bioRxiv Science⌕ Search

Biology subjects

Liu, W.

Publications and source records attributed to Liu, W..

At least 91 records · Page 5Linked to original sources

Rigidity-Aware Geometric Pretraining for Protein Design and Conformational Ensembles

AO_SCPLOWBSTRACTC_SCPLOWGenerative models have recently advanced de novo protein design by learning the statistical regularities of natural structures. However, current approaches face three key limitations: (1) Existing methods cannot jointly learn protein geometry and design tasks, where pretraining can be a solution; (2) Current pretraining methods mostly rely on local, non-rigid atomic representations for property prediction downstream tasks, limiting global geometric understanding for protein generation tasks; and (3) Existing approaches have yet to effectively model the rich dynamic and conformational information of protein structures. To overcome these issues, we introduce RigidSSL (Rigidity-Aware Self-Supervised Learning), a geometric pretraining framework that front-loads geometry learning prior to generative finetuning. Phase I (RigidSSL-Perturb) learns geometric priors from 432K structures from the AlphaFold Protein Structure Database with simulated perturbations. Phase II (RigidSSL-MD) refines these representations on 1.3K molecular dynamics trajectories to capture physically realistic transitions. Underpinning both phases is a bi-directional, rigidity-aware flow matching objective that jointly optimizes translational and rotational dynamics to maximize mutual information between conformations. Empirically, RigidSSL variants improve designability by up to 43% while enhancing novelty and diversity in unconditional generation. Furthermore, RigidSSL-Perturb improves the success rate by 5.8% in zero-shot motif scaffolding and RigidSSL-MD captures more biophysically realistic conformational ensembles in G protein-coupled receptor modeling. The code is available on this repository.

bioinformatics↗

Spin-State Modulation by Atom-Cluster Synergy Steers H2O2 Conversion toward a Catalase-like Decomposition Pathway for Anti-Inflammatory Therapy

Nanozymes have emerged as promising enzyme mimics for anti-inflammatory therapy. However, their catalytic efficiency and substrate selectivity generally remain inferior to those of natural enzymes. Single-atom nanozymes (SAzymes), with isolated metal centers resembling enzymatic active sites, represent an important advance toward rational design of nanozyme, but achieving enzyme-like selectivity remains challenging. Herein, we reported a spin-state modulation strategy to prepare Fe-N-C nanozyme with coexisting single atoms and nanoclusters (FeSA+NC) via reductive-gas pyrolysis. Experimental analyses and density functional theory calculations revealed that Fe nanoclusters induced local symmetry breaking and charge redistribution around FeN4 sites, shifting the Fe centers toward a higher spin configuration and thereby modulating the free energy changes of the H2O2 conversion pathway. As a result, FeSA+NC showed dramatically enhanced catalase (CAT)-like activity (333.79 U mg-1) and suppressed peroxidase (POD)-like activity (38.49 U mg-1), achieving superior selectivity compared to Fe SAzymes (FeSA), which showed comparable CAT- and POD-like activities (62.39 and 60.39 U mg-1, respectively). Moreover, FeSA+NC achieved a higher superoxide dismutase (SOD)-like activity (929.27 U mg-1) than FeSA (249.68 U mg-1), enabling efficient SOD-CAT cascade. FeSA+NC effectively scavenged excessive intracellular reactive oxygen species, suppressed M1 macrophage polarization, and enhanced the therapeutic efficacy of intra-articular stem cell injection in a rat model of rheumatoid arthritis, a representative chronic inflammatory disease. This work highlights an atom-cluster synergy strategy for steering H2O2 conversion towards antioxidant pathway, offering a general design principle for safer, more controllable and more efficient nanozyme-based anti-inflammatory therapeutics.

bioengineering↗

Non-invasive brain stimulation biases temporal value-aversiveness computations and promotes sustainable decision-making

