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Correction for Wang et al., The proofreading mechanism of the human leading-strand DNA polymerase ε holoenzyme
Designing, validation and evaluation of an mHealth app for prenatal health promotion based on the unified theory of acceptance and use of technology: A mixed methods study protocol
A multifunctional anti-O-Antigen human monoclonal antibody protects against <i>Shigella sonnei</i> infection in vivo
Shigellosis is a global public health challenge that mostly affects low- and middle-income countries and causes considerable morbidity and mortality among children under 5 y of age. Multi- and extensively drug-resistant Shigella sonnei strains associated with recent outbreaks in high-income countries exacerbate the problem and have prompted the World Health Organization to include Shigella spp. among the high-risk pathogens for which novel prophylactic and therapeutic tools are urgently needed. Among the most promising and cutting-edge solutions, monoclonal antibodies are gaining considerable attention in the infectious diseases field. Here, we report the discovery of human monoclonal antibodies against S. sonnei , a species whose prevalence is constantly increasing worldwide and is associated with frequent drug-resistant infections. We isolated antibodies generated in response to an experimental S. sonnei vaccine followed by a controlled human infection and screened them by using a panel of high-throughput assays. We identified a molecule which exhibited potent bactericidal activity in vitro, inhibition of invasion of epithelial cells and conferred full protection from S. sonnei infection in vivo. Overall, our study provides a candidate antibody that can rapidly progress to industrial development for application as a prophylactic, therapeutic, and diagnostic tool against shigellosis.
Diagnosis of unilateral vocal fold paralysis using auto-diagnostic deep learning model
SETDB1 ensures the continuity of embryonic to adult neural stem cells through metabolic alterations in the dentate gyrus
Embryonic neural progenitors give rise to adult neural stem cells (aNSCs), which share transcriptomic similarities with astrocytes while sustaining neurogenesis in the adult brain. How embryonic neural progenitors transit into aNSCs while preventing astrocyte fate to maintain the aNSC pool remains unclear. Here, we found that the Setdb1 -mediated metabolic state is essential for the transition from embryonic neural progenitors to aNSCs. Loss of the histone methyltransferase SETDB1 during dentate gyrus development leads to increased astrocyte production at the expense of aNSCs and ultimately constraining neurogenesis. Single-cell RNA sequencing reveals a specific metabolic alteration following Setdb1 loss, notably implicating the cytochrome c oxidase, subunit 6b2 ( Cox6b2 )—a component of the mitochondrial complex—as a key target of SETDB1. COX6B2 modulates oxidative phosphorylation (OXPHOS) to control aNSC fate over astrocyte differentiation. Elevated Cox6b2 levels promote astrocyte fate during dentate gyrus development. Thus, our findings reveal a mechanism underlying the continuity of neural progenitors to generate aNSC enabling the production of new neurons in the adult brain, highlighting the potential therapeutic strategies for transforming astrocytes into neurons via aNSCs.
Spatial distribution of exotic lumbricid earthworm Octolasion tyrtaeum in endangered Taxus contorta stands across Northwest Himalayan moist temperate forests
Implementation science aims to improve healthcare by validating effective interventions
Correction: Comparison of outcome between sole operation and operation after tube thoracostomy in late phase empyema
Hydrogen cyanide and hydrocarbons mix on Titan
This work reveals a striking exception to the well-established rule in chemistry that polar and nonpolar compounds do not spontaneously mix: insertion of methane, ethane, and other small hydrocarbons into the crystal lattice of hydrogen cyanide (HCN), a highly polar molecule. By mixing these components at cryogenic temperatures, we can observe distinct shifts in vibrational modes using Raman spectroscopy. Our computational predictions confirm that cocrystal structures of HCN and ethane, which match our experimental vibrational shifts closely, are thermodynamically and kinetically stable. Given that methane, ethane, and HCN are major components of the atmosphere and surface of Saturn’s moon Titan—where they play key roles in shaping chemistry, weather, and landscape—our findings may prove instrumental for explaining Titan’s chemical and geological evolution.
