Biology subjects

Zuo, Y.

Publications and source records attributed to Zuo, Y..

At least 19 recordsLinked to original sources

bioRxiv2026

Unifying physical and molecular coordinate systems across modalities in spatial biology

Establishing a unified physical and molecular coordinate system from fragmented multi-modal data is a longstanding challenge in biology. Here, we present MAPS, a modality-agnostic platform for spatial biology comprising (1) MAPS-alignment for ultrafast alignment of any modality, (2) MAPS-integration for both anchored and unanchored integration across orthogonal modalities for 3D multi-modal reconstruction, and (3) MAPS-Explorer for large-scale interactive 3D analysis. MAPS outperformed existing methods across extensive benchmarks on 34 datasets spanning 16 technology platforms and 6 modalities, while delineating fine-grained multi-modal tissue architectures across diverse biological systems in mouse and human. At cross-consortium scale, MAPS integrated 434 slices comprising 21 million cells from 18 atlases and 5 modalities to construct the most comprehensive 3D multi-modal mouse brain atlas. At individual laboratory scale, MAPS empowered routine 2D spatial assays to reconstruct continuous 3D multi-modal landscapes of human hepatocellular carcinoma, revealing the limitations of 2D spatial relationships and uncovering depth-dependent immune-state transitions.

bioinformatics↗

bioRxiv2026

Mechanically-mediated low-pressure cell membrane poration enables tunable intracellular delivery of traditionally impermeable cargoes in high throughput and clinical scale formats

Traditional intracellular delivery methods suffer from cargo inefficiencies, non-linear delivery kinetics, and cellular trauma. We designed a mechanically-mediated poration platform governed by deterministic, passive diffusion operating at low pressure which enables dose-dependent, cargo-agnostic intracellular delivery and preserves cellular homeostasis; key advantages include high-fidelity multiplexing, transient cell engineering, and direct-to-biology live-cell target engagement enabling development of novel intracellular delivery applications across drug discovery and cell therapy. We demonstrate examples including live-cell DEL discovery and MOA studies, complex and rapid cell therapy manufacturing, and assay development in sensitive primary cell types.

cell biology↗

bioRxiv2026

Transcription initiation profiling defines the regulatory logic of astrocyte gene regulation

Astrocytes are central regulators of neuroinflammation, yet the mechanisms by which they convert common inflammatory signals into cell type-specific transcriptional responses remain poorly understood. Here we mapped transcription initiation genome-wide in primary mouse astrocytes stimulated with interleukin-1B (IL-1B) and defined the active regulatory elements that drive astrocyte reactivity. We find that inducible enhancer transcription in astrocytes is encoded by a transcription-initiation grammar in which lineage-restricted transcription factors, particularly NFIA and TEAD4, cooperate with inflammatory transcription factors such as NF-{kappa}B, AP-1 and IRF to drive stimulus-dependent transcription activation. The motifs of these inflammatory transcription factors show a strong positional bias upstream of induced transcription start sites, supporting their direct role in controlling initiation upon stimulation. Moreover, NF-{kappa}B and TEAD4 motifs are preferentially associated with sites showing altered patterns of transcription initiation in response to inflammatory stimulus. Comparison with stimulated macrophages revealed that, despite substantial overlap in induced genes, astrocytes exhibit a largely distinct enhancer repertoire, indicating that shared inflammatory signals are interpreted through cell type-specific regulatory landscapes. Finally, transcribed astrocyte regulatory elements are functionally conserved in human astrocytes and are enriched for genetic risk variants associated with neurological disorders. Together, these findings define a cell type-specific regulatory logic for astrocyte inflammatory responses and link astrocyte enhancer regulation to human disease susceptibility.

genomics↗

bioRxiv2026

Dissociating the Hallucinogenic and Neuroplastic Effects of Psilocybin

It is unclear how serotonin 2A receptors (5-HT2ARs) in cortical layer 5 pyramidal neurons (L5 PyrNs) differentially contribute to psilocybin-induced hallucinations versus neuroplasticity. Here we show that psilocybin promotes synapse formation and maturation while accelerating the elimination of pre-existing synapses. Cell type-specific manipulation further demonstrated that 5-HT2AR signaling in L5 PyrNs is necessary and sufficient for psilocybin-induced synaptic remodeling but dispensable for the head-twitch response, a rodent proxy of hallucination.