Environmental sustainability depends on widespread adoption of sustainable behaviors, yet the neurocomputational mechanisms supporting such choices remain poorly understood. We developed a temporal-value decision model (TVDM) to explain sustainability-related decision-making. Behavioral data showed that sustainable decisions often carry immediate aversiveness while associated outcome values that are delayed and therefore discounted, jointly limiting sustainable decisions. We replicated these effects in an independent sample and then investigated whether these mechanisms could be externally influenced. Non-invasive transcranial direct current stimulation (tDCS) targeting the dorsolateral prefrontal cortex (DLPFC) increased sustainability and this behavioral shift was accompanied by higher overall outcome valuation, reduced aversiveness, and a selective level shift for the discounting function for outcomes (but not for aversiveness). These effects were absent under sham stimulation and an active control condition. Together, the findings indicate that sustainable behavior is constrained by a temporally structured value-aversiveness conflict yet can be shifted via non-invasive brain stimulation.

neuroscience↗

Mitigating activity mixing with personalized whole-brain modeling

Mechanistic neuroimaging-based biomarkers based on localized brain activities or interactions are a central tenet in precision and personalized psychiatry. However, their accuracy may be limited by Activity Mixing that is a novel construct indicating the entanglement of any local neuronal activity with activities elsewhere in the network through long-range spatiotemporal correlations, which degrades the localization of brain-symptom associations. Here, we posit that the ill-posed inverse problem of activity mixing can be mitigated by fitting of generative whole-brain models. We developed a multi-objective fitting approach to estimate subject-specific local- and inter-areal brain-dynamics control parameters from neuroimaging observables. By integrating both synchronization and criticality metrics, this approach yields personalized parameters capture individual brain network dynamics more accurately than raw observables. In silico validation demonstrated that fitted model parameters improved brain-symptom correlation estimates by 30-85% and reduced false-negative rates by approximately [~]67% relative to conventional observables-based analyses. As in vivo proof-of-concept, resting-state magnetoencephalography (MEG) data from 230 patients with major depressive disorder (MDD) showed that aberrant brain criticality in the alpha-frequency band (11 Hz) was a significant predictor of disability with a correlation coefficient of 0.236 (95% confidence interval (CI) = [0.206, 0.266]) in 27 (CI = [23, 31]) significant cortical parcels. Model fitting both improved this correlation estimate by [~]56% up to 0.368 (CI = [0.341, 0.405]) and localized it [~]25% more narrowly to 20 (CI = [18, 22]) parcels. These findings suggest that model fitting can mitigate the effects of activity mixing and provide control-parameter estimates that delineate mechanistic biomarkers for brain disorders more accurately than the raw brain imaging observables.

neuroscience↗

Gene III Ergothioneine ameliorates alcoholic fatty liver disease: A dual strategy of accelerated ethanol elimination and reducing oxidative stress

BackgroundAlcoholic fatty liver disease (AFLD) is a progressive hepatic pathology triggered by chronic ethanol consumption, serving as the initial stage of severe liver injury. Currently, there are no FDA-approved pharmacological interventions that specifically target alcohol-induced hepatic steatosis or prevent disease progression, highlighting an urgent need for effective preventive strategies. This study evaluated the preventive efficacy and underlying mechanisms of Gene III Ergothioneine (EGT) in a clinically relevant preclinical model. MethodsC57BL/6 mice were randomized into five groups: a Control group, an alcoholic fatty liver Model group, a Positive control group treated with Silybin (100 mg/kg), and three EGT treatment groups (10, 30, and 50 mg/kg). The NIAAA mouse model was utilized to induce alcoholic fatty liver. Various biochemical, histological, and molecular markers were assessed to evaluate liver damage, alcohol metabolism, lipid profiles, oxidative stress, and inflammation. ResultsGene III EGT treatment significantly ameliorated hepatic steatosis and necrosis, as confirmed by H&E and Oil Red O staining. Notably, EGT accelerated alcohol clearance, reducing serum ethanol levels by up to 54.4% in a dose-dependent manner. Furthermore, EGT restored liver function markers (ALT, AST, GGT) and corrected dyslipidemia by lowering TG, TC, and LDL-C while elevating HDL-C. Mechanistically, EGT suppressed pro-inflammatory cytokines (IL-6, IL-1 {beta}) and mitigated oxidative stress by reducing malondialdehyde (MDA) accumulation and restoring superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. ConclusionGene III Ergothioneine prevents alcoholic liver injury through a dual mechanism: accelerating ethanol metabolism and enhancing hepatocyte antioxidative and anti-inflammatory defenses. These findings position EGT as a promising therapeutic candidate for AFLD management.