A new method of task aggregation and optimization allocation for multiple groups collaborative task networks
Abstract As task diversity and inter-task relationship complexity grow, optimal formation power allocation is key to improving task execution efficiency. This paper proposes a task optimization allocation method with multiple groups collaboration, constructing a task network based on analysis of task static characteristics and inter-task relationship attributes. Firstly, the Lasswell 5W model is introduced to explore task characteristics, extend inter-task relationship types, and propose a generalized quantitative description method of the task network based on binary groups. Secondly, considering task allocation requirements, space–time constraints, resource capacity and demand constraints, the multi-group collaborative task allocation problem is transformed into a multi-constraint multi-objective optimization problem, establishing a multi-group task allocation mathematical model. Subsequently, the large-scale task network is decomposed into sub-task networks. The clustering cost function for tasks is constructed by analyzing the similarity between formation force locations and resource requirements, and between sub-task locations and resource requirements. The initial allocation strategy for subsets of formations and tasks is established. Finally, an adaptive mechanism is introduced to optimize the genetic algorithm’s crossover and mutation strategies, proposing a new adaptive optimal allocation algorithm for multiple groups tasks. Experimental results show that the proposed method achieves efficient task assignment under complex and diverse task planning scenarios.
Threonine phosphorylation of STAT1 safeguards gut epithelial integrity and restricts interferon-mediated cytotoxicity
Barrier tissues such as the intestine are constantly challenged by environmental stressors and must adapt to maintain integrity and prevent excessive inflammation. Although traditionally viewed as a proinflammatory effector of interferon (IFN) signaling, STAT1 is shown here to play a protective role in intestinal epithelial cells (IEC) by promoting resilience to damage and restraining IFN-induced cytotoxicity. We identify phosphorylation of threonine 748 (Thr748) on STAT1 as an evolutionarily selected adaptation—highly conserved between humans and mice—that reciprocally regulates IEC integrity and IFN responsiveness. Mice expressing a phospho-deficient T748A Stat1 mutant exhibit severe colitis-induced tissue damage comparable to Stat1-deficient littermates, underscoring the critical role of Thr748 phosphorylation in mediating Stat1-driven protection during intestinal inflammation. Bone marrow transfer experiments further demonstrate that this protective effect is nonhematopoietic. Integrated genomic and transcriptomic analyses reveal that Thr748 phosphorylation modulates STAT1 DNA binding, directly activates the Itgb4 promoter, and enhances integrin β4 expression in IEC following inflammation. In intestinal organoid models, gain- and loss-of-function experiments demonstrate that Thr748 phosphorylation drives integrin β4 expression and epithelial resilience independently of IFN-induced Tyrosine 701 (Tyr701) phosphorylation. In contrast, IFN stimulation via Tyr701 induces Zbp1—a cytotoxic nucleic acid sensor—while repressing integrin β4, resulting in epithelial injury that is mitigated by Thr748 phosphorylation. Together, these findings reveal a modular architecture of STAT1 signaling in which Thr748 phosphorylation functions as a molecular rheostat that safeguards epithelial integrity while tempering IFN-driven cytotoxic responses.
Ribosomal protein L5 induces cellular senescence via p53-p21-pRb pathway to mediate relapse of acute myeloid leukemia
A quantitative figure of merit for battery SEI films and their use as functional solid-state electrolytes
As a key passivation film that governs battery operation, the solid electrolyte interphase (SEI) has long been credited for enabling high-performance batteries or blamed for their eventual death. However, qualitative descriptions of the SEI often found in the literature (e.g., “conductive,” “passivating”) highlight our incomplete understanding of this layer, where even the most basic properties foundational to SEI function remain difficult to measure. Here, we quantify SEI conductivities and SEI transference numbers using a separator-free Cu|SEI|Li architecture that treats the SEI as a functional solid-state electrolyte (SSE). We find that while any SEI property alone (e.g., electronic conductivity) is weakly correlated (R 2 < 0.67) with battery performance (e.g., Coulombic efficiency), a strong correlation (R 2 > 0.99) can be achieved by defining the “SEI cT number” as a product between the SEI transference number ( T ) and the ratio of SEI conductivities ( c ). Analogous to the thermoelectric figure of merit (i.e., zT ), SEI cT quantitatively benchmarks the holistic impact of SEI properties on battery performance and underscores the pitfalls of citing such properties in isolation. Perhaps most strikingly, we demonstrate that Li metal deposition and stripping at room temperature is possible in our separator-free Cu|SEI|Li cell, confirming that the SEI can function precisely as an SSE. Together, these results enrich our understanding of the SEI, not just as a passivation layer but as a functional structure that can potentially have important implications for solid-state batteries.
