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An accurate and efficient framework for modeling multimetal competitive adsorption on clay minerals
Multiple toxic metal elements usually coexist and thus their competitive adsorption always occurs in natural and engineered clay-rich systems. Currently, however, the competitive adsorption mechanisms of multicomponent metal systems on clay mineral surfaces are still unclear, hindering the accurate prediction of toxic metal distribution in soil-water environments. In this study, we uncovered the microscopic mechanism of competitive adsorption of multimetals on heterogeneous clay mineral surfaces using first principles calculation, which indicates that metal ion size largely dominates their complexation on clay mineral surfaces, and competitive adsorption of metals plays a key modulatory role in the adsorption process on clay minerals. By integrating theoretically and experimentally derived multiscale information, a state-of-the-art surface complexation model (SCM) framework has been developed for modeling competitive adsorption. Extensive tests showed that the SCM framework accurately and efficiently reproduces the toxic metal distribution, which enables the quantitative prediction and understanding in realistic environmental conditions. Our results have wide applications in future fundamental studies and the design of environmental materials for toxic metal removal from aquatic systems.
Microplastics and Nanoplastics: A New Perspective in Cardiovascular Prevention
Academic journals’ AI policies fail to curb the surge in AI-assisted academic writing
The rapid integration of generative AI into academic writing has prompted widespread policy responses from journals and publishers. However, the effectiveness of these policies remains unclear. Here, we analyze 5,114 journals and over 5.2 million papers to evaluate the real-world impact of AI usage guidelines. We show that despite 70% of journals adopting AI policies (primarily requiring disclosure), researchers’ use of AI writing tools has increased dramatically across disciplines, with no significant difference between journals with or without policies. Non-English-speaking countries, physical sciences, and high-OA journals exhibit the highest growth rates. Crucially, full-text analysis on 164 k scientific publications reveals a striking transparency gap: Of the 75 k papers published since 2023, only 76 (~0.1%) explicitly disclosed AI use. Our findings suggest that current policies have largely failed to promote transparency or restrain AI adoption. We urge a reevaluation of ethical frameworks to foster responsible AI integration in science.
Response by Schumacher and Cousino to Letter Regarding Article, “The Impact of Fontan Circulatory Failure on Heart Transplant Survival: A 20-Center Retrospective Cohort Study”
mtDNA leakage promotes neuron–glia crosstalk to induce epilepsy by cGAS–STING-driven neuroinflammation and serine metabolic reprogramming
Epilepsy is increasingly recognized as a disorder involving metabolic dysregulation beyond neural hyperexcitability, yet the underlying metabolic mechanisms remain poorly defined. Here, we identify a mitochondrion–immunity–metabolism axis that drives spontaneous chronic epilepsy. Brain-specific deletion of Mic19 impairs mitochondrial cristae structure and mitochondrial integrity in neurons, leading to activation of the Z-mitochondrial DNA (mtDNA)–ZBP1–RIPK3–mixed lineage kinase domain-like protein (MLKL) axis and p-MLKL-mediated pore formation on the mitochondrial membrane. This process results in cytosolic and extracellular leakage of mtDNA, which is subsequently taken up by microglia and triggers cyclic GMP-AMP synthase (cGAS)–STING-dependent inflammatory signaling. The resulting neuroinflammation promotes sustained activation of astrocytes. Critically, reactive astrocytes undergo profound metabolic reprogramming, marked by upregulated glycolysis and enhanced L-serine biosynthesis. Astrocyte-derived L-serine is subsequently transferred to neurons and converted into D-serine, a key NMDA receptor coagonist that enhances neuronal excitability. This metabolic shift in astrocytes exacerbates excitotoxicity and sustains epileptic activity. Importantly, pharmacologic inhibition of STING with H-151 treatment markedly suppresses seizures, reinforcing the therapeutic potential of targeting immunometabolic crosstalk in epilepsy. Our findings reveal that mtDNA-mediated cGAS–STING activation and D-serine act as important drivers of epilepsy initiation, offering mechanistic insights into neuron–microglia–astrocyte crosstalk and highlighting immunometabolic modulation as a promising therapeutic strategy for epilepsy.
