Biology subjects

Yi, J.

Publications and source records attributed to Yi, J..

At least 19 recordsLinked to original sources

bioRxiv2026

Refactored intracellular domains enhance CAR expression and function

Chimeric antigen receptor (CAR) intracellular domains (ICDs) couple antigen recognition to T-cell activation. Here we worked with AI agents to refactor CAR ICDs, proposing designs and refining them as measurements accumulated over three rounds. This approach yielded KRGR-{zeta}1-40, a 45-amino-acid ICD less than a third the length of the clinical 4-1BB-CD3{zeta} (BB{zeta}) ICD. Compared with BB{zeta}, KRGR-{zeta}1-40 increased CAR surface expression and antigen-driven IFN-{gamma} release, without detectable antigen-independent IFN-{gamma} release. KRGR-{zeta}1-40 extended CAR expression and target-cell killing after transient mRNA delivery, supported the expression of four CARs from a shared mRNA dose, and enhanced B-cell depletion after lentiviral and lipid-nanoparticle delivery. These results show that iterative agent-guided design with experimental feedback can yield compact ICDs that enhance CAR expression and sustain CAR T-cell function.

bioengineering↗

bioRxiv2026

Oscillatory correlates of visuomotor control under varying amount of feedback delay

A weighted integration of visual and proprioceptive movement feedback is key for an adaptive body representation by the brain. Previous work has suggested a relationship between alpha and beta oscillations in sensory cortices and inter-sensory attentional control under visuo-proprioceptive incongruence compared with congruence; and frontal theta oscillations as a marker of the related cognitive-attentional control and response inhibition. Here, we asked whether these oscillatory correlates indicate a gradual adjustment of attention and the corresponding sensory weights, rather than merely a response to conflict per se. Thus, we adopted a recently developed virtual reality based hand-target phase matching task: Participants had to track a target oscillation with recurrent grasping movements of a virtual hand, which they controlled via a data glove. We added a small or a large delay to the virtual hands movements, introducing varying amounts of visuo-proprioceptive conflict. Concurrent EEG recordings revealed a delay-dependent modulation of (i) sensorimotor beta oscillations, (ii) oscillations "entrained" at key movement frequencies over central-parietal sensors, and (iii) mid-frontal theta oscillations. Granger causality analysis suggested that entrained oscillations were more strongly predictive of visual kinematic signals, whereas the prediction of somatosensory kinematics was attenuated depending on the amount of delay. Finally, phase-amplitude couplings suggested that sensorimotor beta coupled with the movement-related oscillations as well as mid-frontal theta. Our results thus establish key oscillatory correlates that scale with the amount of visuo-proprioceptive conflict during visually guided action.

neuroscience↗

bioRxiv2026

Learning shapes neural codes for sensory-motor integration in the tail of the striatum

Separating meaningful sensory stimuli from irrelevant ones requires learning sensorimotor associations, but how sensory-linked striatal circuits acquire and maintain these associations is unclear. We longitudinally imaged direct- and indirect-pathway (D1 and A2a) spiny projection neurons (SPNs) in the tail of the striatum (TS) as mice learned to push or pull a joystick in response to auditory cues in either a stimulus-response association (go/omit) task or a two-alternative forced choice (2AFC) task. Learning in both tasks increased the fraction and strength of task-modulated TS SPNs across the sound, action, and reward epochs, yet individual neuron selectivity often switched over days between behavioral epochs. In spite of individual neuron variability, population activity of direct and indirect pathways became aligned with characteristic behavioral features during learning: D1-SPNs dominated the action category, A2a-SPNs were biased toward the mixed category (multiple epochs), and both SPN types showed sound category specificity that depended on the sound-action association. Trial-wise modeling revealed a reweighting of behavioral predictors within the action window, with reward gaining and movement losing predictive weight. Learning the two-choice task led to a higher prevalence of association-preferring neurons and better behavioral decoding within the sound window than in the action/reward window, reflecting a task-dependent prioritization of sensory information. Association-preferring neurons also showed a stable local distance-similarity relationship, with nearby neurons more similar than distant neurons across learning. Together, our results support a population mechanism in TS during learning in which neurons from both direct and indirect pathways are recruited and take on distinct behavioral roles that vary with performance and task complexity.