neuroscience↗

bioRxiv2026

Dysregulation of a novel autophagosome-mitochondria contact contributes to autophagy dysfunction and neurodegeneration in tauopathy

Mitochondria engage in extensive communication with other organelles through membrane contacts. Perturbed mitochondria-organelle interactions are indicated in a variety of neurodegenerative diseases, but the underlying mechanisms remain poorly understood. Here, we report a new class of mitochondria-organelle communication: autophagosome/autophagic vacuole (AV)-mitochondria (Mito) contact, which exhibits hyper-tethering in tauopathy neurons, consequently hampering AV retrograde transport. Such defects are attributed to accelerated turnover of the contact release factor TBC1D15, triggered by mitochondrial bioenergetic deficit-induced hyperactivity of the AMP-activated protein kinase (AMPK). Increasing TBC1D15 levels or repressing AMPK activity normalizes AV-Mito contact release and restores retrograde transport of AVs, thereby increasing autophagic cargo clearance and reducing tau burden in tauopathy axons. Furthermore, overexpression of TBC1D15 enhances autophagic clearance and attenuates tau pathology, alleviating neurodegeneration and cognitive dysfunction in tauopathy mice. Taken together, our study provides new insights into AV-Mito contact dysregulation in tauopathy-related autophagy failure, laying the groundwork for the development of potential therapeutics to combat tauopathy diseases.

neuroscience↗

bioRxiv2026

Targeting insulo-frontal pathway to reduce stress-evoked cognitive rigidity

The anterior insular cortex (aIC), a central hub of the salience network, is engaged by cognitive flexibility tasks1,2; it is also implicated in stress-related mental disorders3-5, where cognitive rigidity is a common but poorly treated symptom1. While the insular cortexs roles in interoception and emotional regulation are extensively studied6-10, its causal contribution to cognitive rigidity remains unclear. Using attentional set-shifting tasks (AST) in mice, we identify aIC neurons projecting to the medial prefrontal cortex (mPFC) as key regulators of adaptive decision-making. These neurons show heightened activity following incorrect--but not correct--trials. This elevated activity persists into subsequent trials, providing a salience signal that enhances mPFC outcome-dependent updating and promotes convergence of neural activity patterns across trials. Optogenetic manipulation of aIC[->]mPFC projections during the pre-decision phase disrupts mPFC updating and impairs AST performance. Moreover, stress disrupts the outcome-dependence of aIC activity and impairs set-shifting. Crucially, selectively reinforcing aIC[->]mPFC activity after incorrect trials via optogenetics enhances mPFC updating, improves neural activity convergence across trials, and restores cognitive flexibility in stressed mice. These findings reveal a previously unrecognized role of the aIC[->]mPFC circuit in linking trial outcomes to adaptive decision-making and identify this pathway as a promising target for treating stress-induced cognitive rigidity.

neuroscience↗

bioRxiv2026

A lightweight, ultrafast and general embedding framework for large-scale spatial omics data

Deciphering ultra-large-scale omics data with minimal resources while maintaining high computational efficiency is a longstanding challenge in biology. Here, we present Local Pooling (LP), a lightweight, ultrafast and general framework that leverage neighbor-indexing strategy and local pooling module to generate omics embedding and compatible with variety of downstream analyses. We developed its adaptation for spatial omics, SpaLP, and evaluated it on over 20 large-scale datasets spanning 9 technology platforms. SpaLP consistently outperformed baseline methods across multiple benchmarks, including niche identification, expression reconstruction, multiple slices integration, 3D organ construction, multi-omics integration and cross-platform generalization. Notably, SpaLP processed a 1.35-million-cell mouse embryo slice in just 47 seconds, achieving up to 300-fold increase in computational efficiency compared to Graph Neural Network (GNN)-based methods. Meanwhile, SpaLP increased the average adjusted rand index (ARI) by over 30% for niche identification in simulated and realistic settings. Furthermore, we applied SpaLP to integrate 8.4 million mouse brain cells within 4 minutes on a single GPU and constructed a 3D spatial atlas. Finally, we explored SpaLPs ability of cross-platform generalization and potential for developing an omics foundation model. As a novel and general framework, we believe that LP could help more researchers develop new model on large-scale data and overcome the research barriers caused by computing resources in more fields.

