Biology subjects

Park, J.

Publications and source records attributed to Park, J..

At least 73 records · Page 4Linked to original sources

bioRxiv2026

Additive manufacturing of PEDOT:PSS electrodes on collagen substrates for soft and bioactive electronics

Traditional bioelectronic devices are limited by poor biointerfacing due to their substantial mismatch in mechanical and biochemical properties. In tissue engineering, soft and bioactive materials support biointegration by harnessing or mimicking the natural extracellular matrix (ECM). Building bioelectronic devices from ECM should improve their biointegration, yet there are limited methods to fabricate them due to current manufacturing approaches. An additive manufacturing strategy is presented here for collagen-based bioelectronic interfaces that integrates conducting polymer electrodes with ECM-based substrates or encapsulation layers. Addition of poly(ethylene glycol) diglycidyl ether (PEGDE) to poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) colloidal dispersions enables direct extrusion-based patterning under mild conditions compatible with collagen substrates, and forms aqueous stable and highly conducting printed patterns (2788 S m-{superscript 1}). The resulting interfaces maintain stable electrochemical performance over 7 days in physiological environments, and support primary human cell adhesion, viability, and proliferation across both material regions. A sacrificial patterning strategy using 3D printed cacao butter further enables spatial control of collagen encapsulation. This approach establishes a framework for fabricating functional bioelectronic devices based on ECM to further enhance device biointerfaces for tissue models and implantable systems.

bioengineering↗

bioRxiv2026

Organoid modeling of tumor-associated macrophages reveals phagocytosis checkpoint blockade-induced conversion to an immunosuppressive SPP1+ phenotype

Tumor-associated macrophages (TAM) exert essential functions during the immune response to cancer. However, investigations of TAM within a native human tumor microenvironment (TME) have been impeded by a lack of appropriate model systems. Here, patient-derived organoids (PDO) from air-liquid interface (ALI)-grown tumor fragments, containing a human TME that encompassed stroma and immune subsets, robustly preserved TAM that were maintained by endogenous CSF-1 and appropriately responded to polarization signals. Antibody blockade of the CD47 regulatory checkpoint in organoids stimulated phagocytosis and remodeled TAM cytokine secretion profiles that were confirmed in anti-CD47 phase I trial patients. Amongst PDO histologies screened, anti-CD47 tumor killing was notable in clear cell renal cell carcinoma (ccRCC) which was associated with increased TAM infiltration. PDO contained diverse previously described TAM subsets; however, anti-CD47 reprogrammed organoid TAM toward an immunosuppressive SPP1+ phenotype, highlighting a negative feedback mechanism. Our findings uncover a resistance circuit engaged by macrophage checkpoint blockade and position ALI PDO as a robust translational platform for dissecting human macrophage biology and informing precision immunotherapy.

cancer biology↗

bioRxiv2026

Label-free quantitative 3D mapping of collagen architecture by holotomography

Fibrillar collagen architecture regulates tissue mechanics and cell-matrix interactions, but following how collagen-rich matrices assemble and remodel in three dimensions requires non-destructive measurements that can link structure to matrix-associated mass without exogenous labels. Here we present holotomography (HT) as a label-free platform for volumetric imaging and quantitative profiling of reconstituted fibrillar collagen. Volumetric RI tomograms resolved fibrillar collagen networks without exogenous labels, and co-registration with second-harmonic generation (SHG) microscopy supported the correspondence between HT-resolved RI structures and SHG-positive fibrillar collagen. Curvelet-transform-based segmentation of representative axial sections converted the tomograms into fiber-level descriptors, including morphology, orientation and RI-derived fiber-associated dry mass. At the matched 0.8 mg/mL condition, HT resolved distinct network organization, with type I forming thicker, more sparsely distributed fibers and type III a finer, denser network, while mean fiber-associated RI remained comparable between subtypes. Across the concentration series, type I showed stronger increases in fiber width and RI-derived mass, whereas type III remained comparatively fine. Time-lapse HT further captured RI dynamics during type I fibrillogenesis and visualized local cell-matrix reorganization in HT1080 cell-embedded gels, capturing cells and surrounding matrix in a single label-free measurement. Together, these results position HT as a complementary label-free approach for volumetric visualization and RI-based quantification of collagen-rich extracellular matrices.

