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Wang, Q.

Publications and source records attributed to Wang, Q..

At least 91 records · Page 5Linked to original sources

MVCBench: A Multimodal Benchmark for Drug-induced Virtual Cell Phenotypes

Drugs induce coordinated phenotypic changes across multiple modalities, including transcriptional reprogramming and cellular morphological remodeling. Predicting these drug-induced modality changes is central to drug discovery, mechanism-of-action studies and precision therapeutics, however, prediction performance depends critically on how both drug compounds and cellular states are represented. Despite rapid advances in drug molecular and gene representation methods, a systematic evaluation of these methods remains lacking. Herein, we introduce MVCBench, a comprehensive benchmarking framework for evaluating drug molecular and gene representation methods in predicting drug-induced multimodal virtual cell (MVC) phenotypes. MVCBench leverages large-scale transcriptomic and high-content imaging data and systematically evaluates 24 representation methods (12 drug molecular and 12 gene representation methods) across nearly 1.1 million drug-induced profiles, under both in-distribution and out-of-distribution settings spanning unseen compounds, cell lines, assay plates and datasets. Our benchmarking reveals a pronounced modality-dependent asymmetry: advanced drug molecular representations substantially improve the prediction of drug-induced morphological phenotypes but provide only limited gains for gene expression prediction relative to classical fingerprints, whereas task-specific gene representations outperform general-purpose foundation models in predicting drug-induced transcriptomic responses. Predictive performance also deteriorates sharply under distribution shift, highlighting persistent challenges in cross-dataset and cross-platform generalization. We further show that integrating transcriptomic and morphological modalities consistently improves prediction accuracy, and derive practical design principles for MVC architectures, including modality-aware loss calibration and fusion strategies. Together, MVCBench provides a systematic foundation for evaluating representation methods and offers guidance for developing robust MVC models of drug-induced cellular responses.

bioinformatics↗

PARP1 regulates the genomic ribonucleotide processing activity of TOP1 to prevent the formation of toxic TOP1-DNA adducts and the associated mutations.

Ribonucleotides are frequently incorporated into our genome during replication. Canonically, RNase H2 is responsible for the removal of these embedded ribonucleotides. Alternatively, DNA topoisomerase 1 (TOP1) has also been shown to have genomic ribonucleotide processing activity. When this process occurs at short tandem repeat (STR) sequences, it can lead to 2-5 bp deletions. These deletions are the result of two sequential cuts by TOP1 at sites of ribonucleotide incorporation. In this study, we have determined that PARP1 regulates the TOP1-mediated excision of ribonucleotides by preventing the formation of TOP1-DNA adducts that occur through a second cleavage following the initial ribonucleotide cut by TOP1. We biochemically defined the mechanism by which this regulatory inhibition of TOP1 occurs, which involves both PARP1 physically restricting TOP1 from the cleavage site followed by the inhibitory PARylation of TOP1. We also show that this activity means that PARP1 prevents the TOP1-dependent deletions at STRs in cells. In the absence of both a functional RNase H2 complex and PARP1, we demonstrated that cells appear to be in a senescent state provoked by the accumulation of TOP1-DNA adducts, which are a result of TOP1 being unimpeded to remove genomic ribonucleotides. Our work has elucidated the role of PARP1 in preventing the deleterious consequences of the processing of genomic ribonucleotides by TOP1. Understanding this mechanism could help us develop therapies that better sensitize tumors to PARP inhibitors, especially in cancers that present loss-of-function RNase H2 mutations (seen in certain chronic lymphocytic leukemia and prostate cancers).

biochemistry↗

Identification of scavenger receptor BI as a scavenger of free heme that is essential for protection against hemolysis

