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Liu, W.

Publications and source records attributed to Liu, W..

At least 73 records · Page 4Linked to original sources

HYPER-Net: Physics-Conditioned Self-Supervised Reconstruction for Fourier Light-Field Microscopy

The rapid convergence of optical innovation and machine intelligence is reshaping biological imaging by enabling platforms that jointly advance image formation and computational reconstruction for highspeed, high-resolution volumetric microscopy. However, broadly accessible three-dimensional imaging at high spatiotemporal resolution remains limited by the reliance of existing supervised methods on large modality-matched training datasets, the computational burden of conventional iterative reconstruction, and sensitivity to optical mismatch arising from small deviations in the spatial-angular point spread functions. Here, we introduce HYPER-Net, a physics-conditioned self-supervised framework for Fourier light-field microscopy that integrates scan-free volumetric acquisition with fast, robust three-dimensional reconstruction. HYPER-Net incorporates experiment-specific point-spread functions into the learning process in two complementary roles: as the forward operator that enforces measurement consistency and as a conditioning signal that adaptively modulates intermediate feature representations. This design reduces reliance on paired experimental ground-truth volumes, improves robustness to system variation, and enables generalizable reconstruction across diverse biological contexts. Using human colon organoids, embryonic Xenopus laevis hearts, hiPSC-derived cardiac spheroids, and freely moving Caenorhabditis elegans, we demonstrate high-fidelity volumetric imaging of tissue morphology, cardiac function, calcium-contraction coupling, and locomotion-associated neural and muscular dynamics. These results position HYPER-Net as a versatile framework for rapid volumetric imaging and quantitative analysis of dynamic biological systems across basic research and biomedical applications.

bioengineering↗

A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

BackgroundAlcohol consumption influences cardiovascular disease, but whether it does so by affecting endothelial plasticity is unknown. We tested whether alcohol regulates endothelial-to-mesenchymal transition (EndMT) to influence arterial pathology. MethodsHCAEC and HUVEC were exposed to inflammatory cytokines (TGF{beta} {+/-} IL1{beta}) or hypoxia in the presence of ethanol (0-100 mM). EndMT was assessed by changes in cell marker expression, SNAIL levels, and migration assays. In vivo, carotid ligation was performed in mice gavaged with/without either daily moderate ethanol (2-drink equivalent/d) or episodic binge exposure (7-drink equivalent, 2 days/week) and myo-endothelial cell population assessed. ResultsCytokines and hypoxia induced EndMT in vitro, characterized by loss of endothelial markers, increased mesenchymal markers, elevated SNAIL, and enhanced migratory capacity. Low-to-moderate dose ethanol (5-25 mM) attenuated these changes, preserving endothelial phenotype, whereas high dose ethanol (50-100 mM) either had no effect or exacerbated EndMT. The inhibitory effect of moderate ethanol on cytokine- and hypoxia-induced changes in SMA and Cdh5 expression was abrogated by {gamma}-secretase inhibition, consistent with involvement of Notch signaling. Carotid ligation induced neointimal formation and accumulation of myo-endothelial cells indicative of EndMT. Daily moderate ethanol significantly attenuated neointimal hyperplasia and diminished the myo-endothelial cell population, whereas in contrast, episodic binge ethanol exposure increased pathologic remodeling and myo-endothelial cell abundance. ConclusionsAlcohol modulates endothelial trans-differentiation in a biphasic manner. Low-to-moderate alcohol exposure suppresses EndMT and limits pathological remodeling, whereas binge-level exposure promotes these processes. These findings identify regulation of endothelial plasticity as a potential novel mechanism linking alcohol consumption patterns to vascular disease risk. NEW AND NOTEWORTHYWe identify a previously unrecognized biphasic effect of alcohol on endothelial phenotypic plasticity. Low-to-moderate dose alcohol suppresses endothelial-to-mesenchymal transition (EndMT), whereas high-level (binge) exposure promotes this pro-atherogenic process. Given the central role of EndMT in vascular remodelling and atherosclerosis, these findings provide a mechanistic framework linking alcohol consumption patterns and cardiovascular disease risk - potentially explaining both the protective effect at low/moderate levels, and the detrimental impact of heavy alcohol use. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=142 SRC="FIGDIR/small/718463v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@1febae2org.highwire.dtl.DTLVardef@9f5ff1org.highwire.dtl.DTLVardef@153ea69org.highwire.dtl.DTLVardef@42b1ed_HPS_FORMAT_FIGEXP M_FIG C_FIG Injurious stimuli can trigger endothelial cells (EC) to undergo endothelial-to-mesenchymal transition (EndMT) that contributes to arterial remodeling and disease. EndMT is regulated in a biphasic manner by alcohol with low-to-moderate levels (1-3 drink equivalent) suppressing EndMT and attenuating vascular remodeling, whereas higher level/binge exposure (7 drink equivalent) promotes these processes. Graphic created using Biorender.