cell biology↗

bioRxiv2026

IscR-mediated morphological regulation confers virulence and stress resistance by reducing stress molecule uptake in Acinetobacter baumannii

Living organisms must adequately respond to stress to survive and proliferate. Bacterial pathogens face multiple stressors during infections, including oxidative stress from host innate immune cells and antibiotic treatment from clinical therapy. The pathogenic bacterium Acinetobacter baumannii is considered the most critical threat to public health due to its broad antibiotic resistance. However, it is poorly known how A. baumannii properly responds to antibiotics and stress molecules during infection. Here, we investigate the mechanisms by which A. baumannii regulates its morphology to reduce the uptake of stress molecules under oxidative stress and antibiotic exposure, thereby conferring virulence and survival during infection. The transcriptional regulator IscR responds to oxidative stress by upregulating pbp1a, which encodes an enzyme involved in peptidoglycan biosynthesis. Under oxidative stress, bacteria undergo a morphological shift from a rod to a coccoid form, reducing their surface area and thus decreasing their absorption of reactive oxygen species. Inactivation of either iscR or pbp1a results in an elongated morphology characterized by an elevated surface area, thereby reducing A. baumannii survival under oxidative stress. Furthermore, IscR-mediated morphological control is essential for survival under antibiotic treatment. Moreover, IscR-mediated morphology regulation is required for A. baumannii survival in macrophage and mouse models. These findings elucidate a strategy by which A. baumannii uses IscR to adapt to stress through morphological control, facilitating its survival during infections against both immune response and antibiotic therapy. IMPORTNACEAcinetobacter baumannii is a major cause of nosocomial infections. It poses a critical threat due to its extensive antibiotic resistance. This study reveals that the pathogen can change its cellular shape to survive immune system attacks and antibiotic treatment. This change represents a previously unknown survival strategy. A. baumannii transitions to a coccoid morphology under oxidative stress and antibiotic treatment. It does so by activating the peptidoglycan synthesis gene pbp1a through the IscR transcriptional regulator. This rapid morphological adaptation helps A. baumannii evade host defenses and resist antibiotic treatment by reducing uptake of stress molecules. Our findings advance understanding of how pathogens adapt to hostile environments and identify new therapeutic targets. By blocking this shape remodeling ability, it may be possible to render pathogenic bacteria more vulnerable to immune responses and antimicrobial treatments. This offers a promising strategy for combating this multidrug-resistant pathogen.

microbiology↗

bioRxiv2026

Multi-point convective delivery overcomes mass transport barriers for myocardial therapeutics

Angiogenesis-promoting macromolecules reduce adverse remodeling and preserve cardiac function in rodents following myocardial infarctions, yet repeatedly fail to translate across length scales in humans. Through mass transport studies in human and swine myocardium, we found that dense, anisotropic myocardial fibers limit therapeutic diffusion and convection to millimeter scales for existing approaches including bolus intramyocardial injections, shear-thinning hydrogels, and epicardial patches. Furthermore, distributions are confined to one dimension along fibers. To increase myocardial drug distribution to centimeter length scales in vivo in swine, we engineered a three-dimensional multi-injection drug delivery array. Our device performs up to 40 simultaneous 120 {micro}L injections of functional macromolecules, hydrogels, or mRNA lipid nanoparticles. Injections are precisely placed in relation to fiber alignment, achieving near-complete coverage of the left ventricular myocardium.

bioengineering↗

bioRxiv2026

Tuned inhibitory control of neuronal firing thresholds explains predictive sensorimotor behavior

Prior expectations guide sensorimotor behavior when sensory information is uncertain, yet the cellular mechanisms underlying this integration remain elusive. Here, we investigate how priors in sensory motion direction shape neural population dynamics by combining recurrent neural network (RNN) modeling with macaque smooth pursuit behavior and middle temporal area (area MT) electrophysiology. Our RNN model reveals that prior expectations are implemented by elevating firing thresholds in neurons tuned away from the expected direction. This selective inhibition sharpens population tuning and reduces behavioral variability under weak sensory information conditions. We validated this prediction in vivo: delta-band local field potentials in area MT, where the phase reflects neural excitability states, exhibited direction-specific phase shifts that scaled with the deviation from the expected direction. These findings demonstrate that prior expectations enhance behavioral reliability through tuned inhibitory control of neuronal excitability, providing a mechanistic link between Bayesian inference and cortical circuit dynamics.