pharmacology and toxicology↗

Gene III Ergothioneine Ameliorates Exercise-Induced Fatigue by Attenuating Oxidative Stress, Inflammation, and Modulating the AMPK/PGC-1α Signaling Pathway

BackgroundExercise-induced fatigue is a complex physiological phenomenon involving oxidative stress, inflammation, and metabolic disturbances. Ergothioneine (EGT), a naturally occurring amino acid with potent antioxidant properties, has garnered interest for its potential health benefits. This study aimed to evaluate the anti-fatigue effects of Gene III(R) EGT in a mouse model of exhaustive exercise and to elucidate its underlying mechanisms. MethodsMale C57BL/6 mice were randomly divided into five groups: a control group (CTL), low-dose EGT (EGT-L, 10 mg/kg), medium-dose EGT (EGT-M, 30 mg/kg), high-dose EGT (EGT-H, 50 mg/kg), and a positive control group (Coenzyme Q10, 50 mg/kg). Mice were subjected to a 4-week treadmill training protocol, followed by an exhaustive running test. We measured exercise performance and collected blood and skeletal muscle samples at multiple time points to assess biochemical markers, inflammatory cytokines, antioxidant status, and key signaling proteins. ResultsGene III(R) EGT supplementation, particularly at medium and high doses, significantly extended the time to exhaustion and running distance. Compared to the control group, EGT treatment significantly reduced post-exercise levels of lactic acid (LA), lactate dehydrogenase (LDH), and blood urea nitrogen (BUN). Furthermore, Gene III(R) EGT suppressed the exercise-induced increase in pro-inflammatory cytokines, including IL-1{beta}, IL-6, and TNF-. The anti-fatigue effect of EGT was also associated with a reduction in malondialdehyde (MDA) and an increase in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Mechanistically, EGT promoted the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1) in skeletal muscle, while also increasing the Bcl-2/Bax ratio, suggesting enhanced mitochondrial biogenesis and reduced apoptosis. ConclusionsOur findings demonstrate that Gene III(R) EGT effectively enhances exercise performance and alleviates fatigue. The underlying mechanisms involve the mitigation of oxidative stress and inflammation, as well as the activation of the AMPK/PGC-1 signaling pathway to promote mitochondrial function and cellular protection. These results highlight the potential of Gene III(R) EGT as a nutritional supplement for combating exercise-induced fatigue.

pharmacology and toxicology↗

NRF2 pathway activation and SPP1⁺TREM2⁺ macrophages drive chemoradiotherapy resistance in esophageal squamous cell carcinoma

Esophageal squamous cell carcinoma (ESCC) is among the most aggressive cancers, with low rates of durable response to chemoradiotherapy and limited therapeutic options for relapsed disease. To uncover mechanisms of treatment resistance and relapse, we performed comprehensive multi-omics profiling of >100 pre-treatment and post-relapse ESCC tumors from a prospective clinical trial (NCT04694391), integrating whole-exome/genome sequencing, bulk RNA-sequencing, single-cell RNA sequencing, and spatial transcriptomics. We identify somatic alterations in NFE2L2/KEAP1 in nearly 40% of relapsed patients, which are associated with upregulation of NRF2 signaling targets in resistant tumors and cell line models. At single-cell and spatial resolution, relapsed tumors are enriched for NRF2-activated epithelial cells that physically co-localize with immunosuppressive SPP1TREM2 macrophages. This co-localization suggests a synergistic interaction between NRF2-driven tumor programs and macrophage-mediated immune suppression that promotes relapse after chemoradiotherapy. Our findings nominate NFE2L2/KEAP1 mutations as predictive biomarkers for patient stratification and highlight therapeutic targeting of NRF2 signaling and SPP1TREM2 macrophages as rational strategies to overcome resistance in ESCC.