cell biology↗

ARID1A deficiency unleashes centromeric RNA transcription to drive chromosomal instability and boosts PKMYT1 inhibitor efficacy via RNA sensing

Cancer gene-associated mutations and molecular hallmarks of chromosomal instability (CIN) are unexpectedly common in histologically normal cells and tissues. These emerging findings challenge the binary distinction between "normal" and "cancerous" cells and suggest that early tumorigenesis may commence against a background of widespread yet largely tolerated genomic instability. However, it remains largely unexplored how a cancer gene-associated mutation can initiate the development of CIN-like states in non-malignant cells and drive tumor evolution. ARID1A, a chromatin remodeling factor, was identified as the most frequently mutated gene in both gastric normal epithelium and tumors. This distinctive molecular convergence presents an opportunity to elucidate the mechanisms by which a cancer-associated gene facilitates the initiation of early CIN phenotypes and develop effective antitumor strategies. In the present study, using primary human gastric organoids, we employed optical genome mapping (OGM) and live-imaging technologies to demonstrate that ARID1A depletion induced a wide spectrum of structural variants (SVs), copy number variants (CNVs), and chromosomal segregation errors, characteristic features of CIN at a very early stage of gastric tumorigenesis. Mechanistically, ARID1A bound centromere repetitive satellite DNA (satDNA) sequences. Its SWI/SNF-associated chromatin remodeling activity was required for suppressing satDNA transcription and the production of -SatRNA, through restricting RNAPII elongation. Consequently, ARID1A depletion led to overexpression of -SatRNA, and a higher incidence of sister chromatid exchange (SCE), a sensitive indicator of CIN. Importantly, the elevated -SatRNA expression in ARID1A-deficient cells further established a dual therapeutic vulnerability for G2/M checkpoint blockade, such as PKMYT1 inhibitor (PKMYTi), by concurrently aggregating CIN-induced cell death and activating self-dsRNA sensing-mediated innate immune response. Notably, PKMYTi markedly promoted -SatRNA expression, aberrant release of these self-derived dsRNAs into the cytosol and a robust activation of the RIG/MDA5-MAVS-depenent type-I interferon response in ARID1A-depleted cells. As expected, PKMYTi potentiated the efficacy of immunotherapy in ARID1A-deficient gastric tumors. Together, our findings reveal that ARID1A deficiency unleashes centromeric -SatRNA transcription, which sets the molecular stage for tumor evolution and targeted therapy by coordinately inducing CIN and self-dsRNA-induced innate immune responses.

cancer biology↗

The ENL-USP7 Complex Regulates HIV Latency Through BRD4 Stabilization

HIV-1 persists in CD4 T cells and brain microglia through host factors that enforce viral latency, yet the mechanisms that stabilize key transcriptional regulators remain incompletely understood. Here, we identify the YEATS domain-containing protein ENL and its associated deubiquitinase USP7 as a host complex that maintains HIV-1 latency. USP7 stabilizes BRD4 by deubiquitination, suppressing HIV transcription and sustaining viral quiescence. Disruption of the ENL-USP7 complex using selective PROTACs reactivates latent HIV in cell line models, as well as in resting CD4 T cells and microglia isolated from people with HIV on antiretroviral therapy. These findings uncover a critical ENL-USP7-BRD4 axis that enforces HIV-1 latency and highlight USP7 as a potential target for latency-reversing strategies. HighlightsO_LIENL, a YEATS domain-containing crotonylation reader, acts as a suppressor rather than an activator of HIV-1 transcription. C_LIO_LIENL recruits USP7 to stabilize BRD4 and enforce viral latency. C_LIO_LIDisruption of the ENL-USP7-BRD4 axis reactivates latent HIV in T cells and microglia. C_LIO_LITargeting USP7 or ENL reveals a therapeutic vulnerability in HIV reservoirs. C_LI

