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Sun, X.

Publications and source records attributed to Sun, X..

At least 55 records · Page 3Linked to original sources

Investigation of In Vivo Silk Scaffold Degradation by Decoupling Tissue Ingrowth Using a GPR-Driven Digital Twin Framework

Pelvic organ prolapse (POP) reconstruction is increasingly performed utilizing knitted silk meshes (KSM), yet tracking in vivo degradation kinetics remains challenging due to complex host tissue integration. This study developed an AI-driven semi-empirical framework utilizing Gaussian Process Regression (GPR) to bridge the kinetic mismatch between in vitro and in vivo environments. KSM scaffolds underwent 32 weeks of accelerated in vitro enzymatic degradation, with morphology (SEM), molecular conformation (FTIR), and mass loss being coupled with mechanical decay to train the GPR model. In vitro results revealed a multi-stage physical disintegration via a topochemical erosion pathway that preserved crystalline {beta}-sheet structures despite macro-scale mass and mechanical loss. When validated in a rat abdominal wall defect model, traditional tracking metrics encountered severe bottlenecks. Heterogeneous dye labeling caused premature fluorescence quenching by Week 16, while extensive tissue ingrowth masked gravimetric and SEM signatures. Intriguingly, a bi-phasic in vivo mechanical trajectory was identified, where initial degradation-led failure was followed by a secondary mechanical recovery driven by biomechanical synergy with neo-muscular tissue. Importantly, despite premature quenching, this work presents the first optical imaging approach to visually mapping the complete chronological breakdown of the scaffolds peripheral boundary layer in vivo, proving that outer functionalized layers eroded prior to internal silk cores. Furthermore, our GPR framework elegantly resolved the perennial technical barrier of tissue-mesh overlapping. By mathematically decoupling intrinsic polymer degradation from confounding tissue ingrowth, the model successfully achieved a first-of-its-kind prediction of the bare scaffolds long-term structural fate in a non-adhered state, providing a robust digital twin methodology for lifetime predictions of degradable biomaterials.

bioengineering↗

Methylmalonic acid: a new target for Hadamard-edited MRS

BackgroundMethylmalonic acidemia (MMAemia) is a genetic metabolic disorder characterized by an accumulation of methylmalonic acid (MMA) and impaired energy metabolism leading to increased lactate (Lac). The signals of MMA (1.23 ppm) and Lac (1.33 ppm) overlap, making their separation using conventional MRS challenging. An MRS method to differentiate the two metabolites could enhance pathophysiological understanding and improve treatment monitoring - Hadamard-edited MRS has the potential to achieve this. PurposeTo develop a Hadamard-encoded J-difference editing approach for independent detection of MMA and Lac at 3T. MethodsA novel Hadamard-encoded editing scheme was implemented and evaluated with density-matrix simulations, phantom and in vivo experiments. The new four-step scheme uses frequency-selective editing pulses, applied at 3.2 ppm and 4.1 ppm to modulate the J-coupled methyl resonances of MMA and Lac, respectively. Hadamard combinations of the four sub-experiments yield the separate difference-edited spectra for each target metabolite. ResultsSimulations and phantom experiments clearly illustrate the separated signals of MMA and Lac. In vivo validation experiments show a Lac signal (but no MMA) in a healthy infant, and both Lac and MMA (separated into their respective Hadamard-combination spectra) in a patient with MMAemia. ConclusionHadamard-encoded editing at 3T can separate MMA and Lac signals and shows promise for studying altered metabolism in patients with MMAemia.

biochemistry↗

Single-Cell Transcriptomic Mapping of PD-L1/TLR4 Remodeling Informs Topical Immunoprevention Timing in Skin Carcinogenesis