neuroscience↗

bioRxiv2026

Gut-derived metabolic reprogramming drives immune aging and tissue degeneration

Aging is characterized by changes in gut microbiome, metabolic imbalance and chronic inflammation, yet how these processes integrate to drive tissue degeneration remains poorly defined. Using age-related macular degeneration (AMD) as a model of tissue aging, we identify a diet-induced metabolic-immune axis that promotes systemic and retinal degeneration. In mice, a high-fat, cholesterol-enriched (HFC) diet induced perturbations in the gut structural integrity and microbiome repertoire, as well as systemic metabolic aging signatures, prominently marked by reduced circulating histidine. Plasma histidine levels were similarly decreased in AMD patients and inversely correlated with body mass index (BMI) in control donors. These diet-induced gut microbiome changes and subsequent metabolic alterations promoted peripheral innate immune reprogramming, with expansion of inflammatory neutrophils and monocytes that infiltrated the outer retina in a mouse model. Mechanistically, the gut-derived IGF1R/AKT2 signaling acts as a central regulator of global epigenetic remodeling and systemic immune aging under high-fat conditions in C. elegans. In a mouse model with an age-dependent dry AMD-like pathology, distinct retinal pigment epithelium (RPE) subpopulations exhibited downregulation of the histidine transporter SLC7A5, linking metabolic stress to activation of MIF/CD74-dependent inflammatory signaling between RPE and infiltrating immune cells. Histidine supplementation or AKT2 phospho-state modulation attenuated systemic immune activation and rescued retinal degeneration. These findings identify histidine-axis dysregulation as a mechanistic bridge between diet-induced microbiome changes, metabolic stress, immune aging, and retinal degeneration.

cell biology↗

bioRxiv2026

Computational aberration-corrected volumetric imaging of single retinal cells in the living eye

The eye offers a unique non-invasive window for accessing single-cell level structures and functions of the central nervous system (CNS) throughout the retina. However, strong and space-varying ocular aberrations, along with limited volume rates, challenge large-scale cellular imaging in living eyes and stymie the full potential of possible biological and pathological studies in retina. Here, we present plenoptic illumination scanning laser ophthalmoscopy (PI-SLO), a 3D fluorescent retinal imaging modality that enables high-speed, widefield, volumetric single-cell imaging with low phototoxicity. By capturing multiple angular images of fluorescence signals from the entire volume, PI-SLO enables digital aberration correction and 3D imaging across a >20{o} FOV with >23 Hz volume rate. We leverage this structural and functional imaging modality to investigate three key aspects of CNS physiology through the living mouse retina, including: microglial process dynamics, vascular perfusion, and light evoked calcium fluxes in inner retinal neurons. PI-SLO is a versatile non-invasive platform for in vivo investigation of retinal and CNS physiology at the cellular level.

bioengineering↗

bioRxiv2026

Genome-scale mapping of variant, enhancer and gene function in primary human CD4+ T cells

CD4+ T cells harbor a disproportionate enrichment of immune disease risk loci and represent the primary cellular context for immune disease biology, yet the genes and regulatory programs these variants affect remain largely unknown. We combined targeted Perturb-seq of 1,032 cis-regulatory elements (CREs) overlapping 4,724 variants across 14 immune diseases with genome-wide Perturb-seq of all expressed genes in primary human CD4+ T cells, spanning 4.1 million cells. We identified 626 CRE-gene pairs, and connected CRE targets to downstream regulatory cascades. At the TYK2 and DEXI/CLEC16A loci, we resolved target genes and linked noncoding variants to inflammatory and metabolic programs. Across diseases, we revealed that dispersed variants converged on shared and disease-specific programs. Our work provides a framework for tracing variant-to-CRE-to-gene-to-network in disease-relevant primary cells.

genetics↗

bioRxiv2026

Deciphering Cell Cycle Dynamics and Cell States in Single-cell RNA-seq data with SPAE

Rapid advances in single-cell RNA sequencing (scRNA-seq) technology have enabled the investigation of gene expression changes at the single-cell level, particularly for elucidating the heterogeneity among cells and complex biological processes. This technique reveals subtle molecular differences within individual cells, thereby offering a unique viewpoint for the investigation of cell cycle progression, cellular differentiation, and disease pathogenesis. However, accurately identifying and analyzing cell cycle dynamics in scRNA-seq data remains challenging due to the complexity of the data and the subtle differences between cell states. To address this challenge, we developed the integrated Sinusoidal and Piecewise AutoEncoder (SPAE), an autoencoder-based piecewise linear model, for characterizing the cell cycle dynamics and cell states in scRNA-seq data. Compared with existing methods, SPAE demonstrates substantially improved accuracy and robustness in cell cycle characterization. Additionally, SPAE can accurately predict cancer cell cycle transitions and effectively facilitate the removal of cell cycle effects from gene expression data. SPAE is available for non-commercial use at https://github.com/YaJahn/SPAE.