microbiology↗

Serial Thermal Ablation Induces Abscopal Antitumor Immunity and Reveals Targetable CSF1R-Dependent Resistance in Pancreatic Cancer

Thermal ablation is increasingly used for local control of pancreatic ductal adenocarcinoma (PDAC), but its capacity to induce systemic antitumor immunity and the mechanisms limiting this response remain incompletely defined. Using a bilateral LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx1-Cre (KPC) flank tumor model, we show serial radiofrequency ablation (RFA) enhances local tumor control and induces a robust abscopal response. This effect was associated with increased activation of CD8 T cells and natural killer cells, and was abrogated by CD8 T cell depletion. Single-cell RNA sequencing revealed expansion of cytotoxic immune programs alongside induction of a CSF1R-driven myeloid response consistent with adaptive immune resistance. Although combinatorial blockade of PD-L1 and CD73 augmented systemic antitumor responses, and the addition of CSF1R inhibition in this context further enhanced both local and distant tumor control. These findings identify a CSF1R-dependent myeloid resistance program which constrains ablation-induced systemic immunity and demonstrate that rational combination immunotherapy can potentiate the systemic efficacy of tumor ablation in PDAC. STATEMENT OF TRANSLATIONAL RELEVANCERadiofrequency ablation is a local thermal therapy that induces tumor destruction and modulation of the tumor microenvironment used for treatment of many solid tumors, including pancreatic cancer. Serial thermal ablations induce a CD8+ T cells and NK cell antitumor immunological response; however, Nt5e (CD73) is increased in tumor cells, PD-1 is increased in CD8+ T cells, and serial ablations increase a CSF1R+ macrophage cluster in ablated tumors. Combinational targeting of CD73, PD-L1, and CSF1R alleviates CSF1R-dependent therapeutic resistance and enhances local and systemic tumor control. This study identifies targetable countervailing mechanisms to local ablation therapy and provides a rationale for combinatorial strategies integrating serial tumor ablation with systemic immunomodulatory agents. Future prospective studies should evaluate the influence of timing, dosage, and sequence of ablation on immune priming to improve clinical interventions in pancreatic cancer.

cancer biology↗

Overlapping MHC class I/II Epitopes Program cDC1-like Differentiation of Monocyte-Derived Dendritic Cells via mTORC1 Signaling Inhibition

Viral infection polarizes monocyte-derived dendritic cells (moDC) to initiate type 1 immunity. The availability of overlapping (homologous) MHC class I and II epitopes, an occurrence frequently and primarily associated with intracellular infection, significantly enhances this process; however, the underlying mechanism(s) are unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition leads to NF-{kappa}B-mediated expression of IL-12 and other type I immune polarizing genes. The observed cDC1-like gene signature was also significantly enhanced in clinical moDC vaccine products made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel and previously unrecognized mechanism of immune governance that might also be exploited in cancer immunotherapy. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=167 SRC="FIGDIR/small/716309v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@15475borg.highwire.dtl.DTLVardef@ffe5fborg.highwire.dtl.DTLVardef@53c761org.highwire.dtl.DTLVardef@46c4ef_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Volumetric Scattering Microscopy