Severe hemolysis is a life-threatening condition with limited therapeutic options. Although haptoglobin and hemopexin sequester hemoglobin and heme, these protective systems are rapidly saturated during acute hemolysis, leading to the accumulation of cytotoxic free heme. In this study, we identify scavenger receptor BI (SR-BI) as a critical mediator of free heme clearance. SR-BI binds heme and facilitates its hepatic uptake under pathological conditions. Mice lacking hepatic SR-BI exhibit impaired heme clearance and increased susceptibility to heme- and hemolysis-induced lethality. Pharmacological upregulation of hepatic SR-BI via imatinib or adenoviral delivery confers protection against heme toxicity. Using a humanized model of sickle cell disease (SCD), we further demonstrate that sickle hepatopathy significantly reduces hepatic SR-BI expression compared to non-SCD littermates, potentially increasing vulnerability to heme-induced injury. Notably, adenoviral-mediated SR-BI upregulation rescues SCD mice from heme toxicity. These findings reveal a previously unrecognized mechanism of heme detoxification via hepatic SR-BI and identify a promising therapeutic target for hemolytic disorders. One-Sentence SummaryIdentification of scavenger receptor BI as a targetable scavenger of heme in hemolysis

physiology↗

Hemodynamic phenotypes linked to high-altitude subclinical organ damage

BackgroundChronic exposure to high-altitude hypoxia imposes sustained cardiovascular stress, yet hemodynamic adaptation among healthy high-altitude dwellers is heterogeneous and remains poorly characterized. This study aimed to identify distinct hemodynamic phenotypes in a healthy high-altitude population using unsupervised machine learning and to evaluate their association with multi-system subclinical target organ damage. MethodsThis cross-sectional study enrolled 694 healthy adults permanently residing at [&ge;]3300 m on the Qinghai-Tibet Plateau. Unsupervised K-means clustering was performed on nine hemodynamic variables, including peripheral and central blood pressures, augmentation index (AIx), pulse pressure amplification ratio (pPP/cPP), and systolic pressure amplification (pSBP-cSBP). Differences across phenotypes in carotid intima-media thickness (IMT), estimated glomerular filtration rate (eGFR), left ventricular mass index (LVMI), and pulse wave velocity (PWV) were assessed using one-way ANOVA with Bonferroni-corrected post-hoc tests. ResultsThree distinct hemodynamic phenotypes were successfully identified. The C2 (Balanced Adaptation) phenotype (n = 245) demonstrated the most favorable hemodynamic profile, characterized by the lowest blood pressure and augmentation index (AIx) values, along with the highest peripheral-to-central pulse pressure ratio (pPP/cPP). The C1 (Vascular Stress) phenotype (n = 267) presented with normal peripheral systolic blood pressure (125.9 {+/-} 11.3 mmHg) but exhibited markedly elevated wave reflection indices, including the highest heart rate-adjusted augmentation index (AIx@HR75: 31.9 {+/-} 9.7%) and the lowest pPP/cPP ratio (1.29 {+/-} 0.08). The C3 (High-Load Decompensation) phenotype (n = 182) displayed significantly elevated blood pressures and the greatest overall hemodynamic load. Regarding target organ damage, a clear gradient was observed across the three phenotypes. The C3 phenotype showed the highest carotid intima-media thickness (IMT: 1.162 {+/-} 0.23 mm) and left ventricular mass index (LVMI: 69.18 {+/-} 40.73 g/m{superscript 2}). Conversely, the C2 phenotype exhibited the highest estimated glomerular filtration rate (eGFR: 97.38 {+/-} 16.38 mL/min/1.73m{superscript 2}) and the lowest IMT (0.994 {+/-} 0.26 mm). The C1 phenotype consistently displayed intermediate values for all organ damage indicators. After Bonferroni correction, all pairwise comparisons for LVMI and pulse wave velocity (PWV) reached statistical significance (all P < 0.05). ConclusionsHealthy high-altitude individuals manifest three distinct hemodynamic phenotypes arrayed along a cardiovascular risk continuum. The novel Vascular Stress (C1) phenotype represents a "masked" high-risk state characterized by normal peripheral blood pressure but elevated arterial stiffness and wave reflection, challenging sole reliance on brachial pressure for risk assessment. This phenotype-based stratification provides a framework for precision prevention and early intervention in high-altitude populations.

physiology↗

The Ser83, Arg85, Tyr88, Asn124, Lys192 of C-terminal Lipid-associated membrane hemagglutinin affecting Mycoplasma synoviae agglutination of erythrocyte