cancer biology↗

CROCOpy - A Python toolbox for the analysis of CRitical Oscillations and COnnectivity

CROCOpy is a light-weighted toolbox for the assessment of neuronal oscillations, and multiple observables of functional connectivity (phase synchronization, amplitude coupling, and cross-frequency coupling) and critical dynamics (avalanches, long-range temporal correlations, bistability, and functional excitation-inhibition ratio). It was developed to simplify the analysis of continuous electrophysiological recordings and, in addition to metric computation, also includes methods for narrow-band filtering and statistical analysis. It is device-agnostic and supports both GPU and CPU computations. The toolbox also provides detailed tutorials.

neuroscience↗

Antibody Responses Against Coronaviruses in the Wuhan Population

Prolonged circulation of SARS-CoV-2 may broaden population-level neutralizing antibody responses to diverse coronaviruses; however, the extent of this breadth remains unclear. To address this gap, we assessed serum neutralizing activity in 869 individuals from Wuhan, China, including 78 pre-pandemic samples collected in 2017 and 791 post-pandemic samples obtained in 2025. Specifically, using pseudovirus neutralization assays, sera were tested against a panel of coronaviruses, including circulating SARS-CoV-2 Omicron subvariants XFG and NB.1.8.1. Neutralization was measured at a fixed dilution for all samples and by determination of 50% inhibitory dilution (ID50) for selected sera. In parallel, antigenic cartography and genetic distance analyses were applied to relate functional antigenic relationships to spike protein divergence. Our results showed that, compared with pre-pandemic sera, post-pandemic sera exhibited enhanced neutralizing activity against multiple sarbecoviruses and the merbecovirus MjHKU4r-CoV-1, with mean inhibition increases ranging from 1.7% to 76.5% at a 1:20 dilution. Notably, the largest increases from 51.8% to 76.5% were observed against clade 1b sarbecoviruses. In contrast, neutralizing activity against human alphacoronaviruses and MERS-CoV showed no meaningful enhancement. Moreover, neutralizing titers in post-pandemic sera were strongly correlated across sarbecoviruses, particularly among clade 1b viruses. Antigenic mapping further revealed that several zoonotic sarbecoviruses were antigenically closer to ancestral SARS-CoV-2 than contemporary Omicron subvariants, despite substantially greater genetic divergence. Taken together, these findings demonstrate that cumulative SARS-CoV-2 exposure promotes broadly cross-neutralizing antibody responses within the sarbecovirus subgenus and provide a quantitative framework to inform the rational design of pan-sarbecovirus vaccines and antibody-based countermeasures for future coronavirus preparedness.

microbiology↗

Z-RNA-ZBP1 axis drives Tau-mediated neurodegeneration

Although the causes of Tau aggregates vary, once Tau aggregates are formed, their neurotoxicity significantly contributes to neuronal death and cognitive decline in tauopathies, with Alzheimers disease (AD) being the most well-known example. Despite its central pathogenic role, however, effective therapeutic strategies targeting neurotoxicity of Tau remain poor. Here we demonstrate the pathogenic role of neuronal cell death in Tau-related neurodegeneration. Tau-expressing neurons undergo cell death through Z-DNA-binding protein 1 (ZBP1) activation triggered by endogenous Z-RNAs. These Z-RNAs are derived from reactivated transposable elements (TEs) that are typically silenced within heterochromatin. Tau aggregates show a strong affinity for H3K9me3-modified chromatin, effectively sequestering these epigenetic marks from Heterochromatin Protein 1 (HP1), thereby disrupting the condensation of constitutive heterochromatin. Clinically, an inverse correlation between ZBP1 expression levels in excitatory neurons and cognitive performance in AD patients was observed. Importantly, Zbp1 haploinsufficiency significantly ameliorated cognitive deficits in aged Tau-transgenic mice (24-month-old), highlighting the therapeutic potential of ZBP1 inhibition to strive against neurodegeneration in tauopathies.

neuroscience↗

Differential pairings of MAT1-1-1 and MAT1-2-1 protein variants with heteromorphic tertiary structures produced by Ophiocordyceps sinensis strains