Optical scattering in biological tissues fundamentally limits fluorescence imaging by disrupting spatial and angular information, thereby restricting volumetric visualization. Although hardware-intensive and computational approaches have advanced scattering microscopy, practical three-dimensional imaging through tissue remains constrained by instrumental complexity and axial ambiguity. Here, we present volumetric scattering microscopy (VSM), a scan-free, optical-computational framework for three-dimensional fluorescence imaging in scattering biological media. VSM captures angularly resolved speckle-encoded fluorescence using an aperture-segmented Fourier light-field configuration and reconstructs volumetric structure through adaptive feature-based descattering and joint sub-pupil alignment. This hybrid strategy preserves angular information embedded in scattered light without wavefront measurement or mechanical scanning, while maintaining the simplicity of a standard epi-fluorescence architecture. We demonstrate high-fidelity volumetric reconstruction across phantoms, engineered cellular systems, ex vivo tissues with volumetric muscle loss, and intact Xenopus embryos, achieving preserved spatial resolution, enhanced optical sectioning, and quantitative accuracy under strong scattering conditions. VSM supports large-field, robust volumetric imaging in both layered and fully embedded scattering environments. By transforming scattered light into a structured encoding resource, VSM establishes a scalable pathway toward routine three-dimensional fluorescence imaging in complex biological systems.

bioengineering↗

Prefrontal brain-to-brain synchrony during human group hunting: Evidence from fNIRS hyperscanning

Orca, wolves, chimpanzees and humans share a similarly impressive capacity for group hunting, where individuals coordinate behaviour together to capture prey. Studying hunting behaviours has important implications for understanding how behaviour in group contexts may be indicative of cognitive decline. Despite growing interest in brain circuits for prey capture, the brain regions involved in tracking prey during a hunt and the behaviours in group hunt linked to success remain unclear. Here we combined functional near infrared spectroscopy (fNIRS) and a virtual minecraft world to examine behaviour, brain dynamics and brain synchrony involved in group hunting behaviour. We focused on the prefrontal cortex (PFC) due to its known role in planning and social coordination and recorded from pairs of individuals as they either cooperated to hunt another person (prey) or simply followed another person. Hunters were more successful if they managed to keep a smaller distance to the prey and moved at speeds that were more synchronised with their co-predator. At high-range frequencies for fNIRS (0.1-0.2Hz), we found greater brain-to-brain synchrony in lateral and medial (frontopolar) PFC regions during hunting compared with chance levels. Together, these findings provide insights into what behaviours and brain dynamics associated with successful group hunting.

neuroscience↗

Mechanical confinement drives monocyte-to-macrophage differentiation

Cells in vivo experience mechanically diverse microenvironments in which physical confinement is a pervasive but poorly understood regulator of their behavior and fate. Whether and how mechanical confinement governs immune cell differentiation remains unknown. Here, we reveal that a mechanical cue -- long-term confinement is sufficient to drive monocyte-to-macrophage differentiation through a mechanoepigenetic pathway. In vivo, differentiating monocytes exhibited flattened nuclei in the liver capsule, indicative of confinement by surrounding stromal and parenchymal structures. Using a custom cell confiner to recapitulate this confined niche, we found that confinement induces macrophage-like protrusive architectures, enhances motility, and upregulates macrophage-associated genes in RAW264.7 and THP-1 monocyte-lineage cells. Notably, extending this paradigm to primary murine bone-marrow, human umbilical-cord, and tissue-derived hepatic-associated monocytes yielded similar outcomes, thus enhancing phagocytic capacity, directly demonstrating that mechanical confinement can program monocytes into macrophages. Mechanistically, we found that confinement activates KDM6B, leading to H3K27me3 demethylation, which derepresses macrophage-specific transcriptional programs. Pharmacological inhibition of KDM6B with GSK-J4 restored H3K27me3 and blocked macrophage differentiation both in vitro and in vivo. These findings define a KDM6B-H3K27me3 axis that links nuclear mechanics to transcriptional reprogramming, positioning mechanical confinement as a "super-enhancer-like" cue for engineer macrophage function in therapeutic and bioengineering contexts.