neuroscience↗

bioRxiv2026

Deep Learning-Guided Holotomography Reveals Early Structural Remodelling During Pluripotency Exit

Real-time assessment of human pluripotent stem cell (hPSC) quality is critical for reproducibility and safety in regenerative medicine, yet current methods are invasive, labor-intensive, or highly operator-dependent. We present DeepHOPE (Deep-learning-guided Holotomography for Pluripotency Evaluation), a non-invasive, automatizable, and statistics-driven platform that integrates three-dimensional (3D) refractive index imaging with deep learning to assess pluripotency. DeepHOPE performs robustly across diverse contexts, including germ-layer differentiation, retinoic acid-induced differentiation, and mid-reprogramming cultures, enabling streamlined cell production workflows and improving the efficiency of midbrain dopaminergic neuron differentiation through informed colony selection. Mechanistically, DeepHOPE detects minute colony-scale topological changes that precede molecular loss of pluripotency. These early changes are associated with rapid F-actin remodeling, including apical-to-basal redistribution during early differentiation. Consistent with a functional role for cytoskeletal regulation in state transitions, sustained reduction of actomyosin tension decreases pluripotency, identifying cytoskeletal dynamics as an upstream determinant of early pluripotency exit. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/720508v1_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@1d73508org.highwire.dtl.DTLVardef@1dab29aorg.highwire.dtl.DTLVardef@1039f76org.highwire.dtl.DTLVardef@da29a1_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

bioRxiv2026

Landscape-scale navigation unlocks antibody CDR structural logic for AI-guided rescue and therapeutic optimization

While AI offers transformative potential for therapeutic antibody design, the lack of ground-truth data fundamentally constrains our ability to model the epistatic topology of fitness landscapes. Here, we establish a high-throughput workflow to characterize tens of thousands of antibody variants per week with gold-standard biophysical precision. By combinatorially assembling functional variants from deep mutational scanning, we charted antibody fitness landscapes comprising over 17,000 data points, which revealed an extremely rugged, non-navigable epistatic topology. Yet, navigating at this unprecedented scale enabled the discovery of rare peak clusters exhibiting simultaneous enhancements in affinity and productivity. Strikingly, ProteinMPNN predicted the CDR-dependent productivity landscape with remarkable accuracy, suggesting that sequence-structure compatibility within CDRs gates cellular productivity. This insight enabled a structure-guided rescue strategy combining AlphaFold3 and ProteinMPNN, which successfully restored the cellular productivity of high-affinity, low-productivity clones via single amino acid substitutions. Two elite variants drawn directly from peak clusters further demonstrated 20- to 100-fold in vivo efficacy gains in a murine psoriasis model. Our findings establish CDR structural fitness as a fundamental determinant of antibody cellular productivity and validate landscape-scale navigation as a powerful framework for therapeutic antibody optimization.

bioengineering↗

bioRxiv2026

High-variance phenome database reveals important roles of WD40 proteins in the plant pathogenic fungus Fusarium graminearum

WD40 is a highly conserved protein domain in eukaryotes, playing a critical role in various cellular process. We conducted genome-wide functional analysis of WD40 genes in Fusarium graminearum-a phytopathogenic fungus that causes severe yield loss and mycotoxin contamination in major cereal crops. Comprehensive phenome analysis of 119 WD40 gene deletion mutants across 22 distinct phenotypic traits revealed phenotypic divergence within the phenome, establishing a strong correlation between virulence and sexual reproduction. Notably, 21 core WD40 genes were identified, offering valuable insights into divergent biological processes. Pilot interactome studies of Fgwd101 and Fgwd133 provided further insights into their potential pathobiological functions. Our investigation contributes to broadening our knowledge of the biological mechanisms underlying fungal pathogenesis and may assist in the identification of targets for antifungal agents.

molecular biology↗

bioRxiv2026

CXCL-CXCR2 signaling drives cancer-endothelium interactions in SCLC metastatic seeding