Correction to: Abstract Sun602: Lower Survival After Out-of- Hospital Cardiac Arrest in Older Females: The Joint Effect of Age and Sex
Transmission lowers US generation costs, but generator incentives are not aligned
The US electricity grid is rapidly evolving with the entry of low-cost renewable electricity. As a result, new supply is not spatially matched to demand, and the transmission network has become more strained. Better market integration could thus lower US generation costs. We document that eliminating interregional constraints would have reduced electricity generation costs across the lower US 48 states by $5.8 to 7.1 billion in 2022 and $3.4 to 5.0 billion in 2023. But market integration creates winners and losers among generation companies, and we show that producers in some regions have incentives to delay or block grid integration despite the overall system benefits.
Myocardial Recovery With Mechanical Circulatory Support Is Linked to Alternative Splicing and Subcellular Localization of CAMK2D
BACKGROUND: Cardiac reverse remodeling occurs in a small subset of patients with heart failure treated with guideline-directed therapies. This phenomenon, which is defined by reduced ventricular dilatation and improved systolic function, is most common in patients receiving left ventricular assist device (LVAD) therapy. Identifying therapeutic targets for initiating reverse remodeling is an area of great clinical interest, because these patients experience improved outcomes and quality of life. Targets may be discovered among the unique molecular changes associated with LVAD-induced partial myocardial functional recovery; however, the mechanisms underlying this favorable response are incompletely understood. METHODS: To identify molecular signatures of recovery, we studied paired pre-LVAD and post-LVAD myocardial samples from patients with heart failure who received LVAD as a bridge to transplant (10 responders and 9 nonresponders) and controls without heart failure. We performed bulk RNA sequencing, tandem mass tag quantitative proteomics, and tandem mass tag quantitative phosphoproteomics with follow-up mechanistic and functional investigations in primary rat cardiomyocytes and human engineered heart tissues. RESULTS: Alternative RNA splicing was the leading pathway associated with a favorable response to LVAD. Responders had increased RNA splicing factor expression and unique gene splice variant expression compared with nonresponders. Alternative splicing of CAMK2D (calcium/calmodulin-dependent protein kinase 2δ) was a particularly strong predictor of recovery; increased inclusion of exon 14, which encodes the nuclear splice variant CAMK2D-B, was inversely correlated with functional recovery. Nonresponders also displayed hyperphosphorylation near the nuclear localization signal in CAMK2D-B. Investigations in primary cardiomyocytes and subcellular organelle fractions from the human hearts revealed that nuclear localization signal phosphorylation prevented adrenergic stress-dependent nuclear targeting of CAMK2D-B. Expression of a cytoplasm-restricted CAMK2D-B uniquely remodeled the phosphoproteome of primary rat cardiomyocytes compared with a nuclear-competent version and blunted calcium transients in engineered heart tissues. CONCLUSIONS: This is the first study to integrate transcriptome, alternative transcriptome, proteome, and phosphoproteome analyses of heart samples from LVAD-supported patients to investigate myocardial recovery. We identified that increased expression and phosphorylation of the nuclear CAMK2D splice variant predicted poor outcomes. This phosphorylation restricted CAMK2D-B to the cytosol, leading to impaired cardiomyocyte calcium handling. These findings suggest that LVAD nonresponder patients may benefit from therapies that modulate subcellular localization of CAMK2D or inhibit its activity.
Bilingual language processing relies on shared semantic representations that are modulated by each language
Billions of people throughout the world are bilingual, and they can extract meaning from multiple languages. While some evidence suggests that there is a shared system in the human brain for processing semantic information from native and non-native languages, other evidence suggests that semantic processing is language specific. We conducted a study to determine how semantic information for different languages is represented in the brains of bilinguals. Functional magnetic resonance imaging (fMRI) was used to record brain responses while participants read several hours of natural narratives in their native (Chinese) and non-native (English) languages. These data were then used to compare semantic representations between the two languages. We find that semantic representations are largely shared between languages, while there are fine-grained differences in the representation of some semantic categories across languages. These results reconcile current competing theories of bilingual language processing.