bioinformatics↗

bioRxiv2025

Single-Cell Multi-Omics Dissects Transcript Isoform and Immune Repertoire Dynamics in Human Immunosenescence

Immunosenescence, a major hallmark of systemic aging, refers to the progressive functional decline of the immune system. This decline not only compromises host defense and immunological memory but also fuels chronic inflammation and tissue degeneration (collectively known as inflammaging). While single-cell RNA sequencing (scRNA-seq) has revealed transcriptomic alterations in immune aging, analyses restricted to transcript abundance fail to capture deeper regulatory layers, such as transcript isoform diversity and the remodeling of immune receptor repertoires. To address this, we present the human peripheral immune single-cell multi-omics atlas that integrates gene expression, transcript isoforms diversity, and immune receptor repertoires. By combining single-cell full-length transcriptome sequencing (scCycloneSEQ), short-read scRNA-seq, and single-cell immune receptor sequencing (scTCR/BCR-seq), we systematically profiled peripheral blood mononuclear cells (PBMCs) from healthy young and elderly donors. Our analyses uncovered extensive age-related remodeling of immune cell composition, functional states, and TCR/BCR diversity. Notably, we identified in CD4 effector memory T cells exhibited widespread differential isoform usage (DIU), 3'UTR length variation, and a marked reshaping of cytotoxic T lymphocyte (CTL) clonotypes--all closely associated with aging-related inflammation and cellular senescence. This multi-omics atlas delineates key molecular features of immunosenescence and provides a high-resolution resource for deciphering the regulatory architecture underlying immune aging.

immunology↗

bioRxiv2025

A Population-scale Single-cell Spatial Transcriptomic Atlas of the Human Cortex

The genetic and spatial determinants of cell type diversity in human cerebral cortices remain poorly defined. Here, we present a population-level single-cell spatial transcriptomic atlas of human cortices from 71 donors across the lifespan. We identified 906 layer-specific genes showing conserved and divergent laminar expression patterns between humans and other species. Spatial analysis revealed neuronal vulnerability and glial activation during aging, together with a decline in the proportion of superficial SST neurons and their interactions with other cells. Disease-associated genes exhibited high cell-type and layer-specific expression, implicating the pathogenic role of spatially specific gene expression. Spatial cis-eQTL analysis identified regulatory variants linked to genes related to diseases like Tourette syndrome. Cross-species comparison demonstrated glial expansion in the human cortex, accompanied by enhanced neuron-glia communication via the neuregulin signaling. Together, we provide a comprehensive single-cell atlas of the human cortex that is essential for understanding aging, evolution, and disease pathogenesis.

neuroscience↗

bioRxiv2025

MRTX1133 is a potent non-covalent KRAS (G12C) inhibitor with tissue-specific activity

KRAS is a high-value therapeutic target for the treatment of cancer. Two covalent inhibitors, sotorasib and adagrasib, which target a specific codon 12 mutation (G12C), have received accelerated approvals for clinical use. Studies of these inhibitors ushered in the development of new inhibitors such as MRTX1133, that had entered clinical trials as a KRAS (G12D)-selective, non-covalent inhibitor. However, the subsequent failure of sotorasib as monotherapy and the recent termination of an early-phase clinical trial for MRTX1133 indicates that developing clinically effective allele-specific KRAS inhibitors remains a challenge, and that there is a need for further evaluation of KRAS inhibition mechanisms. Here, we show that the reportedly KRAS (G12D)-selective MRTX1133 also binds to G12C mutant KRAS with high affinity and suppresses MAPK signaling in cancer cell lines harboring KRAS (G12C). Intriguingly, its effect on the proliferation of KRAS (G12C) cancer cells is context-dependent; MRTX1133 robustly inhibits the proliferation of the pancreatic cancer cell line MIA PaCa-2 as well as the tumor growth of MIA PaCa-2 mouse xenografts, but it has little effect in lung cancer cells. These findings, together with similar other recent reports, question if allele-specific KRAS inhibitors are truly selective and highlight the need for strategies that take into account tissue and context-specific processes. Significance StatementMRTX1133 is a reportedly selective, non-covalent inhibitor for the KRAS oncogene with a glycine-to-aspartate (G12D) mutation that is present in about 40% of pancreatic cancers. Despite the overwhelming preclinical success, the early-phase clinical trial of MRTX1133 was recently terminated with undisclosed results. Through our in vitro and in vivo studies, we discovered that MRTX1133 is also a potent non-covalent inhibitor of a glycine-to-cysteine (G12C) KRAS mutation that works in pancreatic cancer but not in lung cancer models. Our findings are consistent with other recent reports on the activity of MRTX1133 in non-G12D mutants and highlight challenges in developing true allele-specific KRAS inhibitors via non-covalent mechanisms while also accounting for tissue-specific effects.

cancer biology↗

bioRxiv2025

Persistent cortical excitatory neuron dysregulation in adult Chd8 haploinsufficient mice.