bioinformatics↗

bioRxiv2026

Enhancing volumetric microscopy with blind computational correction of spatially variant aberrations using neural field representation

Studying biological processes across multi-millimeter scales requires imaging systems that combine high spatial resolution with a large field of view (FOV). However, optical aberrations degrade image quality, particularly in large-FOV systems where distortions gradually worsen toward the periphery. Existing methods for correcting field-dependent aberrations are limited and often impractical. Hardware-based solutions such as adaptive optics demand additional components and sample manipulation, increasing system complexity and experimental burden. Computational approaches, while promising, typically rely on exhaustive point spread function (PSF) calibration or large training datasets, restricting their applicability. We introduce a self-supervised algorithm that simultaneously estimates spatially varying aberrations and reconstructs 3D sample structure from a single blurred image--without PSF calibration or training data. Our method was implemented on optically cleared mouse hippocampal neurons and cortical vasculature imaged with oblique plane microscopy (OPM), as well as in vivo mouse retinal vasculature captured with adaptive optics scanning laser ophthalmoscopy (AOSLO), where PSF calibration is infeasible. The algorithm predicts and corrects aberrations across multi-millimeter FOVs, enhances contrast in low signal-to-noise regions, and reveals critical structural details in neuronal and vascular systems that are obscured in raw images. This approach enables high-resolution, large-scale imaging without hardware modifications, expanding the accessibility of advanced microscopy techniques.

bioinformatics↗

bioRxiv2026

Threshold-Free Neural Network Models for Swim Bout Detection of Larval Zebrafish

Accurate detection of swim bouts is essential for decoding motor behavior in larval zebrafish, yet conventional threshold-based methods rely on subjective cutoffs and per-experiment tuning. To address this limitation, we developed threshold-free deep learning models operating on tail-curvature time series: an offline model for post hoc analysis and an online model for real-time detection. Both improved precision over threshold-based methods, particularly for low-amplitude bouts. Using the offline model, we show that a head-fixed, closed-loop preparation largely preserves naturalistic swimming kinematics. Repeated trials reduced bout frequency and increased interbout interval, whereas genetic background primarily affects bout duration and maximum amplitude; notably, casper larvae lacked the late-trial decline observed in wildtype and nacre. We further show that detector choice can alter inferred behavioral outcomes. Together, these results establish a high-throughput framework for robust and reproducible analysis of zebrafish swimming behavior across experimental conditions.

bioengineering↗

bioRxiv2025

Versatile high-speed volumetric imaging from microscopic to macroscopic scale by self-adaptive oblique plane microscopy

There is an increasing need for large-scale high-speed volumetric recording in complex multi-cellular model systems to define dynamic processes. Oblique plane microscopy (OPM) provides a solution that features oblique illumination, rapid optical scanning, and remote focusing to achieve real-time 4D microscopy. OPM implements light sheet imaging via a single primary objective lens, making the entire space below the objective accessible for large specimens, such as living mouse brain. Yet it is challenging to adopt OPM beyond a microscopic scale (i.e. size < 1mm), limiting its broad applications. Here we present a self-adaptive OPM that leverages Abbes sine condition to unlock its flexibility across a range of field-of-views (FOVs) (up to 8 mm2) and resolutions (down to 2.2 {micro}m3). This versatility enables brain-wide single neuron volumetric calcium imaging in behaving larval zebrafish (1x0.4 mm2 FOV at 5 Hz) and capillary blood cell tracking in living mouse brain (>3x3 mm2 FOV) with a sweeping 0.32 mm wide volume section at 100 Hz. In optically cleared mouse brain, the flexibility allows a screen-and-zoom capability by sequentially imaging the whole brain at low-and-high magnifications to locate and resolve subcellular structures such as dendritic tress and spines. By offering a switchable imaging resolution, volume, and speed, the self-adaptive OPM achieves a versatile platform for studying a wide range of multi-cellular model system, whether in vivo or fixed and optically cleared.