Cutaneous squamous cell carcinoma (cSCC) represents a growing public health burden, with incidence projected to increase 23-29% over the coming decade. Topical immunoprevention strategies targeting the PD-L1/PD-1 and TLR4 axes have demonstrated preclinical efficacy, yet optimal intervention timing in humans remains undefined. To address this gap, single-cell RNA sequencing was performed on matched sun-protected (SP), sun-damaged (SD), and actinic keratosis (AK) biopsies from the same individuals, along with independent cSCC cases. Immune checkpoint and innate inflammatory signals were detectable as early as SD skin, prior to histologically confirmed dysplasia. Monotonically increasing expression of CD274 (PD-L1), CTLA4, PDCD1, CD27, and STAT1, alongside progressive TLR4-MYD88 innate immune signaling, was revealed through pseudobulk data analysis, with earliest upregulation at the SD stage. Fuzzy c-means trajectory clustering identified cell-typespecific programs across dendritic cells, macrophages, T cells, fibroblasts, endothelial cells, and keratinocytes. Dendritic cells shifted from early inflammatory antigen-presenting programs toward late PD-L1/IFN-regulatory states; macrophages showed monotonically increasing TLR4-associated myeloid activation; and T cells defined a "hot but exhausted" microenvironment in established cSCC. These findings identify SD and AK as biologically active stages for topical immunoprevention and provide a cellular roadmap for PD-L1/PD-1 and TLR4 blockade strategies.

cancer biology↗

Functional characterization and classification of mechanosensitive bladder afferents

Normal urinary bladder function relies on afferent fibers that detect and integrate mechanical and chemical cues related to bladder distension. Though, the molecular identity and function of the various sensory neuron types involved in bladder function have yet to be fully elucidated. Here, we introduce a novel framework for the functional classification of mechanosensitive bladder afferents based on their differential responses to physiological (15 l/min) and noxious filling (30 s at intravesical pressures of 10, 20, 30, 40, 50, and 60 cmH2O). Our data reveal the presence of three distinct types of mechanosensitive bladder afferents, two that respond to physiological distension (type I and II) and one that is activated by noxious stimulation (type III). Of the two populations that respond to physiological filling, one displays a linear increase in firing with bladder filling (type I), while the firing of the other plateaus as intravesical pressure increases (type II). Fast filling (130 l/min) increases the discharge of all three afferent types, with the effect being most pronounced in those responding to noxious stimulation (type III). Corroborating the existence of three functionally distinct bladder afferent populations, Yoda1, a selective PIEZO1 channel activator, significantly increased the firing rate of types I and III during slow filling and of type III during noxious stimulation. In summary, we present a reliable and reproducible method for studying and classifying bladder afferents, while providing compelling evidence for the existence of functionally distinct populations of mechanosensitive afferents, each activated and regulated by distinct mechanisms. New & NoteworthyUsing a novel approach, we identify three types of mechanosensitive afferents innervating the urinary bladder, two that respond to slow filling and one that is activated only by noxious distension. The three afferent types display distinct firing patterns during rapid filling and in response to the PIEZO1 channel agonist Yoda1.

physiology↗

A Sandwich-Structured Silk Fibroin Mesh with ROS-Responsive and Immunoregulatory Functions for Pelvic Floor Repair

Current biodegradable meshes for pelvic floor repair are constrained by a limited ability to actively modulate the hostile immune microenvironment following implantation. To address these challenges, we developed a functionalized degradable silk fibroin mesh (SFM) integrated with a reactive oxygen species (ROS)-responsive nanocomposite hydrogel. The resulting composite mesh, SFM@Gel-NP, features a "hydrogel-mesh-hydrogel" sandwich structure, wherein the hydrogel layers are loaded with self-assembled nanoparticles (NP-H-CRFP) for the co-delivery of the STING inhibitor H-151 and the ROS-scavenging agent catechin. This design provides immediate mechanical reinforcement while enabling microenvironment-triggered drug release. In vitro, NP-H-CRFP demonstrated efficient cellular uptake, significant ROS clearance, and effective attenuation of macrophage inflammation and apoptosis. In vivo, SFM@Gel-NP remodeled the local immune milieu by inhibiting the ROS/cGAS-STING/NF-{kappa}B axis, thereby promoting a shift from pro-inflammatory M1 toward pro-regenerative M2 macrophage polarization. This immunomodulatory effect, coupled with enhanced and well-organized collagen deposition--particularly of early type III collagen--resulted in improved tissue integration and repair. This work presents a novel strategy that combines structural reinforcement with active immune regulation, offering a promising next-generation solution for durable and functional pelvic floor reconstruction.