The MAT_HMGbox domain in the MAT1-1-1 protein and the HMG-box_ROX1-like domain in the MAT1-2-1 protein play essential roles in DNA binding and regulating the transcription of genes that control sexual reproduction in Ophiocordyceps sinensis. Previous studies have reported differential occurrences, differential transcription, and alternative splicing of the MAT1-1-1, MAT1-2-1, and pheromone receptor genes in Hirsutella sinensis (Genotype #1 among 17 genome-independent genotypes of O. sinensis fungi). In this study, we further demonstrated that the DNA-binding domains of the paired MAT1-1-1 and MAT1-2-1 proteins derived from each of the 20 purportedly "pure" O. sinensis strains exhibit heteromorphic tertiary structures, as predicted by AlphaFold 3D structural modeling. These differentially paired mating proteins are characterized by different truncations, diverse 1-4 amino acid substitutions at distinct sites, altered hydrophobicity and secondary structures, and heteromorphic tertiary structures, indicating divergency in the fungal origins of the mating proteins within the mycologically and genetically impure O. sinensis strains. Our findings support the self-sterility hypothesis for O. sinensis and likely ensure the fidelity and genetic diversity of heterothallic or hybrid reproduction during the lifecycle of the Cordyceps sinensis insect-fungal complex.

biochemistry↗

TREM2 agonist antibody rebuilds the resident synovial macrophage lining barrier in rheumatoid arthritis

Rheumatoid arthritis (RA) can be viewed as a disease of barrier failure, in which CX3CR1+/TREM2+ synovial tissue-resident macrophages that form the lining barrier over cartilage and bone become fragmented and disorganized. However, how to therapeutically rebuild this barrier--and how macrophage states transition during repair--remain unclear. We engineered TR-Ab19, a mouse-selective agonistic antibody against TREM2, as a precision tool to initiate and interrogate barrier repair in vivo. TR-Ab19 engages TREM2-linked downstream signaling and redirects synovial macrophages from Clec4d+ inflammatory/proliferative programs toward TREM2+CX3CR1+Aqp1+ barrier-like states, thereby rebuilding the lining barrier. Across collagen-induced arthritis (CIA) and serum-transfer arthritis (STA) models, TR-Ab19 reduces synovitis, preserves cartilage and bone microarchitecture, limits osteoclastogenesis, and attenuates systemic cytokines and B-cell abnormalities. Single-cell RNA-seq with trajectory and cell-cell communication analyses reveal a TREM2-dependent shift toward a barrier-dominant macrophage ecosystem. Together, these findings establish antibody-mediated reprogramming of resident synovial macrophages as a barrier-centered strategy for RA and provide a framework for instructing macrophage niches in chronic inflammation.

bioengineering↗

p300/CBP-Driven Acetylation Stabilizes PARP7 to Reinforce Negative Feedback on IFN-I Signaling

Immune suppression within the tumor microenvironment (TME) remains a major barrier to effective immunotherapy, yet the molecular mechanisms that constrain type I interferon (IFN-I) signaling in tumor cells are incompletely understood. PARP7 (also known as TIPARP), a mono-ADP-ribosyltransferase, has been reported to suppress IFN-I signaling by modifying TBK1. Here, we identify PARP7 as a previously unrecognized acetylation substrate of the histone acetyltransferases p300 and CBP. We show that p300/CBP-mediated acetylation of PARP7 at lysine 32 markedly enhances its stability, thereby reinforcing repression of the TBK1-IRF3-STAT1 axis and suppressing IFN-{beta}-induced expression of interferon-stimulated genes, including CXCL10. Beyond their established function as transcriptional co-activators that support tumor cell proliferation, our findings uncover a direct role for p300/CBP in shaping innate antitumor immunity. Pharmacological inhibition of p300/CBP catalytic activity by A-485 abolishes PARP7 acetylation, accelerates its proteasomal turnover, and restores IFN-I signaling. In immunocompetent tumor models, this is accompanied by enhanced CD8+ T-cell infiltration and effector function. Together, these findings define a p300/CBP-PARP7 regulatory axis, uncover a non-canonical role for p300/CBP in innate immune suppression, and nominate this pathway as a tractable target for restoring antitumor immunity.