cell biology↗

Foveated Light-Field Compound Imager

Artificial vision systems hold transformative potential for biomedical imaging, diagnostics, and translational research by emulating and extending the capabilities of biological eyes. However, current techniques often face intrinsic trade-offs between spatial resolution, field of view, and depth perception, particularly in compact, biologically relevant settings. Here, we introduce FOLIC, a foveated light-field compound imaging system, which integrates compound-eye-inspired wide angular coverage and chambered-eye-inspired spatial acuity within a unified multi-aperture concave architecture. FOLIC naturally generates peripheral, blend, and foveated zones from a single capture, enabling seamless, depth-extended, multiscale visualization from wide-field context down to single-cell lateral resolution. We validate FOLIC across diverse fluorescent and non-fluorescent specimens, including cellular phantoms, tissue sections, and small organisms, demonstrating its versatility and scalability for biomedical research and related translational applications. We anticipate FOLIC to offer a biologically informed design blueprint for future artificial vision systems. TeaserA bioinspired system unifies compound and chambered eye principles to achieve wide-field volumetric microscopy.

bioengineering↗

The enhanced multi-tissue atlas of regulatory effects in cattle

Cattle are integral to global food security, yet the molecular architecture of their complex traits remains poorly understood. Here, we present the Cattle Genotype-Tissue Expression (CattleGTEx) Phase 1 resource (https://cattlegtex.farmgtex.org/), a substantial expansion of the pilot study. By leveraging 12,422 RNA-seq profiles across 43 tissues and 82 breeds, we characterized 433,972 primary and 161,428 non-primary regulatory effects spanning seven molecular phenotypes. This high-resolution atlas resolves 75% of GWAS signals for 44 complex traits, significantly addressing the "missing regulation" in livestock. We propose a genetic regulatory model demonstrating how variants across multiple biological layers interact with specific biological contexts to shape phenotypic variation. Furthermore, CattleGTEx elucidates mechanisms underlying adaptive evolution between Bos taurus and Bos indicus, as well as artificial selection in dairy and beef breeds. Finally, by mapping evolutionary constraints on these regulatory effects, we demonstrate the translational value of this resource for prioritizing causal variants in human complex diseases. Together, Phase 1 of CattleGTEx provides a transformative framework for functional genomics, precision breeding, and comparative genetics.

genetics↗

Genetically Engineered Biomimetic Nanozymes Reprogram Immune Niches to Intercept Colitis-Carcinoma Transition

Colitis-associated colorectal cancer (CAC) arises from chronic inflammatory niches characterized by persistent oxidative stress and dysregulated immune cell recruitment. Current anti-inflammatory therapies provide only transient symptom relief and fail to prevent malignant progression due to their inability to simultaneously mitigate oxidative injury and immune chemotaxis. Our analysis of clinical samples revealed markedly elevated C-X-C motif chemokine ligand 2 (CXCL2) in intestinal tissues from patients with inflammatory bowel disease (IBD) and CAC, implicating the CXCL2-CXCR2 axis in driving excessive neutrophil and macrophage infiltration and fostering tumorigenesis. Herein, we report a biomimetic nanozymes (PB@ECM) that reprogram inflammatory immune niches to intercept CAC progression. PB@ECM integrates a Prussian blue nanozyme core with genetically engineered macrophage membranes, enabling concurrent scavenging of reactive oxygen species through superoxide dismutase- and catalase-like activities and sequestration of CXCL2 via membrane-displayed CXCR2 receptors. In murine models of colitis and CAC, PB@ECM significantly alleviated intestinal inflammation, suppressed neutrophil and macrophage infiltration, and effectively inhibited colitis-carcinoma transition. By disrupting the pathological crosstalk between oxidative stress and immune chemotaxis, this work establishes a biomimetic nanozyme strategy for preventing inflammation-driven carcinogenesis.

bioengineering↗

Structural insights into antibody responses against influenza A virus in its natural reservoir

While influenza A virus undergoes rapid antigenic drift in humans, at least some subtypes, such as H3, have relatively stable antigenicity in natural waterfowl reservoirs, despite the presence of immune pressure. However, the underlying mechanisms remain poorly understood. This study identified and characterized 187 antibodies to H3 hemagglutinin from experimentally infected mallard ducks, 18 of which were further analyzed by cryo-EM. Compared with human H3 antibodies, duck H3 antibodies exhibited higher glycan-binding propensity, more balanced immunodominance hierarchy, and targeted distinct epitopes. Other unique features of duck H3 antibodies included a convergent CDR H3-independent heavy chain-only binding mode and an N-glycosylated CDR H3 as decoy receptor. By annotating duck immunoglobulin germline genes, we also demonstrated the importance of gene conversion in duck H3 antibodies. Overall, our findings provide insights into how millennia of coevolution have shaped the interplay between influenza A virus antigenic drift and antibody responses in the natural reservoir.

