coding for proteins. We found that these genes mainly encode proteins such as WPP domain-associated protein (WAP) (Fragment), Protein pleiotropic regulatory locus 1 (PRL1) and Phosphomevalonate kinase, peroxisomal (PMK), etc. We found that these proteins may directly or indirectly affect the synthesis of flavonoids, which will provide a data base for molecular breeding and genetic improvement of Xanthoceras sorbifolia.
Navigating the C-Shape Canals: A Case Series on Endodontic Treatment with Bio-ceramic Sealers
Background: Atypical root canal morphologies, such as the C-shaped canal commonly found in mandibular second molars, present persistent diagnostic and therapeutic challenges. These configurations often go undetected due to their complex anatomy, increasing the risk of incomplete debridement, inadequate obturation, and ultimately, treatment failure. Accurate diagnosis, strategic planning, and clinical proficiency, along with the use of advanced diagnostic tools, are essential for achieving successful outcomes. This report presents clinical cases that highlight how effective treatment can be achieved while preserving tooth function through the integration of preoperative radiographs, magnification, and appropriate instrumentation and obturation systems. Case presentation: This case report presents three clinical scenarios in which preoperative assessment using radiographs and magnification loupes facilitated accurate identification of C-shaped canals and their anatomical variations. Management relied heavily on thorough chemical debridement rather than mechanical instrumentation. Bioceramic sealers were selected for obturation due to their excellent flow properties, ability to set in the presence of moisture, bioactivity, enhanced sealing ability, and inherent antimicrobial characteristics. Conclusion: The effective management of C-shaped canal systems is achievable through precise diagnosis, enhanced visualisation using magnification, and the use of modern endodontic technologies. Advanced rotary instrumentation, irrigant activation devices, and reliable obturation techniques such as bioceramic sealers and thermoplasticized filling—play a crucial role in achieving predictable and lasting treatment success.
Genome-scale knockout simulation and clustering analysis of drug-resistant breast cancer cells reveal drug sensitization targets
Anticancer chemotherapy is an essential part of cancer treatment, but the emergence of resistance remains a major hurdle. Metabolic reprogramming is a notable phenotype associated with the acquisition of drug resistance. Here, we develop a computational framework that predicts metabolic gene targets capable of reverting the metabolic state of drug-resistant cells to that of drug-sensitive parental cells, thereby sensitizing the resistant cells. The computational framework performs single-gene knockout simulation of genome-scale metabolic models that predicts genome-wide metabolic flux distribution in drug-resistant cells, and clusters the resulting knockout flux data using uniform manifold approximation and projection, followed by k -means clustering. From the clustering analysis, knockout genes that lead to the flux data near that of drug-sensitive cells are considered drug sensitization targets. This computational approach is demonstrated using doxorubicin- and paclitaxel-resistant MCF7 breast cancer cells. Drug sensitization targets are further refined based on proteome and metabolome data, which generate GOT1 for doxorubicin-resistant MCF7, GPI for paclitaxel-resistant MCF7, and SLC1A5 as a common target. These targets are experimentally validated where treating drug-resistant cancer cells with small-molecule inhibitors results in increased sensitivity of drug-resistant cells to doxorubicin or paclitaxel. The applicability of the developed framework is further demonstrated using drug-resistant triple-negative breast cancer cells. Taken together, the computational framework predicts drug sensitization targets in an intuitive and cost-efficient manner and can be applied to overcome drug-resistant cells associated with various cancers and other metabolic diseases.
Perceived community alignment increases information sharing
Abstract It has been proposed that information sharing, which is a ubiquitous and consequential behavior, plays a critical role in cultivating and maintaining a sense of shared reality. Across three studies, we test this theory by investigating whether or not people are especially likely to share information that they believe will be interpreted similarly by others in their social circles. Using neuroimaging data collected while people who live in the same residential community viewed brief film clips, we find that more similar neural responses across participants is associated with a greater likelihood to share content. We then test this relationship using two behavioral studies and find (1) that people are particularly likely to share content that they believe others in their social circles will interpret similarly and (2) that perceived similarity with others leads to increased sharing likelihood. In concert, our findings support the idea that people are driven to share information to create and reinforce shared understanding, which is critical to social connection.
Intraindividual epigenetic heterogeneity underlying phenotypic subtypes of advanced prostate cancer
Abstract Castration-resistant prostate cancer is a heterogeneous disease with variable phenotypes commonly observed in later stages of the disease. These include cases that retain expression of luminal markers and those that lose hormone dependence and acquire neuroendocrine features. While there are distinct transcriptomic and epigenomic differences between castration-resistant adenocarcinoma and neuroendocrine prostate cancer, the extent of overlap and degree of diversity across tumor metastases in individual patients has not been fully characterized. Here we perform combined DNA methylation, RNA-sequencing, H3K27ac, and H3K27me3 profiling across metastatic lesions from patients with CRPC/NEPC. Integrative analyses identify DNA methylation-driven gene links based on location (H3K27ac, H3K27me3, promoters, gene bodies) pointing to mechanisms underlying dysregulation of genes involved in tumor lineage (ASCL1, AR ) and therapeutic targets (PSMA, DLL3, STEAP1, B7-H3). Overall, these data highlight how integration of DNA methylation with RNA-sequencing and histone marks can inform intraindividual epigenetic heterogeneity and identify putative mechanisms driving transcriptional reprogramming in castration-resistant prostate cancer.