Mycoplasma synoviae is an avian pathogen that causes respiratory disease and synovitis, and its hemagglutinin plays a critical role in host cell adhesion. However, the key residues and structural mechanisms underlying hemagglutination remain unclear. In this study, domain analysis of the hemagglutinin family of Mycoplasma synoviae revealed that it contains long-chain and short-chain types, among which LAM HA (VY93_RS01465) was selected as the bait protein due to its complete C-terminal conserved domain. Through yeast two-hybrid screening, 18 host proteins interacting with LAM HA were identified. Furthermore, five key amino acid residues S83, R85, Y88, N124, and K192 were found to mediate hemagglutination activity. Deletion of these residues reduced the hemagglutination titer of LAM HA under acidic conditions. Secondary structure analysis showed that the deletion mutation decreased the -helix content while increasing the proportions of {beta}-sheet and random coil. Molecular dynamics simulations revealed that the mutant exhibited generally higher root mean square deviation and root mean square fluctuation values than the wild-type under different pH conditions, with a marked decrease in structural stability particularly at pH 5.0 and 6.0. These findings indicate that LAM HA, as a critical adhesin, exerts its hemagglutination function dependent on specific key residues and pH-sensitive conformational stability. IMPORTANCEMycoplasma synoviae (M. synoviae) causes significant economic losses to the poultry industry worldwide. Lipid-related membrane protein hemagglutinin (LAM HA) is a surface adhesin essential for host cell attachment, but its precise amino acid residues and structural features have not been defined. In this study, five key residues (S83, R85, Y88, N124, and K192) were identified as critical for LAM HA-mediated hemagglutination activity. Deletion of these residues altered the secondary structure composition, reduced conformational stability under acidic pH conditions, and decreased hemagglutination activity. These findings reveal a previously unknown structure-function relationship of M. synoviae LAM HA, demonstrating that its hemagglutination activity depends on specific residues and pH-sensitive structural integrity. This provides new insights into the molecular mechanisms of M. synoviae adhesion and offers potential targets for the development of novel intervention strategies against avian mycoplasmosis.

microbiology↗

Low-Intensity Focused Ultrasound Enhances Meningeal Lymphatic Drainage for Preventing Cognitive Decline in Alzheimer's Disease

Meningeal lymphatic vessels (mLVs) are vital for brain waste clearance, making them a promising therapeutic target. However, effective modulation strategies for mLVs with translational potential remain underdeveloped. Here, we develop a low-intensity focused ultrasound (LIFU) strategy that precisely targets the vault cranial meninges to non-invasively facilitate mLVs drainage. Using models of Alzheimers disease (AD) and aging, we demonstrate that this approach promotes CSF drainage, prevents cognitive decline, and reduces pathological biomarkers. Mechanistically, RNA sequencing combined with calcium imaging in vitro reveals that LIFU activates the Piezo1 ion channel in lymphatic endothelial cells, whereas pharmacological inhibition of Piezo1 abolishes LIFUs therapeutic effects. Compliant with FDA safety guidelines, this LIFU protocol demonstrates strong clinical translatability. If its efficacy is clinically confirmed, LIFU offers a promising therapy for neurodegenerative diseases triggered by waste accumulation.

neuroscience↗

AI-Guided Structure-Aware Modeling and Thermal Proteomics Reveal Direct Demethylzeylasteral-ACLY Interaction

Target deconvolution of bioactive natural products (NPs) is frequently hampered by the inability of traditional thermal shift assays to distinguish direct ligand binding from indirect proteomic stabilization. Here, we developed an integrated target discovery framework combining MAPS-iTSA thermal proteomics with a structure-aware graph neural network (HoloGNN). This strategy identified ATP-citrate lyase (ACLY) as a high-confidence target of Demethylzeylasteral, a bioactive triterpenoid from Tripterygium wilfordii. Crucially, orthogonal biochemical assays, including surface plasmon resonance and limited proteolysis, validated its direct binding (KD = 9.86 M) and profound enzymatic inhibition (IC50 = 3.84 M). To establish the relevance of this interaction in the context of the source herb, thermal profiling of Tripterygium wilfordii extract together with ACLY-based affinity-ultrafiltration mass spectrometry supported ACLY engagement and identified Demethylzeylasteral as an ACLY-binding constituent. Given the established role of ACLY-mediated lipid metabolic reprogramming in psoriasis, we further evaluated the pharmacological significance of this interaction. Demethylzeylasteral suppressed keratinocyte proliferation, alleviated imiquimod-induced psoriasiform dermatitis, and reduced inflammatory cytokine expression in vivo. Single-cell RNA sequencing further revealed reversal of ACLY-SREBP-associated lipogenic reprogramming in keratinocytes. Collectively, these findings establish ACLY as a functionally relevant target of DEM and provide a robust AI-chemoproteomic paradigm for mechanism-guided NP drug discovery.