bioengineering↗

Distinct and shared synergistic effects of high-fat and high-iron diets on liver tumorigenesis and transcriptomic remodeling in mice

Background and AimsThe incidence of hepatocellular carcinoma (HCC) is increasingly driven by metabolic risk factors, including obesity and iron overload. Although high-fat and high-iron diets independently promote hepatocarcinogenesis, their shared and distinct molecular effects remain unclear. We sought to define how dietary fat and iron differentially shape HCC development. ApproachMale C3HeB/FeJ mice were exposed to long-term high-fat (HFD), high-iron (HID), or combined (HFD+HID) diets for 16.5 months. Tumor burden, hepatic iron distribution, mTOR signaling, oxidized phospholipid (OxPL) accumulation, and transcriptomic alterations across normal, adjacent non-tumor, and tumor liver tissues were analyzed using biochemical, histological, and RNA sequencing approaches. ResultsAll diets induced HCC with comparable tumor burden. HID increased iron levels in non-tumor liver tissue but resulted in relative iron depletion within tumors, indicating tumor-specific iron utilization. Tumors from all diet groups showed robust mTOR activation and increased OxPL accumulation, with stronger oxidative stress signatures in HFD and HFD+HID tumors. Transcriptomic analyses revealed conserved oncogenic programs alongside diet-specific signatures, with HFD exerting a dominant effect on metabolic reprogramming and gene dysregulation, whereas HID preferentially enhanced immune and inflammatory signaling. Progressive, monotonic changes in gene expression were observed across disease stages. Cross-species analyses linked diet-induced mouse tumors to immunologically "hot" human HCC subtypes. ConclusionsDietary fat and iron promote HCC through overlapping yet distinct molecular pathways, highlighting metabolic and immune mechanisms as key targets in diet-associated liver cancer.

cancer biology↗

Interpretable morphology mapping of peripheral blood leukocytes using annotation-efficient artificial intelligence