immunology↗

L-Lactate reprograms tumor-associated macrophages to drive pancreatic cancer progression via BCL3 lactylation

Metabolic reprogramming fuels pancreatic ductal adenocarcinoma (PDAC) malignancy, creating a nutrient-deprived and waste-rich microenvironment. How this extreme metabolic pressure dictates the phenotypic remodeling of infiltrating immune cells remains largely unclear. Metabolomic profiling of PDAC reveals that robust tumor glycolysis proceeds without a commensurate accumulation of extracellular lactate. Integrated single-cell profiling and tissue multiplex immunofluorescence demonstrate that tumor-associated macrophages (TAMs) act as the primary consumers of tumor-secreted lactate. The uptake of L-lactate directs macrophages toward a pro-tumorigenic state through site-specific L-lactylation of the transcriptional co-regulator BCL3 at lysine 21 (K21). Functioning as a molecular switch, K21 lactylation triggers BCL3 nuclear translocation and enhances its interaction with the NF-{kappa}B p50 subunit. The ensuing BCL3-p50 complex competitively displaces the pro-inflammatory p65 subunit, rewiring the transcriptional output to suppress inflammation and enforce tumor-supporting networks. In vivo, macrophage-specific expression of a lactylation-deficient BCL3 mutant (K21R) abolishes lactate-driven phenotypic shifts and restricts tumor growth. Clinically, a BCL3-lactylated macrophage signature spatially correlates with CD8+ T cell exclusion and predicts poor patient survival, providing a strong rationale for targeting the BCL3-lactylation axis to reverse TAM-driven PDAC progression. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/710237v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@173159eorg.highwire.dtl.DTLVardef@9065f3org.highwire.dtl.DTLVardef@153e0aorg.highwire.dtl.DTLVardef@9c2678_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

ATG5 regulates autophagy-apoptosis-ER stress dysregulation in steroid-induced osteonecrosis of the femoral head (SONFH) pathogenesis

The aim is to investigate how ATG5 regulates autophagy, endoplasmic reticulum stress (ERS), and apoptosis in steroid-induced osteonecrosis of the femoral head (SONFH), and to evaluate ATG5-targeted inhibition as a SONFH intervention. Differentially expressed genes in SONFH were screened using GEO dataset GSE74089. Autophagy/apoptosis/ERS pathway activities were analyzed via GSEA, GO/KEGG enrichment, and GSVA. Rat bone marrow mesenchymal stem cells (BMSCs) were isolated for osteoblast modeling. Groups included: control (A), steroid-treated (B, methylprednisolone), and intervention (C, steroid + ATG5-siRNA). Autophagosome formation, apoptosis rate, and ATG5/PERK/LC3 expression were assessed by electron microscopy, flow cytometry, qPCR, and western blotting. Sixty SD rats were divided into three groups (as above). The SONFH model was established via intramuscular methylprednisolone injection, with intervention group receiving ATG5-siRNA. Bone pathology, cell death, and pathway regulation were evaluated using HE/TUNEL staining, electron microscopy, and molecular detection. Transcriptome analysis revealed synergistic activation of autophagy (ATG5/BECN1), apoptosis (CASP3/9/12), and ERS (PERK) pathways in SONFH, with ATG5 strongly correlating with all three. Steroids upregulated ATG5 to overactivate autophagy, triggering PERK-mediated ERS and ERS-specific apoptosis. ATG5-siRNA intervention inhibited autophagosome formation, reduced apoptosis, downregulated PERK, and alleviated trabecular fractures and empty lacunae. ATG5 deficiency blocked PERK signaling, suppressing both autophagic death and ERS-dependent apoptosis.ATG5 drives autophagy overactivation and ERS-apoptosis cascades via PERK pathway activation, constituting a core SONFH mechanism. Targeted ATG5 silencing effectively blocks this pathology, offering novel preventive/therapeutic strategies.