CHD8 mutations cause autism spectrum disorder, cognitive deficits, and macrocephaly. Chd8+/- mouse models exhibit macrocephaly and transcriptional pathology, with inconsistent findings regarding neurogenesis, neuron function, and behavior. Via stereology and single nucleus transcriptomics (snRNA-seq), we found increased Chd8+/- cortical volume was not explained by increase in neuron number. Differential expression (DE) was present across cortical cell types, with excitatory neurons exhibiting high DE burden and shared and subclass-specific DE signatures. Bulk RNA-seq DE of constitutive Chd8+/- and conditional Camk2a-Cre Chd8+/-mice identified shared transcriptional pathology. DE in synaptosomal versus nuclear mRNA identified overlapping DEGs, but also significant differences and exaggerated synaptosomal changes. Building on DE findings implicating glutamatergic neurons, we found Chd8+/-mice exhibited altered excitatory neuron spine density and dynamics, decreased GCaMP activity correlation, and sleep perturbation. Thus, Chd8 haploinsufficiency causes lasting excitatory neuron dysfunction, perturbs RNA regulation beyond transcription, and impacts neuronal properties, cortical microcircuits, and behavior.

genomics↗

bioRxiv2025

Single-Nucleus Transcriptomics Identifies Neuroblast Migration Programs Sensitive to Reelin and Cannabis in the Adolescent Nucleus Accumbens

The nucleus accumbens undergoes extensive maturation during adolescence, but how drug exposure and genetic vulnerability interact to shape this process remains poorly understood. Here, we used single-nucleus RNA sequencing to examine the effects of chronic adolescent tetrahydrocannabinol (THC) exposure and reduced Reelin signaling in mice. THC produced broader transcriptional changes than Reelin haploinsufficiency, particularly in medium spiny neurons (MSNs). Analysis of cell-cell communication identified a THC-sensitive signaling program in which inhibitory interneurons were the principal receivers of MSN-derived signals related to axon-guidance and synaptic maturation. Despite the dominant effect of THC, both perturbations converged on shared gene networks linked to human genetic risk for substance use and psychiatric disorders. These effects were strongest in a population of immature neurons that we confirmed are generated in the adolescent nucleus accumbens and decline in adulthood. These findings show that adolescent THC exposure and Reelin signaling converge on transcriptional programs that regulate late neuronal maturation in striatal circuits.

neuroscience↗

bioRxiv2025

The Caenorhabditis elegans spe-21 gene that encodes a palmitoyltransferase is necessary for spermiogenesis.

In most animals, spermatids that are produced must further differentiate into fertilization-competent spermatozoa after completing meiosis. In Caenorhabditis elegans, this process is known as spermiogenesis or spermatid activation and it results in the transformation of round, non-motile spermatids into amoeboid, motile spermatozoa. Spermatid activation in C. elegans is also associated with the fusion of Golgi-derived vesicles called the membranous organelles (MOs) with the plasma membrane. This fusion process is required for producing a fertilization-competent surface on the sperm by placing MO-carried, resident proteins onto the spermatozoon membrane. We have identified, cloned, and characterized the role of spe-21, also designated as dhhc-5, during both hermaphrodite and male spermatid activation. spe-21 null mutant worms are severely sub-fertile at all studied growth temperatures. spe-21 mutant spermatids fail to activate either in vivo or in vitro after treatment with known chemical activators. We have found that spe-21 is necessary for MO fusion and pseudopod formation in spermatids. The spe-21 gene encodes a predicted four pass transmembrane protein with a conserved Asp-His-His-Cys (DHHC) tetrapeptide zinc finger motif embedded in a cysteine rich region (DHHC-CRD type zinc finger motif). Generally, proteins with DHHC-CRD motifs catalyze the post-translational addition of palmitate to their protein substrates and are called palmitoyltransferases or palmitoylacyltransferases (PATs). We also found that mNeonGreen-tagged SPE-21 localizes to the MOs in spermatids. Together, our findings show that SPE-21 is an MO localized palmitoyltransferase required for proper spermatid activation and creation of fertilization-competent spermatozoa.