BackgroundPeripheral blood smears (PBS) review is labor-intensive, subjective, and challenging for rare or morphologically heterogeneous cell types in hematologic malignancies. Artificial intelligence (AI) offers a scalable alternative, but broader clinical translation is constrained by annotation burden and limited interpretability. MethodsWe developed an interpretable, annotation-efficient AI framework that learns leukocyte morphology through a two-stage process: label-free representation learning to construct a morphological embedding space, followed by supervised fine-tuning for cell type and morphological attribute classification. The model was trained and evaluated on 5,952 PBS images from cancer patients at MD Anderson Cancer Center, including blast cells, and 17,092 images from public sources. Active learning strategies were assessed to improve label efficiency, and interpretability was examined using saliency and embedding visualization. An interactive web application, HemoSight, was developed to support clinical review. FindingsThe framework achieved a macro-F1 score of 0{middle dot}96 for 9-way leukocyte classification on the internal test split and 0{middle dot}83 on the held-out patient cohort. Active learning substantially reduced annotation requirements, reaching peak performance with only 13{middle dot}3% of available labels and significantly improving learning efficiency across 8 of 9 cell types. The model generalized to classifying 11 leukocyte morphological attributes with a mean F1 score of 85{middle dot}8% and revealed structured morphological landscapes. Saliency maps, embedding visualizations, and the HemoSight application enabled transparent morphological inspection of model predictions, supporting confidence in model behavior and feasibility for clinical integration. InterpretationOur framework enables scalable, annotation-efficient, and interpretable modeling of leukocyte morphology, supporting the integration of AI-assisted PBS review for hematopathology workflows. FundingSeed funding from The University of Texas MD Anderson Cancer Center. Research in ContextO_ST_ABSEvidence before this studyC_ST_ABSPeripheral blood smear review is essential for diagnosing and monitoring hematologic malignancies, but manual case review is time-consuming and variable, particularly for rare or abnormal leukocyte types. Automated hematology analyzers are widely used to flag abnormal cells; however, they provide limited morphological insight and often require frequent manual correction, especially in cancer settings where disease and treatment alter cell appearance. Previous artificial intelligence approaches for leukocyte classification have shown promise, but most rely on fully supervised learning, require extensive expert annotation, focus on a limited set of cell types, and frequently exclude diagnostically important rare cells such as blasts. Interpretability is inconsistently addressed, and few studies provide tools that allow clinicians to inspect and interpret model outputs within routine workflows. Added value of this studyThis study introduces an annotation-efficient framework trained on a large collection of peripheral blood smear images, including cancer patient samples with hematopathologist-verified rare cell types such as blasts. The framework learns leukocyte morphology from unlabeled images and adapts to multiple classification tasks with minimal expert labeling. Performance is evaluated on both internal test splits and a held-out patient cohort to provide a realistic estimate of generalization. Iterative, uncertainty-guided annotation substantially reduces labeling requirements while improving learning efficiency across most leukocyte classes. Beyond cell-type classification, the framework is extended to 11 clinically relevant morphological attributes and reveals a structured morphological landscape. These capabilities are integrated into a web application, HemoSight, enabling real-time inference and transparent morphological inspection of predictions within hematopathology workflows. Implications of all the available evidenceAdvancing artificial intelligence for hematology requires methods that reduce expert labeling demands, provide interpretable outputs, and perform reliably across clinically diverse patient samples. This study shows that learning from largely unlabeled data combined with iterative expert annotation can support scalable and flexible modeling of leukocyte morphology for classification tasks. Integrating quantitative predictions and interactive visualization supports the use of artificial intelligence as an assistive tool for diagnostic peripheral blood smear review, with potential to improve efficiency, consistency, and reviewer confidence.

pathology↗

Modeling human B cell development with pluripotent stem cells

The ability to generate functional B cells from human pluripotent stem cells (hPSCs) would open new opportunities to develop novel B cell-based therapies to treat a range of human diseases and disorders. Towards this goal, we established a protocol that promotes the efficient development of B lineage cells from definitive hematopoietic progenitors generated from different hPSC lines. Flow cytometric and multi-omic scRNA-seq analyses revealed that B cell development from hPSCs transitions through the well-established pro-B, pre-B and naive B cell stages, accurately recapitulating B lymphopoiesis in the human adult bone marrow. Importantly, the naive B cells generated with this approach could be induced to mature into plasma cells that secrete antibodies and undergo class switching. Analyses of signaling pathways that regulate B lymphopoiesis in these cultures uncovered a potent inhibitory effect of IL-7 on functional IgH rearrangement, resulting in the development of abnormal cells that failed to undergo pre-B cell maturation. Finally, analysis of the different hPSC-derived hematopoietic programs revealed that both definitive and yolk sac progenitors display B cell potential, indicating that there are distinct developmental sources of human B lineage cells. Taken together, these findings demonstrate the efficient generation of B cells from hPSCs and, in doing so, provide a system for further investigating the earliest stages of human B lymphopoiesis and a source of appropriately staged plasma cells for future therapeutic applications.