bioengineering↗

bioRxiv2025

An ancient transcription factor functions as the master regulator of primary cilia formation

How ancient transcription factors are repurposed during evolution to drive the functional diversification of conserved organelles remains a fundamental question in biology. Although highly conserved in basic morphology, eukaryotic cilia vary extensively in their sizes and functions. Previously, we showed that an evolutionarily ancient transcription factor, X chromosome-associated protein 5 (Xap5), controls motile ciliogenic transcriptional programs during mouse spermatogenesis (Wang et al., 2025). Here we show that Xap5 functions as the master regulator of primary ciliogenesis. Xap5 associates with the nuclear protein Non-POU domain-containing octamer-binding protein (Nono) to form a regulatory module that directly binds and activates the transcription factors Sox5 and Sox9. Genetic ablation of Xap5 or Nono impairs primary ciliogenesis, and loss of Sox5 disrupts the downstream ciliogenic program, consistent with the established role of Sox9. Collectively, our results provide new insight into how complex ciliary transcription factor networks determine ciliary diversity during evolution, and suggest that defects in this regulatory axis may contribute to the etiology of human ciliopathies.

cell biology↗

bioRxiv2025

A non-canonical AKT1-TERT pathway coordinates autophagy and ERphagy

The retinal pigment epithelium (RPE) sustains lifelong proteostasis under chronic stress, yet how post-mitotic cells activate autophagy when canonical kinase pathways suppress it remains unresolved. Here we demonstrate that AKT1, conventionally regarded as an autophagy suppressor, drives autophagy through a non-canonical transcriptional mechanism triggered by isoform imbalance. In RPE and age-related macular degeneration (AMD) models, AKT2 hyperactivation destabilizes mTORC2 and engages S6K-mediated IRS-1 inhibition, creating a feedforward autophagic arrest. Compensatory AKT1 activation via mTORC2 phosphorylates telomerase reverse transcriptase (TERT) at Serine 824, driving nuclear translocation that is independent of telomere maintenance. In the nucleus, TERT assembles with FOXO3 and MYC into a tripartite transcriptional complex that occupies the EIF2AK3 promoter, enabling PERK transcriptional activation. This activity converts the unfolded protein response from pro-apoptotic to cytoprotective: PERK-ATF4 signaling drives biogenesis of core autophagy machinery while simultaneously inducing selective ERphagy through the receptors TEX264 and CCPG1, which prevents pathological PERK clustering and preserves tubular ER architecture in diseased RPE. Using C. elegans phosphorylation-deficient mutants, mouse models and AMD patient induced pluripotent stem cell-derived retinal pigment epithelium (iPSC-RPE), we establish that AKT1-mediated TERT phosphorylation is an evolutionarily conserved prerequisite for FOXO/DAF-16 nuclear function and lysosomal homeostasis in post-mitotic cells. Pharmacologic targeting of AKT2 with a first-in-class dual-pocket allosteric inhibitor selectively enhances AKT1 compensation, restoring macroautophagic and ERphagy flux across disease models. These findings reveal a kinase-to-transcription axis that reprograms organelle quality control and identify the AKT1-TERT-PERK-ATF4 pathway as a therapeutic target in proteostasis-driven disease.

cell biology↗

bioRxiv2025

CellBin:a generalist framework to process spatial omics data to cell level

Spatial omics has rapidly expanded with increasingly diverse imaging modalities, molecular targets, and chip sizes. However, no general framework currently exists to construct cell level matrices that are robust across platforms and omics types. Here we present CellBin, a universal and scalable frame-work that unifies image stitching, cell segmentation, and spot-to-cell mapping for multiple spatial omics technologies. CellBin integrates a multi-field weighted stitching algorithm for large-area images, a family of U-Net-based models trained across diverse staining modalities, and an optimized computational architecture for high-throughput processing. Across five technological platforms and three omics data types, CellBin achieves robust segmentation and accurate single-cell matrix construction, consistently outperforming seven state-of-the-art methods in F1-score, cell size precision, and annotation accuracy. By providing a generalizable, cross-platform solution, CellBin bridges multiple spatial omics, enabling unified, high-resolution cell level analyses across technologies.

bioinformatics↗

bioRxiv2025

Single nucleus multiomic atlas of human dorsal root ganglia reveals the contribution of non-neuronal cell types to pain