developmental biology↗

bioRxiv2024

Water use efficiency of Cupressus gigantea is higher in mountain slope habitats compared to riverside habitats

Cupressus gigantea is an endemic species of the Yarlung Zangbo River in Tibet, China, and is designated as a national key protected wild plant. It is only distributed in the narrow area along Yarlung Zangbo River from Jiacha County to Danniang village Milin City in various habitats such as the waterline along the Yarlung Zangbo River, terraces, and mountain slopes. In this study, we utilized stable isotope technology ({delta}D, {delta}18O, and {delta}13C), combined with the IsoSource model, to quantitatively determined the sources of water absorption and the water use efficiency of C. gigantea in various habitats, including riverside area, terraces and mountain slopes. The results showed that the content of soil total nitrogen, soil nitrate nitrogen, soil ammonium nitrogen, and soil organic carbon are significantly higher on mountain slope than in the other two habitats, while the total carbon content, water content, and total nitrogen content of C. gigantea leaves are significantly lower on mountain slope than in the other two habitats (P<0.05). The water use efficiency (WUE) of C. gigantea in the mountain slope habitats is 107.8 mol mol-1, which is significantly higher than that of other habitats (P<0.05), with the WUE of C. gigantea in the riverside habitat being the lowest at 35.7 mol mol-1. C. gigantea distributed on the mountain slope and terrace uses soil water as the main water source. During the normal rainy season, the proportion of soil water utilization is the highest, accounting for more than 60%; in the dry season, the utilization of river water and groundwater increases, while soil water utilization decreases. C. gigantea distributed along the riverside mainly absorbs water from the Yarlung Zangbo River, about 63%. In August when the rainfall increases in the rainy season, the use of soil moisture increases, and in the dry season, river water becomes the main water source. This indicates that with the alternation of rainy and dry seasons, the water absorption sources and strategies of C.gigantea adjusted accordingly. The research results provide an important scientific basis for the protection and management measures of the C. gigantea population.

ecology↗

bioRxiv2024

The cornerstone of early diagnosis and immunotherapy of prostate cancer:screening characteristic genes

BackgroundProstate cancer (PCA) has become a common malignant tumor globally, posing a substantial risk to the health of middle-aged and elderly men. However, there is still a lack of effective strategies for early detection and treatment of prostate cancer. The introduction of gene therapy in recent years has shown promise as a potential approach for cancer diagnosis and treatment. Methodology & Theoretical OrientationThe training set data GSE45016, GSE46602, and GSE69223 from the Gene Expression Omnibus (GEO) dataset, along with validation training set data GSE17951, were utilized. Differentially expressed genes (DEGs) between normal individuals and tumor patients were identified by combining the training set data. Subsequent analyses including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) were conducted on the DEGs. WGCNA analysis was then performed on the gene expression matrix to identify module genes highly correlated with PCA, followed by the application of the LASSO algorithm to obtain PCA candidate genes. The candidate genes were validated using the area under the receiver operating characteristic (ROC) curve (AUC) to determine key feature genes. Finally, the relationship between key characteristic genes and immune cells was explored. FindingsA total of 54 DEGs were identified, with 26 down-regulated genes and 28 up-regulated genes. The GO function analysis revealed enrichment in processes such as establishment of protein localization to membrane and protein targeting to membrane. KEGG analysis showed enrichment in pathways like eutrophil degranulation, neutrophil activation involved in immune response, and regulation of cell morphogenesis. GSEA analysis highlighted enrichment in pathways like CTRL_VS_ACT_IL4 AND ANTI_IL12_12H_CD4_TCELL_DN. Through WGCNA and LASSO regression analysis, key characteristic genes MARCKSL1, TMTC4, and TTLL12 were identified, with AUC values greater than 0.8 in both the training and validation sets, and were found to be closely associated with immune cell infiltration. Conclusion & SignificanceMARCKSL1, TMTC4, and TTLL12 emerge as crucial genes in the process of PCA, showing significant relevance to immune cell infiltration.this study offers valuable clinical insights into the diagnosis and treatment of prostate cancer through the identification of specific genes associated with the disease.