Nonlinear behavior of dispersive solitary wave solutions for the propagation of shock waves in the nonlinear coupled system of equations
Human land use promotes range expansion of soil protists from temperate to subtropical regions in China
Land-use changes are reshaping the distribution of aboveground species worldwide. However, the impact of land-use changes on the distribution of soil organisms remains poorly understood. In particular, we lack a mechanistic understanding of the environmental factors reshaping the distribution of soil microbiota in response to global biological homogenization. Here, we used metabarcoding to investigate the biogeography of protists and their relationships with prey and hosts in three human-dominated ecosystem types, i.e., farmlands, residential areas, and parks, along with natural forests, in subtropical and temperate climatic regions across China. We found that human land-use systems extended the distribution range of habitat-generalist protists compared to forests. This human-facilitated spread of protists was highly directional and mainly driven by temperate to subtropical range expansion of soil taxa. Put simply, increases in soil pH associated with human land uses mitigate the natural acidity barrier typically found in subtropical ecosystems, facilitating the temperate to subtropical range expansion of protist species. However, in temperate regions, the northward expansion of subtropical species is likely restricted by a more arid climate with even higher soil pH. The cross-region spread of soil protists was more pronounced in phagotrophs than phototrophs and parasites, reflecting codispersal of phagotroph protists and microbial prey (especially bacteria) related to tight predator–prey specialization and/or similar responses to environmental changes. Our findings indicate that land-use changes create hotspots of potential microbial invasions, particularly in subtropical and tropical regions, highlighting that understudied regions are likely to be strongly affected by biological homogenization related to introduction of exotic species.
Evaluation for the selection of agricultural spraying drones using p, q-Quasirung orthopair fuzzy logic and multi-criteria methods
The Gln-rich protein twip1 promotes high-density {110} twins formation in the shell of the limpet <i>Cellana rota</i>
Aragonite, a polymorph of calcium carbonate (CaCO 3 ), exhibits enhanced mechanical properties due to crystal defects such as twins, which are particularly prevalent in biogenic aragonite and can inhibit crack propagation. Despite the importance, the molecular mechanisms responsible for the formation of aragonite {110} twins in marine organisms have remained poorly understood. Identifying a key inducer for {110} twins could help us understand how crystal defects are controlled in biomineralization. In this study, we explore the role of a protein, twip1, in inducing a high density of {110} twins within the aragonite layers of the limpet Cellana rota shell. Through a combination of layer-specific protein profiling and in vitro aragonite binding assays, twip1 is identified as a potential protein preferentially binding to the aragonite (110) plane. Gene expression analysis via quantitative PCR (qPCR) confirmed that twip1 is specifically expressed in the mantle tissue. To further investigate its function, recombinant twip1 (rtwip1) is produced using an Escherichia coli expression system. X-ray diffraction (XRD) and electron microscopy observations reveal that rtwip1 significantly increases {110} twin density during in vitro aragonite synthesis. Moreover, in vivo knockdown shows that reducing twip1 expression results in abnormal shell growth and {110} twin boundary reduction. Enhancing the formation of {110} twins in aragonite can improve its toughness and elasticity. This research highlights the crucial role of specific proteins in regulating crystal defect formation, offering a promising direction for future biomineralization studies and advanced material design.
Prediction of MGMT methylation status in glioblastoma patients based on radiomics feature extracted from intratumoral and peritumoral MRI imaging
Polyploidy promotes transformation of epithelial cells into nonprofessional phagocytes
Removal of dead and damaged cells is critical for organismal health. Under stress conditions such as nutritional deprivation, infection, or temperature shift, the clearance of nonessential cells becomes a universal strategy to conserve energy and maintain tissue homeostasis. Typically, this task is performed by professional phagocytes such as macrophages. However, nonprofessional phagocytes (NPPs) can also adopt a phagocytic fate under specific circumstances. Similar to professional phagocytes, NPPs undergo transitions from immature to mature states and activation, but the precise cellular and molecular mechanisms governing their maturation, induction, and phagocytic execution remain largely unknown. A notable example of stress-induced phagocytosis is the removal of germline cells by follicle cell–derived NPPs during oogenesis in Drosophila . In this study, we report that the transformation of follicle cells (FCs) into NPPs is dependent on Notch signaling activation during mid-oogenesis. Moreover, Notch overactivation is sufficient to trigger germline cell death and clearance (GDAC). We further show that polyploidy, driven by Notch signaling-induced endoreplication, is essential for the transformation of FCs into NPPs. Polyploidy facilitates the activation of JNK signaling, which is crucial for the phagocytic behavior of these cells. Additionally, we show that polyploidy in epidermal cells, another type of NPPs, is important for their engulfment of dendrites during induced degeneration. Together, these findings suggest that polyploidy is a critical factor in the transformation of epithelial cells into NPPs, enabling their phagocytic functions, which are essential for maintaining cellular and organismal homeostasis during stress conditions.