Small cell lung cancer (SCLC) is a highly metastatic malignancy with tropism to the liver, yet the signals that enable organ-specific metastatic colonization remain largely undefined. During metastasis, disseminated cancer cells first encounter endothelial cells (ECs) at the vascular-tissue interface, positioning cancer-endothelium crosstalk as a key determinant of metastatic success. Defining the signaling pathways underlying this reciprocal communication may uncover actionable vulnerabilities for preventing and treating this lethal disease. Here, we uncover an EC-derived CXCL chemokine program that activates cancer-intrinsic CXCR2-RAC1 signaling as a critical mediator of SCLC liver metastasis. By integrating in vitro and in vivo models, we show that SCLC cells induce robust CXCL chemokine expression from liver ECs, which in turn enhances SCLC migration and reinforces cancer cell-EC interactions. We applied highly quantitative metastatic colony barcode sequencing coupled with individual gene inactivation to demonstrate that CXCR2 is essential for SCLC migration and liver metastatic seeding. Mechanistically, CXCL-CXCR2 signaling activates RAC1-dependent F-actin assembling to drive SCLC motility during CXCL-induced metastatic seeding. Pharmacologic inhibition of CXCR2 or RAC1 suppresses SCLC migration and prevents SCLC liver metastasis. Together, our research defined a chemokine-driven signaling circuit that governs cancer-endothelium communication during the metastatic cascade and nominate the CXCL-CXCR2-RAC1 axis as a promising therapeutic vulnerability for preventing and treating metastatic SCLC.

cancer biology↗

bioRxiv2026

Controlled linking of AAV capsids enables coordinated multi-vector delivery

Adeno-associated virus (AAV)-based delivery of large genetic systems splits cargo across vectors, but functional reconstitution depends on stochastic co-delivery and often requires high viral doses. Here, we present a multi-capsid linking strategy that enables coordinated delivery of AAV vectors carrying distinct or split genetic cargos. Using a substrate-confined linking process, we suppress uncontrolled higher-order aggregation while enabling programmable nanoscale capsid coupling via oligonucleotide linkers. These linkers further enable efficient downstream purification of linked AAVs and recycling of unlinked vectors, yielding [~]70% AAV dimers and trimers in <24 hours. By enforcing coordinated delivery, linked AAVs achieve co-transduction at reduced viral doses and with greater expression uniformity than conventional dual-AAV approaches. This improved coordination enhances reconstitution of split genetic systems and increases targeted prime editing efficiency in vitro and in the mouse brain. This capsid coupling strategy expands the functional scope of AAVs toward dose-efficient and uniform delivery of large genetic systems.

bioengineering↗

bioRxiv2026

Development of host-mimicking legume-based media for robust induction of sporulation in soybean-associated Cercospora species

Cercospora species associated with soybean cause Cercospora leaf spot and purple seed stain, which are major diseases affecting soybean production worldwide and can lead to significant yield and seed quality losses. However, unstable and poor sporulation under laboratory conditions remains a critical challenge, hindering the recovery of genetically homogeneous isolates and the establishment of standardized experimental protocols. These limitations further restrict our understanding of the biology, epidemiology, and pathogenicity of these pathogens. In this study, we developed specialized legume-based culture media derived from soybean and pea tissues to mimic host-associated environmental conditions. We compared the sporulation efficacy of these media with commonly used artificial media, including potato dextrose agar (PDA) and V8 juice agar. Our results demonstrated that legume-based media consistently supported higher levels of sporulation than PDA and V8 across multiple strains, although conidial yields varied depending on the strain and medium concentration. Transcriptional analysis of sporulation-related genes revealed that while abaA, wetA, and steA did not show significant differential expression among media, velB exhibited distinct medium-dependent expression patterns. Further evaluation using additional field isolates confirmed that legume-based media provide a more reliable method for inducing sporulation than PDA. Overall, legume-based media represent a practical and effective approach for promoting sporulation in soybean-associated Cercospora species under laboratory conditions.

microbiology↗

bioRxiv2026

Spatiotemporal Characterization of Amyloidosis-Associated Microglial States Reveals Sex Difference in Early Plaque Formation