cancer biology↗

Synchrony within Aβ mechanoreceptor subtypes governs signal propagation to primary somatosensory cortex

Fast-conducting A{beta} slowly adapting type I low threshold mechanoreceptors (SAI-LTMRs) and A{beta} rapidly adapting type I (RAI-) LTMRs are critical for discriminative touch from glabrous skin. Recent studies used mouse genetic loss-of-function and optogenetic gain-of-function manipulations to determine that signals from these A{beta} LTMRs are integrated subcortically to build the cortical representation of touch. However, the precise influence of each subtype on downstream responses is unclear, in part because previous manipulations lacked the capacity to reproduce physiological firing patterns in individual A{beta} LTMR subtypes. Here, we took advantage of a fast variant of channelrhodopsin, CatCh, which enabled us to generate physiological spiking rates and patterns in either subtype while monitoring responses in mouse primary somatosensory cortex (S1). Doing so revealed that propagation of steady-state signals from sustained responses of A{beta} SAI-LTMRs to neural activity (spiking and local field potential) in S1 is dependent on synchronous activation of multiple A{beta} SAI-LTMRs. Asynchronous activation of the same A{beta} SAI-LTMRs rarely produced sustained responses in S1 measured at the level of single unit spiking as well as local field potentials. This suggests that the irregular firing patterns of A{beta} SAI-LTMRs during static indentations contribute to the preponderance of transient cortical responses. By contrast, both synchronous and asynchronous activation of multiple A{beta} RAI-LTMRs resulted in robust S1 responses. Overall, the temporal patterning and synchrony of activity within A{beta} LTMR subtypes govern how well their signals propagate through the ascending somatosensory system. Key PointsO_LICatCh, a sensitive and fast channelrhodopsin variant, enables pulsed-light generation of physiological spiking patterns in A{beta} low threshold mechanoreceptor (LTMR) subtypes. C_LIO_LIThe synchrony of multiple mechanoreceptors within a subtype controls the extent to which their signals influence activity in primary somatosensory cortex. C_LIO_LIA{beta} rapidly adapting type I (RAI-) LTMRs drive stronger cortical responses than A{beta} slowly adapting type I (SAI-) LTMRs, especially when considering asynchronous activation of A{beta} LTMRs within each subtype. C_LI

neuroscience↗

Twitching in sleeping premature infants provides a sensitive behavioral assay of early motor control

AO_SCPLOWBSTRACTC_SCPLOWLimb twitching is among the earliest observable behaviors in human development and a hallmark of active (REM) sleep. Systematic assessments in full-term infants have revealed functional features that informal observation cannot capture. Because preterm infants spend even more time asleep and are at heightened risk for neurodevelopmental disorders, we provide the first systematic characterization of twitching at 34-35 weeks postmenstrual age. Preterm infants exhibit an immense quantity of twitching across the body, underscoring its developmental significance. The spatiotemporal structure of twitching also changes with age, including a selective increase in finger and toe twitching. Unexpectedly, during periods of trace alternant, a precursor to quiet sleep, twitching appears in brief bouts that are almost exclusively restricted to the legs. These findings show how this abundant but overlooked sleep behavior provides a sensitive assay of the developing neural control of movement, with implications for understanding typical and atypical development.

animal behavior and cognition↗

Automating the Construction of Contextualized Biomedical Knowledge Graphs for Scientific Inference

Biomedical interactions are inherently dynamic, often shifting or even reversing under specific physiological states. However, existing extraction methods simplify these complex mechanisms into context-agnostic binary associations, resulting in semantic loss and contradictory evidence. Here, we present AutoBioKG, an end-to-end framework that constructs context-aware knowledge graphs by leveraging composite triples to encode environmental conditions and entity attributes alongside core relationships. Powered by an open information extraction model trained on BioOpenIE and further refined through self-training with pseudo-labels from unlabeled literature, the framework exhibits broad generalization. Notably, AutoBioKG achieved the highest zero-shot F1 across DDI, ChemProt, and BioRED, outperforming the best-performing baseline on each benchmark by 3.6-17.8 percentage points. Furthermore, AutoBioKG-derived graphs outperformed existing approaches on yes/no, factoid, and list questions in the BioASQ biomedical question-answering evaluation, particularly for queries requiring fine-grained contextual information. Together, these results support AutoBioKG as a scalable framework for transforming unstructured literature into structured, context-aware biomedical knowledge.