2026 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association
BACKGROUND: The American Heart Association annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and cardiovascular-kidney-metabolic syndrome) that contribute to cardiovascular health. The 2026 Heart Disease and Stroke Statistics Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs). METHODS: The American Heart Association, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistics Update with review of published literature through the year before writing. The 2026 Statistics Update is the product of a full year’s worth of effort in 2025 by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year’s edition includes a new chapter on cardiovascular-kidney-metabolic syndrome, as well as an expanded chapter on tobacco and nicotine use and exposure. RESULTS: Each of the chapters in the Statistics Update focuses on a different topic related to heart disease and stroke statistics. CONCLUSIONS: The Statistics Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.
Understanding human metacontrol and its pathologies using deep neural networks
Error monitoring is crucial for inferring how controllable an environment is, and thus for estimating the value of control processes (metacontrol). In this study, we use computational simulations with deep neural networks to investigate its behavioral and neural correlates. We trained both humans and deep reinforcement learning (RL) agents to perform a reward-guided learning task that required adaptation to changes in action controllability. Deep RL agents could only solve the task when designed to explicitly predict action prediction errors that fire in the medial prefrontal cortex. When trained this way, they displayed signatures of metacontrol that closely resembled those observed in humans. Moreover, when deep RL agents were trained to over- or underestimate controllability, they developed behavioral pathologies partially matching those of humans who reported depressive, anxious, or compulsive traits on transdiagnostic questionnaires. These findings open up avenues for studying metacontrol using deep neural networks.
Response by de Veld et al to Letter Regarding Article, “Device-Related Complications in Transvenous Versus Subcutaneous Defibrillator Therapy During Long-Term Follow-Up: The PRAETORIAN-XL Trial”
Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis
Never in mitosis A (NIMA)-related kinase 2 (NEK2) is a serine/threonine kinase that plays a crucial role in cell cycle regulation and is frequently induced across multiple cancer types, where its elevated levels are associated with poor prognosis. Epstein–Barr virus (EBV) and Kaposi’s sarcoma–associated herpesvirus (KSHV), both known to drive various malignancies, were observed to induce NEK2 expression during both primary infection and latent phases of infection. Increased NEK2 expression contributes to chromosomal instability by promoting nondisjunction, leading to a rise in aneuploid cell populations and fostering uncontrolled cell proliferation. Mechanistically, EBV latent protein EBNA2 and KSHV latent antigen LANA were identified as principal regulators of NEK2 upregulation, acting through modulation of RBP-Jκ activities at the NEK2 promoter region. Additionally, we demonstrated that targeting NEK2 impaired EBV- and KSHV-mediated tumor progression, highlighting its potential as a critical driver of virus-induced oncogenesis and a promising therapeutic target.
Response by Shi and Chen to Letter Regarding Article, “Partnership Model of Regionalized Care for Congenital Heart Disease in Resource-Limited Settings: Results From the ASSIST Project”
School shootings and the strategic contributions of gun policy PACs in US House elections
The American public consistently supports stricter gun laws. We show that the gun lobby is most concerned that this support will translate into federal legislative action when fatal school shootings occur. Leveraging a dataset of political action committee (PAC) contributions and school shootings, we implement a staggered difference-in-differences design to estimate the causal effect of fatal school shootings on contributions to House candidates. We find progun Political Action Committees increase contributions by 31% to candidates in districts with fatal school shootings, and 20% for gun safety PACs. Neither show any significant response to nonfatal school shootings or mass shootings. The temporal pattern also reveals strategic behavior: For both progun and gun safety PACs, contribution spikes emerge in the wake of fatal school shootings, with effects dramatically amplified as Election Day approaches; when a shooting occurs within two months of Election Day, contributions from progun PACs increase by 2,820% while gun safety PAC contributions increase by 917%. These effects are concentrated in competitive districts ( ≤ 5% margins) where the two-sided surge in contributions offsets any measurable electoral impact. These results provide robust evidence that PACs strategically deploy contributions after school shootings, with the magnitude and timing suggesting a deliberate mobilization to advance its agenda. Our findings underscore a gap in democratic accountability: While public opinion should drive policy change, campaign contributions are wielded to blunt electoral responsiveness, providing insight into the inability of Congress to adopt broadly supported gun safety measures.