Twice as many women develop Alzheimer's disease (AD) compared to men. Several key aspects, such as genetic risk factors, hormonal vulnerability, social responsibilities, and differences in longevity, contribute to the strong female bias in AD. To assess whether sex differences can be detected during the onset of AD, we examined the amyloid-{beta} (A{beta}) plaque burden--one of the hallmarks of AD--and microglial states in young 5XFAD mouse models of amyloid pathology. We hypothesized that an elevated A{beta} burden will directly correlate with an increase in microglial cell number and phagocytic activity, shaping the appearance of compact dense-core plaques in the cortex from 2 to 6 months of age. As expected, no change in microglial density and phenotype was found in A{beta} plaque-free hypothalamus of 5XFAD male and female mice when compared to age-matched wildtype controls. By quantifying the number and coverage of diffuse and dense-core plaques in the cortex, we discovered a pronounced increase in A{beta} plaques and microglial clustering in 4-month-old female 5XFAD compared to male mice. Conversely by 6 months, higher total plaque load in males and no sex difference in the number of plaque-associated microglial (PAM) cluster was observed. Our spatiotemporal characterization of microglial CD68, Dectin-1 (Clec7a), and CD11c (Itgax) expression revealed transient sex differences in the upregulation of only CD68 among these phagocytic markers in cortical microglia. In 4-months-old males, greater phagolysosomal activity may benefit A{beta} clearance and delay plaque formation. In females, lower microglial phagolysosomal activity and increased microgliosis may have led to the increase in plaque deposition and compaction from 2-4 months. Our results suggest that during early amyloidosis, sex differences in CD68-associated phagolysosomal activity and microglia-driven plaque compaction may cause disproportionate AD risk and severity that is compounded by other exacerbating factors during aging. Taken together, sex-specific targeting of microglial proliferation and phagocytic activity may be a promising intervention in presymptomatic patients with known AD risks.

neuroscience↗

bioRxiv2026

Display functions of dinosaur proto-wings before powered flight

Pennaceous feathers are fundamental to avian flight, yet their early function in non-volant dinosaurs remains unknown. Early-diverging pennaraptorans had simple pennaceous feathers on proto-wings and tails, which were unsuitable for flight but may have enhanced visual signals. However, the visual display hypothesis has not been empirically tested. To address this, we used computer animations of early pennaraptoran displays to measure responses in a well-established animal model of a visually sensitive neural pathway. We show that pennaceous proto-wings and tails enhance the efficiency of motion-based displays across a range of anatomically plausible movements. Integrating these results with comparative and paleontological evidence, we suggest that early pennaceous feathers functioned in diverse signaling contexts and were subsequently exapted for aerodynamic use.

evolutionary biology↗

bioRxiv2026

A structure-informed deep learning framework for modeling TCR-peptide-HLA interactions

The interaction between T cell receptors (TCRs), peptides, and human leukocyte antigens (HLAs) underlies antigen-specific T cell immunity. Despite substantial advances in peptide- HLA presentation prediction, accurate modeling of coupled TCR-peptide-HLA recognition remains underdeveloped, limiting applications such as TCR and neoepitope prioritization in cancer and antigen identification in autoimmunity. Here we present StriMap, a unified framework for predicting TCR-peptide-HLA interactions by integrating physicochemical, sequence-context, and structural features at recognition interfaces. StriMap achieves state-of-the-art performance with improved generalizability and enables applications in both cancer and autoimmunity. As a case study in ankylosing spondylitis (AS), we screened 13 million peptides derived from 43,241 bacterial proteins and identified candidate molecular mimics that were experimentally validated to activate T cells expressing an AS-associated TCR. Notably, a top validated peptide was enriched in patients with inflammatory bowel disease (IBD), suggesting potential shared microbial triggers between AS and IBD. Overall, StriMap provides a generalizable framework for rational immunotherapy design and for dissecting antigenic drivers of autoimmunity.

bioinformatics↗

bioRxiv2026

Spiperone targets HBV cccDNA via ER stress induced innate immune activation and epigenetic silencing

