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On demand laser-induced frequency tuning of coherent magnons in a nanometer-thick magnet at room temperature
Abstract The collective vibrational and magnetic response of a solid to external stimuli is encoded in the dispersion relations of phonons and magnons, respectively. Recently, the coherent drive and nonlinear manipulation of collective lattice and magnetic excitations via laser pulses has been explored, as a route to control the non-equilibrium properties of quantum materials. Device concepts that leverage coupled multiphysical dynamics must exhibit laser-induced frequency tunability controllable through external parameters. Although previous works have shown that optically driven excitations in the midinfrared can manipulate magnon frequencies, inducing deterministic red- or blue-shifts of the magnon frequency in the same material is still elusive. Here we demonstrate this concept in a nanometer-thick magnet at room temperature. Visible light pulses in combination with an external magnetic field (<200 mT) can either raise or lower the magnon frequency by up to 40% of its original value. This effect results from the interplay of the optical excitation, magnetic anisotropy and external magnetic field. Our results show how an efficient manipulation of magnons can be achieved by light and provide perspectives for the realization of logic devices optically reconfigurable on the nanosecond timescale.
Biomass derived nitrogen and sulfur codoped carbon dots as efficient corrosion inhibitors for carbon steel in acidic environment
Interplanetary magnetic correlation and low-frequency spectrum over many solar rotations
Fluctuations and structure across a wide range of spatial and temporal scales are frequently studied in the solar wind. The properties of the low-frequency fluctuations are of relevance to turbulent energy injection into the plasma and the transport of high-energy cosmic rays. Correlation analysis of decade-long intervals of interplanetary data permits study of fluctuations at time scales much longer than suitably defined correlation times, and therefore at frequencies well below those associated with the Kolmogorov inertial range of in situ turbulence. At the frequencies of interest, we study the familiar occurrence of the 1 / f spectral signature. We also study point spectral features due to solar rotation and their relation with the 1 / f signal. We report properties at timescales ranging from minutes up to years, using data selected by wind speed, phase of solar cycle, and cartesian components of the magnetic field. A surprising finding is that the power in solar rotation harmonics is consistent with an extension of the 1 / f spectrum, down to frequencies as low as around 5 × 10 − 7 Hz . The presence of a broadband 1 / f spectrum across different wind types supports the interpretation that 1 / f signals may be related to or even originate from the solar dynamo.
Integrated millimeter-wave cavity electro-optic transduction
Abstract Emerging communications and computing technologies will rely ever-more on expanding the useful radio frequency spectrum into the millimeter-wave and terahertz frequency range. Both classical and quantum applications would benefit from advancing integration and incorporation of millimeter-wave and electro-optic technologies into common devices, such as modulators. Here we demonstrate an integrated triply-resonant, superconducting electro-optic transducer. Our design incorporates an on-chip 107 GHz niobium titanium nitride superconducting resonator, modulating a thin-film lithium niobate optical racetrack resonator operating at telecom wavelengths. We observe a maximum photon transduction efficiency of η OE ≈ 0.82 × 10 −6 and an average single-photon electro-optic interaction rate of g 0 /2 π ≈ 0.7 kHz. We also present a study and analysis of the challenges associated with the design of integrated millimeter-wave resonators and propose possible solutions to these challenges. Our work paves the way for further advancements in resonant electro-optic technologies operating at millimeter-wave frequencies.
Applicability and validation of Franco, Willems and Willems II dental age estimation models in a population of Ceará, Brazil
Abstract Dental age assessment plays a crucial role in clinical and forensic contexts. For safer practices, however, the existing methods need to be tested. This study aimed to evaluate for the first time the applicability of Franco’s, Willems’, and Willems’ II dental age assessment models in a Northeastern Brazilian sample. The sample consisted of 500 panoramic radiographs (250 males, 250 females) of Brazilian individuals between 6 and 15.9 years from the State of Ceará. Chronological (CA) and estimated (EA) ages compared using mean error (ME), mean absolute error (MAE), and root mean square error (RMSE). Statistical comparisons were performed through generalized estimating equations (GEE). The mean CA of the sample was 11.0 years. The mean EA was 11.3 years for Franco’s model, 11.6 for Willems’, and 11.5 for Willems II. Franco’s model showed the smallest bias, with ME values being 0.25 and 0.21 years lower than Willems’ and Willems II, respectively ( p < 0.001). Differences between CA and EA were minimal across sexes and not clinically relevant. Age-group analysis revealed similar performance up to 11.9 years. Overall, Franco’s model demonstrated better error metrics, but all the models showed comparable accuracy and consistency for dental age estimation in children and adolescents from Ceará, confirming their validity and suitability for both clinical and forensic applications in this population.