bioinformatics↗

Development of Integrin α5β1-targeted PET/NIR imaging probes for glioblastoma intraoperative navigation and intracavity targeted radionuclide therapy

Incomplete extent of tumor resection is the major factor of glioblastoma recurrence, leading to its poor prognosis. Developing therapies that enable the minimal tumor cell remnant during surgical resection is a major challenge to combat this aggressive cancer. This study develops a glioblastoma integrin 5{beta}1-selective peptide binder through series strategy screening and labeling it with 68Ga, indocyanine green (ICG), or 177Lu for efficacious multimodal treatment. This strategy combines positron emission tomography (PET) imaging for preoperative diagnosis, intraoperative NIR-II fluorescence-guided surgery for maximal tumor resection, and followed by intracavity targeted radionuclide therapy for elimination of residual tumor cells. We identified GR, with five arginine mutation, exhibiting superior integrin 5{beta}1 binding affinity and brain penetration. [68Ga]GR demonstrated substantial tumor uptake and prolonged retention time in both mouse models and tissues from glioblastoma patients. The guidance of ICG-GR achieved accurately intraoperative tumor imaging and maximal tumor resection in orthotopic mouse glioblastoma models. Notably, combining intracavity administration of [177Lu]GR following ICG-GR guiding resection markedly inhibited tumor growth and reduced possibility of tumor recurrence compared with surgery alone (unguided or ICG-GR-guided) or unguided surgery followed by [177Lu]GR. Therefore, we have reported the integrin 5{beta}1-targeted radionuclide and optical agents for maximal elimination of tumor cells during surgical resection in glioblastoma patients. HIGHLIGHTSO_LIGR is a glioblastoma-specific peptide with both favorable binding affinity superior brain penetration. C_LIO_LIICG-GR is a glioblastoma-targeted NIR probe enabling maximal surgical resection. C_LIO_LIICG-GR-guided surgery with [177Lu]GR-based adjuvant therapy allows robust elimination of tumor cells. C_LI

cancer biology↗

Targeted Chromosomal Sequencing of Wild Bonobos Identifies a Genetically Distinct Subpopulation East of the Lomami River

Bonobos (Pan paniscus), an endangered species, have for decades been genetically understudied, partly due to difficulties in obtaining high-quality samples. The study of their genome is important not only for understanding their evolution, but also for improving conservation efforts, including population management, diversity and inbreeding assessment, and tracking rescued individuals to combat illegal wildlife trafficking. Here, we use chromosome 21 target capture data from 156 non-invasively collected faecal samples from wild bonobos to perform a comprehensive analysis of their population structure. We confirm the existence of three previously suggested subpopulations identified here as Western, Central and Eastern bonobos which are defined by natural barriers of gene flow such as the Lomami River. By estimating levels of inbreeding, diversity and differentiation, we find support for isolation of mainly Western and Eastern populations and add information on the dispersal routes of their ancestors. We infer split times and separation of these populations and apply a genetic framework to geolocalize samples of unknown origin, showing that locations of their potential origin can be estimated with a precision of up to a median of [~]50 km. Our study provides valuable insight into the evolution and population structure of bonobos and reveals how rivers act as strong barriers between populations. It also offers resources for conservation efforts and highlights the need to monitor bonobo populations more closely, in particular isolated ones. ImpactBonobos have been difficult to study genetically due to their remote forest habitat and endangered status. Here we used non-invasive sampling and chromosome 21 target capture sequencing to perform the most detailed analysis to date of their population structure. We find three main subpopulations and genetic differentiation influenced by river barriers, especially with populations found on the Eastern side of the Lomami river. This data will be useful for identifying the geographic origin of confiscated samples and thus aid bonobo conservation efforts.

bioinformatics↗