genomics↗

bioRxiv2023

EfNST: A composite scaling network of EfficientNet for improving spatial domain identification performance

Spatial Transcriptomics (ST) leverages Gene Expression Profiling while preserving Spatial Location and Histological Images, enabling it to provide new insights into tissue structure, tumor microenvironment, and biological development. The identification of spatial domains serves as not only the foundation for ST research but also a crucial step in various downstream analyses. However, accurately identifying spatial domains using computational methods remains a tremendous challenge due to the poor computational performance of many existing algorithms. Here, we propose EfNST, a deep learning algorithm based on a composite scaling network of the EfficientNet Network, designed specifically for the analysis of 10X Visium spatial transcriptomics data. We applied EfNST to three different datasets: human Dorsolateral Prefrontal Cortex, human breast cancer and mouse brain anterior. EfNST outperforms five advanced competing algorithms, achieving the best Adjusted Rand Index (ARI) scores of 0.554, 0.607, and 0.466, respectively. Notably, EfNST demonstrated high accuracy in identifying fine tissue structure and discovering corresponding marker genes with an improved running speed. In conclusion, EfNST offers a novel approach for inferring spatial organization of cells from discrete datapoints, facilitating the exploration of new insights in this field.

bioinformatics↗

bioRxiv2023

Translational modulation by ISRIB alleviates synaptic and behavioral phenotypes in Fragile X syndrome

Fragile X syndrome (FXS) is caused by the functional loss of Fragile X messenger ribonucleoprotein (FMRP), a translational regulator that binds the transcripts of many proteins involved in synaptic function and plasticity. Dysregulated protein synthesis is a central effect of FMRP loss and to date direct translational modulation has not been leveraged in the treatment of FXS. Thus, we examined the effect of the small molecule translational modulator, Integrated Stress Response Inhibitor (ISRIB), in treating synaptic and behavioral symptoms of FXS. Using a combination of population-level single synapse analysis, in vivo two-photon microscopy, and behavioral analysis, we revealed a mechanism for the appearance of dense and immature dendritic spines, which are observed in human FXS patients and Fmr1 knockout (KO) mice. Our data suggest that FMRP loss at the synapse dysregulates synaptic protein abundance and that spines are disproportionately stabilized through increased PSD-95 expression but prevented from maturing through reduced synaptic accumulation of glutamate receptors. ISRIB rescues these molecular and synaptic deficits in FXS and improves social recognition in Fmr1 KO mice. These findings highlight the therapeutic potential of targeting core translational mechanisms and the differential impact of FMRP on synaptic and cellular function in FXS and neurodevelopmental disorders more broadly.

neuroscience↗

bioRxiv2023

Toward single cell tattoos: Biotransfer printing of lithographic gold nanopatterns on live cells

Lithographic nanopatterning techniques like photolithography, electron-beam lithography, and nanoimprint lithography (NIL) have revolutionized modern-day electronics and optics. Yet, their application for creating nano-bio interfaces is limited by the cytotoxic and two-dimensional nature of conventional fabrication methods. Here, we present a biocompatible and cost-effective transfer process that leverages (a) NIL to define sub-300 nm gold (Au) nanopattern arrays, (b) amine functionalization of Au to transfer the NIL-arrays from a rigid substrate to a soft transfer layer, (c) alginate hydrogel as a flexible, degradable transfer layer, and (d) gelatin conjugation of the Au NIL-arrays to achieve conformal contact with live cells. We demonstrate biotransfer printing of the Au NIL-arrays on rat brains and live cells with high pattern fidelity and cell viability and observed differences in cell migration on the Au NIL-dot and NIL-wire printed hydrogels. We anticipate that this nanolithography-compatible biotransfer printing method could advance bionics, biosensing, and biohybrid tissue interfaces. TOC Figure O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=97 SRC="FIGDIR/small/542285v1_ufig1.gif" ALT="Figure 1"> View larger version (54K): org.highwire.dtl.DTLVardef@16f6e1corg.highwire.dtl.DTLVardef@a60bacorg.highwire.dtl.DTLVardef@1485d06org.highwire.dtl.DTLVardef@1d365c9_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