developmental biology↗

Striatal FOXP2 is essential for stable vocal production in non-human primates

The transcription factor FOXP2 is the most well-known language-related gene in humans, yet its role in primate vocalization remains poorly understood. Here we report that knockdown of FOXP2 in the striatum markedly disrupts vocalization stability in the marmoset monkey, a valuable non-human primate model for studying vocal behavior. FOXP2 exhibited high expression in the marmoset striatum, especially during early development. Using the CRISPR-Cas12 system, we achieved specific in vivo editing of the FOXP2 gene and effective knockdown of FOXP2 protein expression in the marmoset striatum. Two neonatal marmosets received bilateral striatal injections of the gene-editing and control virus, respectively, and were raised together in the same family. In three such marmoset pairs, analysis of vocalizations recorded during 6-15 weeks post-injection revealed that striatal FOXP2 knockdown significantly altered vocal features and increased intra-individual variability in phee syllables--the most common marmoset vocalization, often produced repetitively as multi-syllable phee calls. Notably, in FOXP2-edited marmosets, acoustic alterations were minimal in the first syllable of phee calls but became progressively more pronounced in subsequent syllables, which exhibited a marked upward shift in the frequency spectrum over time with progressively steeper slopes. These temporal dynamics in vocal features reflect a reduction in the stability of continuous vocal production. In line with the known striatal functions in motor control, our findings provide the first evidence of FOXP2 in controlling vocalization in non-human primates, thereby opening new avenues for investigating the neural mechanisms underlying FOXP2 function.

neuroscience↗

Multimodal alignments of in vivo imaging and spatial biology datasets at cellular resolution

Parallel revolutions in intravital microscopy and spatial biology techniques have respectively enabled large-scale recordings of cellular dynamics in live animals and multi-dimensional molecular profiling at single-cell resolution. However, due to the challenges of aligning data from different modalities at cellular resolution, these two transformational approaches have generally been applied on separate biological samples, stymying the ability to link activity patterns and molecular attributes in the same exact cells. To enable routine, multimodal investigations of cells in vivo dynamics and molecular content, we created TRU-FACT (Total Registration Under Functional Activity, Connectivity, and Transcriptomics), a broadly applicable experimental and computational pipeline for registering large populations of individual cells across intravital imaging and spatial biology datasets. The pipeline combines three key innovations: an optomechanical tissue handling and alignment method to parallelize specimen planes, a graph-theoretic method to register individual cells based on their geometric relationships to neighboring cells, and a statistical framework that provides for each cell an a posteriori probability of correct registration. We validated TRU-FACT with several preparations for imaging neural Ca2+ activity in cortical and deep brain areas in head-fixed and freely behaving mice, RNA-barcode-expressing viruses for labeling neural projections, and low- and high-plex spatial transcriptomic methods. In mice performing a skilled reaching task, TRU-FACT alignments revealed the movement-related signaling patterns of intratelencephalic, extratelencephalic, and striatum-, superior colliculus-, and thalamus-projecting motor cortical neurons. Overall, TRU-FACT constitutes a scalable, multimodal discovery platform that is applicable to diverse tissue-types and spatial biology techniques, thereby enabling multiscale analyses of many complex biological systems.

neuroscience↗

The discovery of missing taxane C13α-O-deacetylases re-delineates the biosynthetic pathway of paclitaxel

The prevalence of naturally occurring C13-acetoxy taxanes, together with the presence of a native C13-acetyltransferase in yew trees, suggests that the natural biosynthetic pathway for paclitaxel may involve a cryptic C13-O-deacetylation step. However, whether a putative taxane C13-O-deacetylase (T13dA) acts in the pathway of paclitaxel biosynthesis remains elusive. Herein, we functionally characterized two novel taxane C13-O-deacetylases (T13dA1 and T13dA2) from Taxus x media cell cultures, providing experimental evidence for the molecular and biochemical plausibility of C13-O-deacetylation in paclitaxel biosynthesis in Taxus species. Furthermore, T7dA1, a novel taxane C7{beta}-O-deacetylase with higher activity than the reported T7dA was discovered and characterized here. Notably, we reconstituted a new 19-gene pathway enabled by the integration of a C13-O-acetylation-deacetylation module for the de novo biosynthesis of baccatin III in Nicotiana benthamiana leaves, reaching a yield of 71{square} g{square} g-1 DW, much higher than that obtained from the 17{square} gene pathway lacking this module. These findings not only demonstrate the functional importance of the C13-O-acetylation-deacetylation module as a branch within the paclitaxel biosynthetic network, but also expand the multi-branched taxane metabolic network in Taxus and provide novel enzymatic tools and engineering strategies to facilitate heterologous pathway reconstitution and efficient paclitaxel production.