Sensory neurons residing in dorsal root ganglia (DRG) transmit sensory information such as pain, itch, touch, pressure and bodily position to the central nervous system. The activity of sensory neurons is regulated by non-neuronal cell types in the DRG, including satellite glial cells (SGCs), immune cells and fibroblasts. Dysregulated gene expression in DRG cells contributes to sensory nervous system disorders such as chronic pain. Understanding the genetic underpinnings of these conditions requires dissecting transcriptional regulation in human tissue. In this study, we profiled transcriptomic and chromatin accessibility landscapes from postmortem human DRG (hDRG) samples at single-nucleus level. We demonstrate that sequencing depth significantly impacts downstream analysis, with deeper sequencing yielding more detected cells and features, improved data integration, refined clustering and annotation, and more accurate scientific interpretations. We identified nine major cell types, defined their molecular signatures, and mapped cis-regulatory landscapes. Integration of gene expression with chromatin accessibility enabled peak-gene association and transcriptional network analyses, revealing transcription factors, their target genes, regulatory elements and potential partners that cooperatively drive cell-type-specific gene expression programs. This integrative approach identified cell types, genes, and cis-regulatory regions potentially driving pain conditions. Our unbiased genome-wide analysis not only recovered known pain-related genes but also highlighted novel candidate genes and regulatory regions implicated in pain mechanisms. Importantly, our results demonstrate that non-neuronal cells, including endothelial cells, fibroblasts, macrophages, and SGCs, play critical roles in pain pathogenesis and should be investigated as therapeutic targets. One Sentence SummaryOur work provides a comprehensive single-nucleus multi-omic atlas of human dorsal root ganglia, uncovering novel cell-type-specific regulatory mechanisms and candidate therapeutic targets for pain, thereby directly advancing translational insights into human sensory disorders and chronic pain pathogenesis.

neuroscience↗

bioRxiv2025

A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies

The human peripheral nervous system (PNS) consists of many ganglia including sympathetic ganglia (SG) and dorsal root ganglia (DRG). These ganglia house the cell bodies of diverse PNS neurons that transmit autonomic and sensory signals, as well as a much larger number of non-neuronal cells. However, the molecular and cellular diversity of these human PNS cell types and their implications in human disease remain elusive. By generating an integrated single-cell multi-omic atlas of human SG and DRG, we provide comprehensive transcriptional and epigenomic landscapes of various cell types in these peripheral ganglia. While the major cell types and their cell-type-specific transcriptional and epigenomic features are similar between human SG and DRG, we identify key differences between SG and DRG cell types. These differences highlight the distinct molecular and cellular mechanisms underlying their specific functions. We also profiled key genomic regulatory networks that govern cell-type-specific gene expression in these peripheral ganglia. Moreover, by mapping the expression and chromatin accessibility of disease-associated genes in human SG and DRG, we identify cell types that may underlie various peripheral neuropathies. This atlas serves as a valuable resource for understanding the intricate cell-type-specific molecules and interactions in the human PNS and their implications in human health and diseases.

neuroscience↗

bioRxiv2025

Enteric ChAT-expressing neurons as new target for Lactobacillus plantarum ameliorates inflammatory bowel diseases

The gut microbiota plays a crucial role in inflammatory bowel diseases (IBD), yet how specific microbial components influence disease progression remains incompletely understood. Our study reveals that decreased abundance of Lactobacillus species correlates with ulcerative colitis severity in patients. Among tested strains, L. plantarum A736, isolated from traditional fermented foods, demonstrated remarkable efficacy in ameliorating dextran sulfate sodium (DSS)-induced colitis in a mouse model. Strikingly, multi-omics analysis revealed that L. plantarum A736 uniquely enhances choline acetyltransferase-expressing (ChAT+) neurons in the enteric nervous system and elevates acetylcholine (ACh) levels. Further analysis identified that L. plantarum A736 metabolizes tryptophan to produce indole-3-lactic acid (ILA), and supplementation with ILA significantly mimics this strains anti-inflammatory effects by activating ChAT+ neurons. Crucially, selective ablation of colonic ChAT+ neurons completely abolished the therapeutic benefits of both L. plantarum A736 and ILA, establishing their essential role in mediating these effects. These findings demonstrate for the first time that microbial metabolites can directly modulate enteric neuronal circuits to regulate gut immunity. The identified ILA-ChAT+ neuron axis represents a novel neuro-immune pathway that could be targeted for IBD treatment. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/673902v1_ufig1.gif" ALT="Figure 1"> View larger version (63K): org.highwire.dtl.DTLVardef@1e0d3c5org.highwire.dtl.DTLVardef@16f5481org.highwire.dtl.DTLVardef@152283org.highwire.dtl.DTLVardef@18cfad0_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2025