biochemistry↗

Ocrelizumab Modulates Both B and T Cell Immune Capacities in Multiple Sclerosis

To understand the molecular and cellular mechanisms beyond B-cell depletion with the anti-CD20 monoclonal antibody ocrelizumab, we used comprehensive muti-modal flow cytometry and functional assays in a prospective longitudinal multiple sclerosis (MS) cohort. Ocrelizumab depleted the vast majority of B cells and showed selective effects on different B cells subsets. Analysis of residual/replenished B cells revealed relative enrichment of regulatory B cells like CD27+CD43+ B1 and CD24hiCD38hi transitional B cells, and reduction of CD27+ memory B cell subsets and CD19+IgD+CD27-naive B cells at early time points (1-3 month) and before subsequent infusions at 4-7 months, 11-14 months, and >18 months. CD20+ T cells and peripheral helper T-cells (Tph) were also reduced. RNA sequencing analysis showed B1 cells have significantly higher expression of LGALS1, KCNN4, ITGB1, and IL2RB. Compared to transitional B cells, B1 cells also displayed significantly higher expression of tissue homing molecules ITGAX (CD11c), S100A4, ITGB1, and CXCR3. IL10 signaling pathway is increased in these B cells. Ex vivo B cell functional assays indicated the residual/replenishing B cells were anergic following ocrelizumab, with increased IL10/TNF and IL10/IL6 ratios under BCR stimulation. Ocrelizumab treatment may create a self-reinforcing regulatory circuit: the reduction of Tph cells could alleviate suppression of regulatory B cells, which subsequently expand and further promote regulatory T cell networks via IL2RB, LGALS1, and an increased IL-10 signaling pathway.

immunology↗

Effect of dietary Chitosan supplementation on Intestinal Barrier Function and Growth Performance in weaned piglets challenged by Enterohemorrhagic haemolytic Escherichia coli

Enterohemorrhagic Escherichia coli O157:H7 (EHEC) is an important zoonotic pathogen that disrupts intestinal epithelial barrier integrity and induces excessive inflammatory responses, thereby leading to impaired growth performance and intestinal injury. EHEC is also an important cause Hemolytic Uremic Syndrome (HUS) in children and older adults. In pig production, chitosan is considered a promising alternative to antibiotics due to its bioadhesive and antimicrobial properties, but the effects and underlying mechanisms of chitosan (COS) under pathogenic challenge remain to be elucidated. One hundred and eight pigs were randomly divided into three treatments: an unchallenged control group (CON), an EHEC-challenged control group (ECON), and an EHEC-challenged group supplemented with 100 mg/kg COS (ECOS). Results show that EHEC challenge increased the feed conversion ratio (FCR), increased inflammatory cytokine levels, disrupted intestinal morphology, and downregulated tight junction and nutrient transporter gene expression (P<0.05). Dietary COS supplementation significantly improved average daily gain (ADG) and FCR during day 6-14 (P<0.05). Moreover, COS reduced fecal shedding of total E. coli (P = 0.085) and EHEC, attenuated systemic inflammation by decreasing serum TNF- and IL-6 levels, and enhanced humoral immunity as indicated by increased IgA and IgM concentrations (P<0.05). Importantly, COS alleviated EHEC-induced intestinal injury by restoring villus height and villus-to-crypt ratio, with enhanced mucosal digestive enzyme activities, and upregulated expression of tight junction proteins (ZO-1 and occludin) and nutrient transporters (SGLT-1 and PEPT1) (P<0.05). In conclusion, these findings indicate that dietary COS improves growth performance in EHEC-challenged weaned pigs, with enhanced intestinal barrier integrity and nutrient transport capacity.