biochemistry↗

DCN1 inhibitor induces fetal hemoglobin through self-limited regulation of CUL3 neddylation

Few genetic loci are as well-characterized as the globin gene locus, and the substitution of healthy {gamma}-globin (HbF) for missing or mutated {beta}-globin (HbB) is an established therapeutic strategy for {beta}-hemoglobinopathies including sickle cell disease (SCD) and {beta}-thalassemia. Although substantial progress has been made in understanding HbF derepression and globin switching, many current therapeutic strategies involving small molecules increase HbF through broad epigenetic perturbations or cytotoxic stress, raising concerns about dose-limiting cytopenias and off-target effects. By coupling single-cell transcriptomics, genetic perturbations, and functional genomics, we identified an unknown role of neddylation in the regulation of fetal hemoglobin (HbF). Partial impairment of neddylation of cullin ubiquitin ligase 3 (CUL3) through defective in cullin neddylation 1 (DCN1) inhibition leads to highly selective chromatin changes, histone demethylation, and globin locus binding of known activators of HbF transcription. Further, DCN1 inhibition drives globin switching and HbF increases in vitro and in vivo with minimal off-target transcriptional effects and no evidence of cytotoxicity or stress erythropoiesis. To therapeutically target this axis, we report the discovery and characterization of CLY-124, a first-in-class, covalent DCN1 inhibitor with favorable pharmacology properties. In a humanized mouse model, CLY-124 showed a dose-dependent increase in HbF as monotherapy and in synergy with hydroxyurea (HU), a current standard of care. Collectively, these findings highlight the power of single-cell transcriptomics to elucidate undiscovered biologic insights with therapeutic potential, and the promise of DCN-1 inhibitors like CLY-124 to address {beta}-hemoglobinopathies. With an appropriate nonclinical safety profile, a first-in human study of safety, pharmacokinetics and HbF assessments in healthy volunteers and participants with SCD is ongoing for CLY-124. One-sentence SummaryDCN1 is a promising target for {beta}-hemoglobinopathies

molecular biology↗

Mechanotransduction-Aware Causal Omics on Tissue Scaffolds: A Controlled Mechanochemical Framework for Identifying Disease Genes Beyond Pure Omics Analysis

Omics-based disease-gene discovery is typically performed as if molecular states evolve independently of tissue mechanics. Most current pipelines analyze transcriptomic or multimodal molecular data alone and identify abnormal genes using differential expressions, latent trajectories, or association-based recovery under treatment. However, in mechanically active tissues, gene expression is shaped not only by internal regulatory networks but also by mechanotransduction arising from strain, curvature, force transmission, and scaffold geometry. This raises a fundamental question: should disease-gene identification in tissues be treated as a pure omics association problem, or as a causal mechanochemical inference problem? We introduce a mechanotransduction-aware causal omics framework on a Cosserat tissue scaffold. Gene expression evolves through intrinsic regulatory dynamics, spatial diffusion, external control, and a mechanotransduction term driven by scaffold mechanics. To distinguish causation from association, we define a hidden mechano-drug rescue channel in the true data-generating system and compare predictive models that either include or omit mechanotransduction. We show that association-based rankings can incorrectly elevate downstream homeostatic or repair genes, even when the disease gene is the true direct mechanochemical target. By contrast, a causal ranking based on reconstruction of the direct mechanotransduction intervention effect correctly identifies the disease gene as the strongest beneficiary. These results argue that popular pure-omics analysis is insufficient for disease-gene discovery in mechanically structured tissues. Mechanotransduction should be modeled as part of the causal structure of tissue biology rather than treated as a secondary covariate or omitted entirely.