molecular biology↗

CEACAM5/6+ Tumor Cells and IL-1β+ Macrophages Drive Resistance to Chemo-immunotherapy in Gastric Cancer

Chemo-immunotherapy is a first-line treatment for advanced gastric cancer, yet response rates remain limited and resistance mechanisms are poorly defined. Here we generate a single-cell atlas of 542,121 cells from 35 patients treated with anti-PD-1 plus chemotherapy, profiling pre- and post-treatment tumors linked to clinical response. Integrating spatial transcriptomics, immunohistochemistry, and bulk RNA sequencing, we identify two temporally distinct resistance programs. Intrinsic resistance in pre-treatment non-responders is marked by enrichment of CEACAM5/6 tumor cells that form immune-excluded spatial niches characterized by macrophage recruitment and CD8 T-cell exhaustion. Acquired resistance in post-treatment non-responders is driven by expansion of IL-1{beta} macrophages, which induces coordinated NF-{kappa}B activation across tumor and stromal compartments, promoting PD-L1 upregulation, epithelial-mesenchymal transition, and chronic inflammation. These findings delineate an evolutionary trajectory of resistance and nominate CEACAM5/6 and IL-1{beta} as predictive biomarkers and therapeutic targets to improve anti-PD-1-based combination strategies.

cancer biology↗

Co-evolution of Oncogenic KRAS Signaling and LILRBhigh Macrophages Drives Pancreatic Cancer Recurrence

Pancreatic ductal adenocarcinoma (PDAC) frequently recurs after surgical resection, indicating that residual disease is sustained by coordinated tumor-microenvironment interactions. To define the biological basis of recurrence, we leverage large-scale clinical data from 2,710 patients, deeply characterized multi-omics profiling (whole-exome, bulk RNA, and single-nucleus sequencing) of 36 matched primary and locally recurrent PDACs, an in-house multiplex spatial imaging cohort of 190 patients, and extensive public datasets. Recurrent tumors were characterized by increased KRAS mutant allele dosage and reinforced KRAS signaling, accompanied by expansion of basal-like malignant cell states. In parallel, we identified an immunosuppressive macrophage population marked by high LILRB expression that spatially co-localized with KRAS-activated tumor cells. Functional studies showed that LILRB4+ macrophages enhanced tumor cell plasticity and progression, whereas inhibition of macrophage LILRB4 suppressed these phenotypes. Notably, a first-in-class human anti-LILRB4 antibody reduced macrophage-driven tumor traits, and dual targeting of KRAS signaling and LILRB4 achieved superior tumor control in macrophage-containing mouse models. These findings reveal a co-evolved tumor-immune niche underlying PDAC recurrence and nominate the KRAS-LILRB4 axis as a therapeutic vulnerability.

cancer biology↗

PAVR: High-Resolution Cellular Imaging via a Physics-Aware Volumetric Reconstruction Framework

The rapid convergence of advanced microscopy and deep learning is transforming cell biology by enabling imaging systems in which optical encoding and computational inference are jointly optimized for volumetric information capture and interpretation. However, broadly accessible three-dimensional imaging at high spatiotemporal resolution remains constrained by volumetric reconstruction throughput, susceptibility to artifacts, and the burden of collecting modality-matched training data. Here, we introduce PAVR, a physics-aware light-field imaging platform that integrates single-shot volumetric acquisition with fast, end-to-end volumetric reconstruction. PAVR is trained entirely using in silico system responses, avoiding reliance on external high-resolution ground-truth modalities and enabling sample-independent reconstruction across diverse biological contexts. Using fixed and live mammalian cells, we demonstrate multicolor volumetric imaging of subcellular organelles, three-dimensional tracking of autofluorescent particles, and high-speed visualization of organelle remodeling and interactions. We further extend PAVR to quantify coupled morphological and functional dynamics in beating human induced pluripotent stem cell-derived cardiomyocytes under pharmacological perturbation. Together, PAVR establishes a scalable hardware-software platform for high-throughput volumetric imaging and quantitative analysis of dynamic cellular systems in both basic and translational settings.

bioengineering↗