microbiology↗

Gradient Multinozzle 3D Printing

Direct ink writing is compatible with an expansive materials palette. While enabling diverse applications, this materials versatility brings significant bottlenecks in ink formulation, often requiring the mixing, printing, and testing of dozens to hundreds of ink compositions over the course of a project. To accelerate ink-space exploration, we introduce gradient embedded multinozzle (GEM) printheads that combine the high-throughput parallelized printing of multinozzles with combinatorial ink mixing. These printheads allow simultaneous mixing of two-, three-, and four-input inks which are distributed to printer nozzles to create complex 3D structures with graded compositions of inks. Using a two-way GEM printhead, we vali-date cell compatibility by printing scaffolds containing various concentrations of fibroblasts and observing non-linear compaction behaviours. We next test a three-way GEM multinozzle to print ten compositions of di- and multi-functionalized poly(ethylene-glycol) diacrylate hydrogel tri-leaflet valves, optimizing for stiffness, swelling ratio, and toughness. Our GEM multinozzles are compatible with open-source printers and either pressure- or volume-driven extrusion systems and promise to accelerate iterative ink design and testing.

bioengineering↗

Endothelial ACKR1 expression regulates neutrophil infiltration and breast cancer metastatic engraftment in the lung metastatic niche

The formation of the premetastatic niche prepares distant tissues for tumor cell engraftment. Endothelial cells are critical mediators of premetastatic niche formation, orchestrating extravasation of circulating tumor cells and critical pro-tumor immune cells, such as neutrophils. In mouse models of breast cancer, we show that primary tumors upregulate the non-signaling chemokine receptor ACKR1 in the endothelium of the lung premetastatic niche. ACKR1-expressing venules were found to be preferential sites of neutrophil and tumor cell localization within lung tissue. A newly generated conditional ACKR1 allele was used to show that endothelial-specific removal of ACKR1 expression significantly reduces metastatic engraftment in the lung. When ACKR1 is activated by tumor-secreted factors, endothelial ACKR1 functions to promote neutrophil recruitment within the lung parenchyma. We conclude that ACKR1 is a critical component of the endothelial response to tumors at the metastatic site of the lung, leading to neutrophil recruitment and promotion of tumor cell metastasis. SUMMARYEndothelial cells play critical roles in breast cancer metastasis. ACKR1 is upregulated in the endothelium of the lung metastatic niche in response to primary mammary tumors. Endothelial ACKR1 expression was found to promote neutrophil infiltration into the metastatic niche and support breast tumor cell metastasis to the lung.

cancer biology↗

Training constrains neural routes to knowledge assembly

A hallmark of human intelligence is the ability to rapidly restructure existing knowledge when new information reveals unexpected connections, a capacity termed knowledge assembly. This cognitive flexibility distinguishes human learning from artificial systems, which catastrophically forget when acquiring new relationships. Understanding the mechanisms underlying flexible knowledge reorganization thus has implications for continual learning in both humans and algorithms. Here, using electroencephalography we show that successful knowledge assembly depends on temporally orchestrated reactivation of prior neural representations. Critically, training schedules bias learners toward different representational strategies: blocked training promotes compressed certainty-weighted codes, while interleaved training yields high-dimensional factorized representations. Vanilla recurrent networks failed to develop human-like certainty geometries despite identical training, revealing missing computational principles in current artificial systems. These findings demonstrate that cognitive flexibility emerges through creative reuse of learned representations, with training history constraining available neural routes to reorganization.

neuroscience↗

IgG Propels Atherosclerosis by Noncanonically Activating Macrophages

Despite being a central component of adaptive immunity and a highly abundant serum protein, the contribution of IgG to the milieu of atherosclerosis remains unappreciated. Here, we identify a pro-atherogenic role for IgG as it activates an innate immune cascade, independent of its classical antigen-neutralizing function. Analyses of human coronary artery plaques reveal a positive correlation between IgG and cardiovascular and cerebrovascular disease severity. Integrated single-cell plaque analyses localize IgG, coinciding with its recycling receptor FcRn, to pro-inflammatory and foamy macrophages. Genetic ablation of FcRn in myeloid cells prevents IgG from accumulating in mouse atherosclerotic lesions, diminishing plaque size and inflammation. Mechanistically, IgG acts as an endogenous ligand for TLR4, triggering NF-{kappa}B-NLRP3 inflammasome signaling without requiring its antigen-binding domain. Additionally, IgG accelerates macrophage foam cell formation through upregulation of downstream effector LCN2. Our work uncovers a role for previously overlooked adaptive immune molecules in the pathogenesis of atherosclerosis through a noncanonical mechanism linked with innate immunity.