bioinformatics↗

Predicting Pre-treatment Resistance or Post-treatment Effect? A Systematic Benchmarking of Single-Cell Drug Response Models

Intratumoral heterogeneity drives variable drug responses in cancer. Single-cell RNA sequencing (scRNA-seq) enables characterization of such heterogeneity and prediction of drug response at single-cell resolution. Accordingly, various computational models have been developed to infer drug response from scRNA-seq data. However, their performance, robustness, and generalizability across different biological contexts remain insufficiently evaluated. To address this gap, we benchmarked representative single-cell drug response prediction models using 26 curated datasets comprising over 760,000 cells across 12 cancer types and 21 therapeutic agents. We constructed balanced and imbalanced scenarios to reflect realistic drug-response label distributions. To address the lack of ground-truth labels in conventional scRNA-seq datasets, we incorporated lineage-tracing data with experimentally validated drug-response annotations, enabling evaluation in a clinically relevant pre-treatment prediction setting. Our results show that prediction performance was markedly higher in cell lines than in tissue samples. Under imbalanced conditions, most methods exhibited sharp performance declines, whereas scDEAL demonstrated the highest robustness. Independent validation using an in-house pancreatic ductal adenocarcinoma dataset further confirmed scDEALs robustness and ability to capture biologically meaningful state transitions. Label-substitution experiment revealed that this robustness was partially driven by the models specific training-label construction. However, benchmarking with lineage-tracing data revealed a fundamental limitation: most models capture drug-induced transcriptional changes but struggled to predict intrinsic resistance before treatment. In summary, our study defines the performance boundaries of current approaches and highlights their limitations in addressing intratumoral heterogeneity, class imbalance, and intrinsic resistance prediction, emphasizing the need for the next-generation single-cell drug response models with stronger clinical relevance.

bioinformatics↗

MolClaw: An Autonomous Agent with Hierarchical Skills for Drug Molecule Evaluation, Screening, and Optimization

Computational drug discovery, particularly the complex workflows of drug molecule screening and optimization, requires orchestrating dozens of specialized tools in multi-step workflows, yet current AI agents struggle to maintain robust performance and consistently underperform in these high-complexity scenarios. Here we present MolClaw, an autonomous agent that leads drug molecule evaluation, screening, and optimization. It unifies over 30 specialized domain resources through a three-tier hierarchical skill architecture (70 skills in total) that facilitates agent long-term interaction at runtime: tool-level skills standardize atomic operations, workflow-level skills compose them into validated pipelines with quality check and reflection, and a discipline-level skill supplies scientific principles governing planning and verification across all scenarios in the field. Additionally, we introduce MolBench, a benchmark comprising molecular screening, optimization, and end-to-end discovery challenges spanning 8 to 50+ sequential tool calls. MolClaw achieves state-of-the-art performance across all metrics, and ablation studies confirm that gains concentrate on tasks that demand structured workflows while vanishing on those solvable with ad hoc scripting, establishing workflow orchestration competence as the primary capability bottleneck for AI-driven drug discovery.

bioinformatics↗

Targeting TPO/MPL Signaling to Mitigate JAK2V617F-driven Cardiac Microvascular Disease