Recovery of retinal terminal fields after traumatic brain injury: evidence of collateral sprouting and sexual dimorphism

The central nervous system is characterized by its limited regenerative potential, yet striking examples of functional recovery after injury in animal models and humans highlight its capacity for repair. Little is known about repair of pathways/circuits after traumatic brain injury (TBI), which results in disruption of connectivity. Here we utilize a mouse model of diffuse traumatic axonal injury (Impact-acceleration TBI) in order to explore, for the first time, the evolution of structural and functional changes in the terminal fields of the injured visual system. Retinal ganglion cell (RGC) axons and synapses were genetically labeled via AAV transduction, while anterograde and transsynaptic tracers were used to mark terminals and postsynaptic cells. Functional connectivity and visual integrity were assessed by monitoring c-Fos expression following light stimulation and pattern-reversal visual evoked potentials (pVEPs). Our findings demonstrate that, although TAI results in approximately a 50% loss of RGC axons and terminals, surviving RGCs undergo collateral sprouting, a form of compensatory branching of surviving axons, that restores terminal density to pre-injury levels. Transsynaptic tracing and c-Fos mapping confirmed the reestablishment of connectivity, which was also associated with significant improvements in visual function as measured by pVEPs. Interestingly, the recovery process exhibited sexual dimorphism, with female mice showing delayed or incomplete repair. Moreover, collateral sprouting proceeded normally in Sarm1 knockout mice, evidence of some independence from Wallerian degeneration. Our findings show that collateral sprouting may be an important mechanism of circuit repair in TAI and may represent a promising target for therapeutic interventions. SignificanceHomotypic collateral sprouting -the process by which uninjured axons from the same neuronal source extend new branches to reinnervate targets deprived of their original connections- is a fundamental yet understudied mechanism for CNS repair following injury. Unlike heterotypic sprouting, involving sprouting from unrelated pathways, homotypic sprouting offers potential to restore circuit architecture after partial lesions. Here, we employed a model of diffuse axonal injury in the mouse visual system to examine this mechanism. Our research demonstrates surviving retinal ganglion cell axons can re-establish terminal fields, achieving structural and functional connectivity. Importantly, we discovered significant sex differences: female mice showed delayed/incomplete recovery compared to males. These findings provide evidence of repair of brain circuits perturbed by TBI and the role of homotypic sprouting.

neuroscience↗

bioRxiv2025

Multimodal retinal imaging by visible light optical coherence tomography and phosphorescence lifetime ophthalmoscopy in the mouse eye

SignificanceOxygen metabolism is important to retinal disease development, but current imaging methods face challenges in resolution, throughput, and depth sectioning to spatially map microvascular oxygen. AimTo develop a multimodal system capable of simultaneous phosphorescence lifetime imaging scanning laser ophthalmoscopy (PLIM-SLO) and visible light optical coherence tomography (VIS-OCT) to capture capillary-level oxygen partial pressure (pO2) and structural volumes in rodents. ApproachC57BL/6 mice were imaged by VIS-OCT with high-definition (10 kHz raster) and Doppler (100 kHz circular) protocols. Phosphorescent probe Oxyphor 2P was retro-orbitally injected to enable intravascular PLIM-SLO imaging (200 {micro}s pixel dwell time), while a tunable lens was used to adjust the focal depth. The extracted phosphorescence lifetimes were used for pO2 calculation. Simultaneous imaging utilized a shared imaging path and synchronized data collection. ResultsVIS-OCT images revealed detailed anatomy and Doppler shifts, while PLIM-SLO provided capillary pO2 at multiple depths. A hemoglobin oxygen dissociation curve related retinal arterial pO2 to systemic oxygen saturation as inhaled oxygen was varied. Registered simultaneous images were captured and pO2 was empirically adjusted for the combined excitation. ConclusionsDetailed anatomical structures and capillary pO2 levels can be simultaneously imaged, providing a useful tool to study oxygen metabolism in rodent disease models.

bioengineering↗