immunology↗

IR-AMES uncovers structure and composition of Alzheimer' s tau oligomers

The structure and composition of biomolecular assemblies shape their biological functions and disease processes. Yet existing approaches either require homogeneous samples or lack chemical specificity and sensitivity, limiting the elucidation of transient oligomeric species under native conditions. Here we report infrared absorbance-modulated evanescent scattering (IR-AMES) that enables ultrasensitive structural and compositional profiling of individual biomolecular assemblies in aqueous environments. This capability is achieved by photothermally encoding mid-infrared vibrational absorption into scattering contrast using a total-internal-reflection geometry. Applying IR-AMES to recombinant tau assemblies, we resolve random-coil monomers and the emergence of heterogeneous oligomers beyond ensemble-averaged measurements. In Alzheimer's disease brain-derived tau, IR-AMES reveals enrichment of antiparallel {beta}-sheet structures and RNA components in oligomers. Using lipid nanodiscs as membrane mimics, we find that pathological tau oligomers exhibit enhanced interactions with anionic membranes. IR-AMES enables spectroscopic imaging of diverse biomolecular assemblies, opening opportunities to elucidate structure-function relationships in heterogeneous biomolecular systems.

biophysics↗

Microencapsulation of a novel Bacteroides thetaiotaomicron strain: a promising strategy to fortify intestinal barrier fortification in weaned pig model

Porcine Bacteroides thetaiotaomicron LYH5 demonstrated in vitro antimicrobial activity, suggesting probiotic potential. Due to poor gastric juice tolerance, LYH5 was encapsulated via extrusion using sodium alginate (SA) and gellan gum. Box-Behnken design optimization yielded optimal parameters: SA 1.5%, gellan gum 0.4%, CaCl2 0.9%, bacteria:glue ratio 1:4, achieving an encapsulation rate of 84.22{+/-}0.17%. Its effect on weaned piglet intestinal health was evaluated using 78 piglets (7.69{+/-}0.52 kg) randomly assigned to 4 groups for 40 days: CON (control), T (basal diet + LYH5 live bacteria, 1x10{superscript 1} CFU/mL), TJ (basal diet + LYH5 microcapsules, 1x10{superscript 1} CFU/mL, J (basal diet + empty capsules). The results of this experiment showed that compared with the control group, LYH5 microcapsule can improve the intestinal barrier function without affecting the growth performance of piglets, and provide ideas and references for the development of human next-generation probiotics (NGP). IMPORTANCEThis study addresses the key bottleneck of poor gastric acid tolerance of probiotics via microencapsulation and provides a practical reference for the development of human next-generation probiotics.

microbiology↗

TMEM106B mediates ACE2-independent replication of the SARS-CoV-2 S-E484D variant in airway-derived cell models

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to cause significant respiratory disease, particularly in vulnerable populations. Although ACE2 is the primary receptor for viral entry, previous studies have identified a naturally occurring, ACE2-independent entry pathway in certain airway-derived cell lines. Utilization of this pathway depends on surface heparan sulfates and requires the E484D substitution within the receptor-binding domain of the viral Spike (S) protein. In this study, we expand the panel of airway-derived cell lines that support ACE2-independent, S-E484D-dependent replication and identify the host lysosomal transmembrane protein TMEM106B as a critical host factor for infection. Knockout of TMEM106B completely abolishes infection by SARS-CoV-2 SE484D in NCI-H522 and NCI-H661 cells. Moreover, ectopic expression of the luminal C-terminal domain (CTD) of TMEM106B-either alone or redirected to the plasma membrane - is sufficient to enable viral entry and infection in otherwise non-permissive cells. We further show that Fc-TMEM106B-CTD decoy protein blocks infection by SARS-CoV-2 SE484D, supporting a direct interaction between the S-E484D protein and TMEM106B-CTD. Finally, passaging experiments with a chimeric VSV-SARS-CoV-2 SE484D identify additional mutations within the heptad repeat 1 that enhance TMEM106B utilization and viral spread in the ACE2-independent cell models. Together, these findings demonstrate that TMEM106B is a key mediator of a naturally occurring ACE2-independent pathway in multiple airway-derived cells lines and suggest that variation in the Spike protein can expand receptor usage by SARS-CoV-2. IMPORTANCESevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to acquire mutations in the viral spike (S) protein as it circulates in humans. How these mutations influence the cell and tissue tropism of SARS-CoV-2 remains poorly understood. While ACE2 is the canonical host cell receptor for SARS-CoV-2, previous studies revealed the presence of a naturally occurring ACE2-independent entry pathway in multiple airway-derived cell lines that can be utilized only by a SARS-CoV-2 variant bearing the E484D substitution within the viral S protein. Here we expand the airway-derived cell line models that support ACE2-independent and S-E484D-dependent entry and show that the host lysosomal transmembrane protein, TMEM106B, is an essential viral entry factor. Although the E484D substitution is currently rare in human isolates, our findings raise the possibility that small mutations in SARS-CoV-2 S can allow the utilization of alternative entry pathways that broadens its cell and tissue tropism.