BackgroundIndividuals with JAK2V617F-mutant myeloproliferative neoplasms or clonal hematopoiesis of indeterminate potential have a markedly increased risk of cardiovascular disease, yet the mechanisms by which mutant blood cells drive vascular and cardiac dysfunction remain incompletely understood. Although the thrombopoietin (TPO) receptor MPL is central to hematopoiesis and is expressed in vascular endothelial cells (ECs), its role in JAK2V617F-associated cardiovascular complications is unknown. Methods and ResultsWe generated chimeric mice with JAK2V617F-mutant blood cells and wild-type endothelium by bone marrow transplantation and challenged them with a high-fat/high-cholesterol diet to model cardiometabolic stress. These mice developed a distinct cardiovascular phenotype characterized by microvascular disease, increased left ventricular mass, and relatively preserved left ventricular ejection fraction. Histological analysis revealed coronary arteriole stenosis, perivascular fibrosis, reduced microvascular density, and endocardial injury, without evidence of epicardial coronary stenosis or myocardium infarction. Single-cell RNA sequencing revealed activation of inflammatory, stress-response, and endothelial-to-mesenchymal transition gene signatures in ECs, most prominently within the endocardial ECs. Immunohistochemistry identified MPL expression predominantly in endocardial ECs. TPO/MPL signaling was upregulated in endocardial ECs in mice with JAK2V617F-mutant hematopoiesis, and treatment with an anti-MPL neutralizing antibody markedly improved cardiac pathology, restored endocardial integrity, and increased coronary microvascular density despite persistent systemic inflammation. ConclusionsJAK2V617F-mutant hematopoiesis induces coronary microvascular dysfunction. Endocardial ECs represent a key cellular target under cardiometabolic stress, and endocardial MPL signaling constitutes a potential targetable pathway in JAK2V617F-associated cardiovascular disease. Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=122 SRC="FIGDIR/small/715884v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@15dcebdorg.highwire.dtl.DTLVardef@1b00a2eorg.highwire.dtl.DTLVardef@6c6f98org.highwire.dtl.DTLVardef@1128f75_HPS_FORMAT_FIGEXP M_FIG C_FIG Key PointsO_LIJAK2V617F-mutant hematopoiesis induces cardiac microvascular disease C_LIO_LIMPL is expressed in endocardial ECs and MPL inhibition restores endocardial integrity and improves cardiac microvascular function C_LI

cell biology↗

Complete genome-derived metabolic interactions reveal impact of gut ecology on human health

Metabolic interactions govern gut microbiome assembly, yet functional rules remain obscured by genomic incompleteness and fragmentation. Here, we leverage 1,150 complete genomes to construct genome-scale metabolic models, demonstrating that draft genomes introduce systemic artifacts missing critical transport functions. We observe that metabolic interactions are intrinsically driven by genomic traits and niche specialization rather than random association. We stratifies strains into four ecological groups, including active players, resource predators, utilizers, and contributors, each of which exhibits distinct metabolite exchange/competition signatures. This functional architecture is strongly coupled to secondary metabolism. Applying this framework to inflammatory bowel disease revealed distinct temporal dynamics of ecological groups across disease subtypes, where group-specific dysbiosis predicted clinical phenotypes better than whole community profiles. Furthermore, integrating metabolic and co-occurrence networks to identify keystone for classifiers as features significantly improved disease diagnosis. Our study provides novel insights into gut metabolic interaction landscape, bridging the gap between genomic potential and clinical utility for precision microbiome therapeutics.

microbiology↗

The population structure and genetic health of European wolves

Once nearly eradicated from Europe, grey wolves (Canis lupus) have recently undergone a remarkable demographic recovery, but their long-term survival remains precarious. By analyzing 1,001 genomes, we uncover a mosaic of distinct evolutionary lineages, not a single recovering population. Northern populations exhibit Asian wolf ancestry, while southern populations preserve ancient Holocene lineages, with dog introgression varying by region. Isolated wolves from the Scandinavian, Italian, and Iberian peninsulas harbored particularly high levels of inbreeding and fixed deleterious mutations. Signatures of genome erosion were widespread across Europe, with many populations falling well short of the minimum size recommended for long-term survival. Our study reveals the complex tapestry of wolf ancestry and variation across Europe, which calls for nuanced, regional conservation plans founded in genetic monitoring.

genomics↗