Metabolomic profiling reveals the potential of fatty acids as regulators of exhausted CD8 T cells during chronic viral infection
Chronic infections induce CD8 T cell exhaustion, marked by impaired effector function. While intrinsic drivers are well studied, the role of the surrounding metabolic environment in shaping exhausted CD8 T cells (Tex) is less understood. Using untargeted metabolomics and the murine lymphocytic choriomeningitis virus infection model, we investigated systemic metabolite changes following acute vs. chronic viral infections. We identified distinct short-term and persistent metabolite shifts, with the most significant differences occurring transiently during the early phase of the sustained infection. This included nutrient changes that were partially associated with CD8 T cell–induced anorexia and lipolysis. One remarkable observation was the elevation of medium- and long-chain fatty acids (FA) and acylcarnitines during the first week after chronic infection. Consistently, virus-specific CD8 T cells from chronic infection exhibited increased lipid accumulation and uptake compared to their counterparts from acute infection, particularly the stem-like Tex (Tex STEM ), which generates Tex INT that directly limit viral replication. Notably, only Tex STEM increased oxidative metabolism upon ex vivo FA exposure, while short-term administration of FA during late chronic infection exclusively increased Tex STEM and their mitochondrial potential. The last-mentioned treatment also led to reduced Tex INT and enhanced PD-1 across all Tex subsets, which coincided with compromised viral control. Our study offers a valuable resource for investigating the regulatory role of specific metabolites during acute and chronic viral infections and highlights the potential of FA to fine-tune Tex subsets during protracted infections.
Ferroelectric switching of interfacial dipoles in α-RuCl3/graphene heterostructure
NFBC: an efficient FPGA based NFSR-oriented lightweight block cipher suitable for embedded system
Social networks and international migration in Honduran villages
Social relationships are central to shaping international migration patterns, yet the link between widescale network structure and mobility decisions remains poorly understood. Here, we investigate two key mechanisms by which social networks influence migration behavior: transmission of information and resources, and comparison of social status. These mechanisms suggest distinct sets of alters that an ego may emulate with respect to their migration behaviors, resulting in divergent mobility trajectories within and across communities. Leveraging longitudinal data from 73 Honduran villages ( N = 15 , 480 individuals) over six years, we use a Linear Network Autocorrelation Modeling framework to disentangle the effects of kinship, friendship, and economic ties on international migration decisions. Our findings reveal that incorporating social network factors as predictors significantly improves model fit. While indicators for resource-sharing processes substantially contribute to model performance, the inclusion of structural comparison mechanisms does not provide additional explanatory power. These results underscore the critical role of information and resource transmission within social networks in facilitating migration behaviors.
Intrathecal CRISPR-edited allogeneic IL-13Rα2 CAR T Cells for recurrent high-grade Glioma: preclinical characterization and phase I trial
Tracking the protein conformational motions driving HIV-1 membrane fusion
Differential roles of type I topoisomerases in regulating HPV pathogenesis
High-risk human papillomaviruses (HPVs) activate the Ataxia Telangiectasia Mutated and Ataxia Telangiectasia and Rad3-Related pathways by inducing DNA breaks through the action of viral oncoproteins E6 and E7, which target factors such as topoisomerases. Type I topoisomerases cleave and religate a single strand of DNA, and little is known about how they regulate HPV pathogenesis. The levels of type I topoisomerases, TOP1α, TOP3α, and TOP3β, were all elevated in cells maintaining high-risk HPV genomes, as well as in squamous cell carcinomas. Only TOP1α and TOP3β, but not TOP3α, bound to HPV genomes and were critical for regulating viral gene transcription and replication with little effect on cell growth. Furthermore, the knockdown of TOP1α or TOP3β reduced levels of DNA breaks and differentially altered the expression of genes in key pathways. TOP1α knockdown reduced the expression of IL6 and activation of the procytokine signaling pathway. In contrast, TOP3β targeted EGR3, which regulates growth and differentiation. Finally, TOP1α and TOP3β differentially regulate the formation of R-loops, which are critical for viral replication. These findings demonstrate the differential roles of type I topoisomerases in HPV pathogenesis.