microbiology↗

SR2P: an efficient stacking method to predict protein abundance from gene expression in spatial transcriptomics data

Spatial transcriptomics data are largely available with RNA expression alone, limiting the detection of cell states defined by surface protein abundance. The lack of multi-omics spatial data limits the ability to identify immune cells and their signaling in the tumor microenvironment, as most solid tumors are immunologically poor and exhibit protein-RNA abundance discordance in critical immune cell surface markers. Although emerging technologies enable spatial multi-omics profiling, technical and cost constraints remain a hurdle. We introduce SR2P, a stacking-based machine-learning framework for predicting spatial protein abundance from RNA expression. SR2P integrates 11 complementary predictive models and consistently outperforms existing methods across multiple spatial multi-omics benchmark. We showcased an application of SR2P recovered macrophage-enriched regions and identified potential immune markers associated with therapeutic response from head-and-neck squamous cell carcinoma patients. SR2P enables protein-abundance inference from RNA-only spatial data, extending the analytical capabilities of current spatial platforms for studies of tumor immunology.

bioinformatics↗

Comparative study on the inhibition of copper oxide, nickel, and sodium tungstate on microbially induced concrete corrosion under sewer conditions

Microbially induced concrete corrosion (MICC) is a significant issue that reduces the service life of sewer systems. Bacteriostatic agent in concrete can inhibit microbial activity and the process of MICC to some extent. However, a systematic comparison of the inhibition effects of various bacteriostatic agents on MICC remains lacking. In this study, three bacteriostatic agents (copper oxide, nickel, and sodium tungstate) were investigated for their inhibitory effects on MICC. For each inhibitor, the cement mortar coupons with 0.05 wt%, 0.1 wt%, and 0.2 wt% of the inhibitor were prepared. The coupons were partially submerged in sewage of a controlled laboratory corrosion chamber (20 {+/-} 5 ppm H2S) to simulate the tidal region of gravity sewer. During the 56 days of exposure, the intensification of pores, cracks, surface erosion, and spalling was observed on all coupons. After 56 days of exposure, the sulfate concentration and adenosine triphosphate (ATP) content of coupons without inhibitor were 10.65 mg/cm2 and 30.17 {+/-} 3.87 mol/cm2, respectively. They were higher than those of coupons containing 0.05 wt%, 0.1 wt%, and 0.2 wt% of copper oxide and 0.05wt% of nickel. The temporal profiles of ATP of coupons without inhibitor was similar to those of coupons containing sodium tungstate. After exposure for 28 days, the surface pH of coupons without inhibitor was 7.45, meanwhile of those coupons containing 0.2 wt% of copper oxide and 0.05 wt% of nickel were 9.42 and 9.93, respectively. Those results indicated that the bacteriostatic effect of copper oxide and nickel (0.05 wt %) was found to be the most prominent. The findings indicate that a single bacteriostatic agent is only effective during specific corrosion stages, suggesting that a combination of multiple agents may be a promising strategy to combat the multi-stage MICC process over the long term. This study provides a theoretical basis for the selection and development of protective materials against concrete corrosion in sewer networks.

microbiology↗