Aerophilic debubbling
Gas bubbles frequently accumulate at liquid interfaces, compromising throughput, selectivity, and stability across scales from microfluidics to natural ecosystems. Here, we experimentally show that highly permeable aerophilic membranes placed on a liquid–air interface annihilate bubbles within milliseconds. This ultrafast regime appears only above a critical permeability threshold, where the flow departs from classical Darcy-driven dynamics in micropores. We quantitatively characterize this aerophilicity-mediated debubbling process by examining local interactions at the scale of single bubbles approaching the membrane and identify three asymptotic evacuation regimes, the physics of which we capture through simple scaling laws.
The Nemp1–Nesprin complex mediates cellular responses to matrix mechanics
Nuclear Envelope Membrane Protein 1 (NEMP1) is crucial for metazoan fertility; loss of Nemp1 causes death of primordial oocytes that reside in the mechanically challenging ovarian cortex. Here, we show that softening the ovary rescues oocyte loss and restores fertility in N emp1 knockout (KO) mice. In cell culture, NEMP1 depletion on stiff substrates leads to death, while cells remain viable on soft substrates. We further show that NEMP1 regulates YAP nuclear translocation, essential for mechanotransduction. Mechanistically, Nemp1-depleted cells on stiff substrates or subjected to stretching exhibit reduced nuclear YAP localization, and expressing nuclear YAP5SA restores cell viability. Loss of NEMP1 disrupts actin organization. Inducing actin polymerization partially rescues nuclear YAP, indicating a role for F-actin in NEMP1 mediated mechanotransduction. NEMP1 forms a complex with NESPRIN’s Klarsicht, Anchorage (ANC)-1, Syne Homology (KASH) domain, strengthening the actin cytoskeleton to withstand mechanical forces, independent of SUN proteins. Thus, the Nemp1–Nesprin complex supports a mechanosensitive pathway parallel to the LINC complex, enabling cellular response to mechanical stress in vitro and in vivo.
Multispecies analysis of social effects on same-sex sexual behavior challenges mistaken identity hypotheses in insects
Same-sex sexual behavior (SSB) in insects has historically been considered a byproduct of sex recognition failure, or “mistaken identity,” and consideration of other hypotheses lags behind that of vertebrates where it is often thought to adaptively mitigate aggressive interactions. Comparative analyses to help disentangle the functions of insect SSB are lacking. To address this, we quantified male–male interactions in controlled trials across eight North American field cricket species ( Gryllus spp.). While limited taxonomic sampling precluded a formal phylogenetic comparative analysis, we were able to assess variation across species with structural equation models. Using this technique, we distinguished focal from partner influences and evaluated support for mistaken identity vs. other models of SSB. SSB expression varied extensively across species. It was always associated with reduced aggression, but the strength of this association and the balance of focal vs. partner effects varied. Temporal analysis of behavioral interactions showed that males exhibited SSB while able to discern the sex of their partner. These findings, along with observations of a previously undescribed sexual behavior not seen in different-sex interactions, imply a history of adaptive evolution inconsistent with mistaken identity SSB.
Uniqueness and predictability in evolution and the history of mollusks
Evolution is a historical process whose trajectories are determined in part by the introduction of new phenotypes. Although most phenotypes have evolved repeatedly within and among clades of organisms, others are unique and apparently originated only once, and even the earliest occurrences of repeated traits were unique for their time. To investigate the timing and circumstances of these unique events, we compiled adult skeletal phenotypes with single origins and first occurrences of repeated traits as recorded in the fossil record in the phylum Mollusca. Of the 24 unique and 72 repeated traits we considered, 46 (48%) originated during the first 96 m.y. of molluscan history (frequency 1 per 2.1 m.y.) and only 50 in the 444 m.y. since then (frequency 1 per 8.9 m.y.), with secondary peaks of frequency in the Triassic and Cenozoic. We interpret this finding to mean that molluscan evolutionary history has become substantially more predictable over time despite increasing diversity. Expansions of the phylum from its ancestral marine epifaunal benthic environment to other habitats including fresh water and dry land were generally not associated with unique or earliest occurrences of repeated phenotypes. Most of the innovations enhanced individual defense or activity and were therefore honed by interactions within and among species, although it remains possible that they originated in temporarily permissive conditions in which genetic and other constraints were relaxed.