Rapid enantioselective fluorescence recognition and chiral separation of free amino acids
An improved Wexler algorithm for electrical impedance tomography using finite element method and gradient based overrelaxation
Design of solubly expressed miniaturized SMART MHCs
The precise recognition of specific peptide–major histocompatibility complex (pMHC) complexes by T cell receptors (TCRs) plays a key role in infectious disease, cancer, and autoimmunity. A critical step in many immunobiological studies is the identification of T cells expressing TCRs specific to a given pMHC antigen. However, the intrinsic instability of empty class-I MHCs limits their soluble expression in Escherichia coli and makes it very difficult to characterize even a small fraction of possible pMHC/TCR interactions. To overcome this limitation, we designed small proteins which buttress the peptide binding groove of class I MHCs, replacing β2-microglobulin (β2m) and the heavy chain α3 domain, and enable soluble and partially soluble expression in E. coli of H-2D b and A*02:01, respectively. We demonstrate that these soluble, monomeric, antigen-receptive, truncated (SMART) MHCs retain both peptide- and TCR-binding specificity and that peptide-bound structures of both allomorphs are similar to their full-length, native counterparts. With extension to the majority of HLA alleles, SMART MHCs should be broadly useful for probing the T cell repertoire in approaches ranging from yeast display to T cell staining.
Deep learning guided design of protease substrates
Abstract Proteases, enzymes that play critical roles in health and disease, exert their function through the cleavage of peptide bonds. Identifying substrates that are efficiently and selectively cleaved by target proteases is essential for studying protease activity and for harnessing it in protease-activated diagnostics and therapeutics. However, the vast design space of possible substrates (c.a. 20 10 amino acid combinations for a 10-mer peptide) and the limited accessibility of high-throughput activity profiling tools hinder the speed and success of substrate design. We present CleaveNet, an end-to-end AI pipeline for the design of protease substrates. Applied to matrix metalloproteinases, CleaveNet enhances the scale, tunability, and efficiency of substrate design. CleaveNet generates peptide substrates that exhibit sound biophysical properties and capture not only well-established but also previously-uncharacterized cleavage motifs. To control substrate design, CleaveNet incorporates a conditioning tag that steers peptide generation towards desired cleavage profiles, enabling targeted design of efficient and selective substrates. CleaveNet-generated substrates were validated experimentally through a large-scale in vitro screen, even in the challenging case of designing highly selective substrates for MMP13. We envision that CleaveNet will accelerate our ability to study and capitalize on protease activity, paving the way for in silico design tools across enzyme classes.
Nonlinear compartmental modeling of COVID-19 with dual dose vaccination using Mason graphs and variational iteration method
Abstract In this research work, a novel non-linear mathematical model has been proposed considering susceptible, quarantined, infected, recovered, and removed compartments before and after the 1st dose and 2nd dose of vaccination. For this dynamics model, the novel coronavirus COVID-19, a contagious disease, is taken as a case study in which its transmission, impact of vaccination, and mitigation have been discussed. This model may be helpful in numerous fields of epidemiology and dynamical systems; moreover, Mason Graph has been used to describe the mathematical model. The stability analysis and disease-free equilibrium points have been deliberated for the model. In this work, the semi-analytical technique Variational Iteration Method has been employed, which will assist researchers in the future by showing that if the rate of immunized personnel rises, then the infection rate decreases. It has been observed that the non-vaccinated personnel decrease with the passage of time due to the awareness campaign programs of the governments. Furthermore, it was observed that the removed rate also decreases with the passage of time as the immunized personnel rises. Mathematical software MAPLE has been used to calculate the analytical solutions of the aforementioned mathematical model.
Peripheral nerve injury reduces macrophage efferocytosis to facilitate neuropathic pain
For reasons not fully understood, proresolving immune processes sometimes fail to engage after peripheral nerve injury (PNI), leading to enhanced neuropathic pain and inflammation. Here, we implicate reduced efferocytosis due to proteolytic cleavage of surface MER tyrosine kinase (MERTK) from macrophages at the site of PNI. After PNI, the proportion of macrophages expressing MERTK progressively decreased, while soluble (cleaved) MER increased. Using male and female knock-in mice encoding cleavage-resistant Mertk , we demonstrated that cleavage of MERTK from macrophages at the PNI site led to exaggerated pain-related behaviors. PNI-induced hyperactivity of TRPV1 + sensory neurons and damage to myelin and myelinated axons was exacerbated by MERTK cleavage. Cleavage of MERTK led macrophages to adopt a proinflammatory phenotype. It also reduced their efferocytotic capacity, increasing accumulation of TUNEL + (apoptotic) and RIPK3 + (necroptotic) cells at the injury site. The pronociceptive damage-associated molecular patterns (DAMPs) interleukin-33 and heat shock protein-90 were increased, consistent with passive release from uncleared cell corpses. These corpses can also release de novo antigens along with DAMPs to trigger autoimmunity, recently implicated in neuropathic pain through a mechanism involving secretion of immunoglobulin G (IgG). Indeed, MERTK cleavage led to accumulation of IgG at the injury site and dorsal root ganglia. All outcomes were further worsened when Mertk was conditionally deleted from macrophages. Our findings identify cleavage of MERTK from macrophages at the injury site as a pivotal regulator of pronociceptive and tissue-damaging neuroimmune signaling after PNI.