Chronic hepatitis B persists due to the stability of nuclear covalently closed circular DNA (cccDNA), which maintains viral transcription despite prolonged antiviral therapy, highlighting the need for strategies that suppress cccDNA via host-targeted mechanisms. Here, we identify Spiperone, a clinically approved compound, as a repurposed anti-HBV candidate with strong translational potential. Spiperone robustly reduced HBsAg, HBeAg, viral DNA, and pgRNA across HepG2.2.15, HBV-infected HepG2-NTCP-C4 and HepaRG cells, and multiple in vivo models, including HBV transgenic, hydrodynamic injection, and AAV- HBV1.04x models. Notably, intrahepatic cccDNA was significantly diminished. In combination, Spiperone potentiated tenofovir activity, exhibiting synergistic effects, while both intraperitoneal and oral administration reduced antigenemia and viremia. Mechanistically, Spiperone activated the PERK-eIF2-ATF4 arm of the ER stress response, coupled with mitochondrial perturbation and cytosolic release of oxidized mitochondrial DNA, leading to activation of IFI16-STING-IRF3 signaling. This cascade induced type I interferon (IFN-I) and interferon-stimulated genes. ChIP-qPCR further demonstrated reduced enrichment of activating histone marks on cccDNA, consistent with transcriptional repression. Collectively, these findings position Spiperone as a host-directed antiviral that converges ER stress-linked innate immunity and epigenetic repression to suppress cccDNA, supporting its advancement in combination strategies toward a functional cure for chronic HBV infection.

microbiology↗

bioRxiv2026

A retrospective public external benchmark of healthy-to-stroke lower-limb EEG transport identifies constraints from source construction, adaptation burden, and confound sensitivity

BackgroundLower-limb EEG is a rehabilitation-facing control signal for stroke neurorehabilitation and future non-invasive brain-spine interfaces, but a public external benchmark that jointly audits source construction, minimal adaptation burden, and confound sensitivity is lacking. We therefore tested whether lower-limb effort-versus-rest decoders trained on healthy public EEG transport to a stroke target domain. MethodsWe conducted a retrospective public-data external benchmark using three public EEG datasets harmonised to a common lower-limb effort-versus-rest target. Classical and deep models were compared under zero-shot transport, 10-shot temperature calibration, and 10-shot fine-tuning. For few-shot analyses, each target participant contributed a trial-disjoint subject-internal support set of 10 labelled trials per class and a held-out remainder test set. Prespecified analyses audited source construction, support-resampling sensitivity, and montage controls. Uncertainty was summarised with participant-level bootstrap confidence intervals. ResultsWithin this benchmark, healthy-to-stroke zero-shot transport was weak. The best zero-shot result was classical rather than deep, with CSP+LDA reaching area under the receiver operating characteristic curve (AUROC) 0.603, whereas EEGNet remained near chance (AUROC 0.527). Ten-shot calibration improved operating behaviour more than discrimination: for CSP+LDA, expected calibration error fell from 0.267 to 0.035 and specificity increased from 0.180 to 0.485, whereas AUROC remained essentially unchanged (0.603 to 0.604). Ten-shot fine-tuning produced only modest gains; the best overall AUROC was 0.605 for pooled dataset-balanced CSP+LDA, numerically tied with pooled raw CSP+LDA (0.605). MILimbEEG-only source training was consistently weak, exploratory deep domain-generalisation variants did not rescue transport, and frontal and temporal montage controls remained relatively competitive. ConclusionsWithin this public benchmark, source construction and minimal adaptation burden mattered more than model novelty, and retrospective montage controls limited motor-specific interpretation. The results support harmonised prospective validation of lower-limb EEG transport over further retrospective model iteration.

neuroscience↗

bioRxiv2026

Self-severing circuits facilitate passage of ingestible electronic sensor-guided therapeutics

Ingestible electronics enable the tracking and treatment of gastrointestinal and systemic diseases. However, bulky batteries and circuit boards require large capsules that can result in bowel obstruction, a medical emergency. Here, we engineered a 9 x 26 mm electronic pill capable of triggered severing into tiny pieces with sizes clinically proven to reduce obstruction risk. Our capsule enables multicomponent circuit boards to connect with separately encapsulated powering elements via conductive, interlocking connections. Heat induced softening of polyethylene glycol/polycaprolactone channels activates a spring to separate encapsulated components into inert 9 x 15 mm segments, facilitating intestinal passage. Separation triggers included closed-loop sensors and time-delay circuits. In vivo swine studies demonstrate the ability of our capsules to sense luminal oxygen changes via an optoelectronic sensor, locally trigger upadacitinib delivery, and facilitate safe excretion.

bioengineering↗