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Li, C.

Publications and source records attributed to Li, C..

At least 415 records · Page 23Linked to original sources

Modular Nano-Scaffold Biocatalysis for Superior PET Depolymerization and Valorization

The global crisis of polyethylene terephthalate (PET) waste demands new strategies for sustainable management. Biocatalytic recycling offers a promising route, but direct depolymerization under moderate conditions is often limited by kinetic constrains of individual enzyme. Here, we engineer and optimize modular protein scaffolds that utilize orthogonal interaction domains, including the cohesin-dockerin pairs from bacterial cellulosomes and the SH3 ligand/domain pair from mouse Crk, to assemble complementary hydrolases (PETase, MHETase, and ICCG) into a synergistic multi-enzyme cascade. This architecture overcomes intermediate inhibition, efficiently converting PET hydrolysis products into the final monomers, terephthalic acid (TPA) and ethylene glycol (EG), outperforming previous multi-enzyme systems. The systems application is further evaluated by stability enhancement via immobilization on metal-organic frameworks (MOFs), coupling depolymerization to the valorization of EG into glycolic acid (GA), and adapting the system for scalable whole-cell biocatalysis. This scaffold-based multi-enzyme approach provides a new strategy for developing integrated biocatalytic systems to advance a circular PET economy.

synthetic biology↗

Biomolecular condensation of ERC1 recruits ATG8 and NBR1 to drive autophagosome formation for plant heat tolerance

Macroautophagy (hereafter autophagy) is essential for cells to respond to nutrient stress by delivering cytosolic contents to vacuoles for degradation via the formation of a multi-layer vesicle named autophagosome. A set of autophagy-related (ATG) regulators are recruited to the phagophore assembly site for the initiation of phagophore, as well as its expansion and closure and subsequent delivery into the vacuole. However, it remains elusive that how the phagophore assembly is regulated under different stress conditions. Here, we described an unknown Arabidopsis (Arabidopsis thaliana) cytosolic ATG8-interaction protein family (ERC1/2), that binds ATG8 and NBR1 to promote autophagy. ERC1 proteins translocate to the phagophore membrane and develop into classical ring-like autophagosomes upon autophagic induction. However, ERC1 proteins form large droplets together with ATG8e proteins when in the absence of ATG8 lipidation activity. We described the property of these structures as phase-separated membraneless condensates by solving the in vivo organization with spatial and temporal resolution. Moreover, ERC1 condensates elicits a strong recruitment of the autophagic receptor NBR1. Loss of ERC1 suppressed NBR1 turnover and attenuated plant tolerance to heat stress condition. This work provides novel insights into the mechanical principle of phagophore initiation via an unreported ERC1-mediated biomolecular condensation for heat tolerance in Arabidopsis.

plant biology↗

Target protein identification in live cells and organisms with a non-diffusive proximity tagging system

Identifying target proteins for bioactive molecules is essential for understanding their mechanisms, developing improved derivatives, and minimizing off-target effects. Despite advances in target identification (target-ID) technologies, significant challenges remain, impeding drug development. Most target-ID methods use cell lysates, but maintaining an intact cellular context is vital for capturing specific drug-protein interactions, such as those with transient protein complexes and membrane-associated proteins. To address these limitations, we developed POST-IT (Pup-On-target for Small molecule Target Identification Technology), a non-diffusive proximity tagging system for live cells, orthogonal to the eukaryotic system. POST-IT utilizes an engineered fusion of proteasomal accessory factor A (PafA) and HaloTag to transfer Pup to proximal proteins upon directly binding to the small molecule. After significant optimization to eliminate self-pupylation and polypupylation, minimize depupylation, and optimize chemical linkers, POST-IT successfully identified known targets and discovered a new binder, SEPHS2, for dasatinib, and VPS37C as a new target for hydroxychloroquine, enhancing our understanding these drugs mechanisms of action. Furthermore, we demonstrated the application of POST-IT in live zebrafish embryos, highlighting its potential for broad biological research and drug development.

pharmacology and toxicology↗

GDF11 secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis

Here, we present a combination of cell and gene therapy that harnesses the regenerative properties of GDF11 in age-related pulmonary fibrosis. Our genome-edited FailSafeTM-GDF11 mouse ESC line provides controlled proliferation and efficient derivation to lung progenitors while inducibly expressing GDF11. When these cells were transplanted into bleomycin-injured aged mice, they acted as a source of reparative cells, restoring the damaged alveolar epithelium. Furthermore, the transplanted cells acted as an "in situ factory", enabling the production of GDF11 in response to the inducer drug. This approach attenuated age-associated senescence and led to the successful resolution of fibrosis. Our study presents a promising method for treating pulmonary fibrosis. Additionally, this approach offers a versatile tool that can be expanded to incorporate other regenerative and anti-aging factors. This helps overcome limitations such as high production costs and a short half-life of therapeutic factors. One of the strengths of our system is its ability to allow precise regulation of factor-expression when needed to address specific aging phenotypes.

developmental biology↗

GenoM7GNet: An Efficient N7-methylguanosine Site Prediction Approach Based on a Nucleotide Language Model

N7-methylguanosine (m7G), one of the mainstream post-transcriptional RNA modifications, occupies an exceedingly significant place in medical treatments. However, classic approaches for identifying m7G sites are costly both in time and equipment. Meanwhile, the existing machine learning methods extract limited hidden information from RNA sequences, thus making it difficult to improve the accuracy. Therefore, we put forward to a deep learning network, called "GenoM7GNet," for m7G site identification. This model utilizes a Bidirectional Encoder Representation from Transformers (BERT) and is pretrained on nucleotide sequences data to capture hidden patterns from RNA sequences for m7G site prediction. Moreover, through detailed comparative experiments with various deep learning models, we discovered that the one-dimensional convolutional neural network (CNN) exhibits outstanding performance in sequence feature learning and classification. The proposed GenoM7GNet model achieved 0.953 in accuracy, 0.932 in sensitivity, 0.976 in specificity, 0.907 in Matthews Correlation Coefficient and 0.984 in Area Under the receiver operating characteristic Curve on performance evaluation. Extensive experimental results further prove that our GenoM7GNet model markedly surpasses other state-of-the-art models in predicting m7G sites, exhibiting high computing performance.

bioinformatics↗

Decreased Astrocytic CCL5 by MiR-324-5p Ameliorates Ischemic Stroke Injury via CCR5/ERK/CREB Pathway

Following ischemic stroke, Ccl5 mRNA expression increased, while miR-324-5p expression decreased in the peri-infarct cortex of middle cerebral artery occlusion (MCAO) mice. However, the roles of CCL5 and miR-324-5p in stroke remained largely unclear. Here, we show that inhibiting CCL5 using antibodies or miR-324-5p not only reduced infarct area and preserved neurological function in MCAO mice but also attenuated astrocyte reactivity and microglial activation, protected dendritic structures, and maintained spine density. In an astrocyte-neuron co-culture system after oxygen-glucose deprivation (OGD), inhibiting astrocytic CCL5 by antibody or miR-324-5p decreased neuronal apoptosis and preserved dendritic structure. Importantly, the suppression of CCL5 enhanced ERK/CREB pathway signaling both in vivo and in vitro. Consistent with these findings, the application of Maraviroc, a CCR5 antagonist, reduced infarct size, decreased neuronal apoptosis, and upregulated the ERK/CREB pathway in neurons treated with OGD. In conclusion, targeting the CCL5 pathway via miR-324-5p represents a promising therapeutic strategy for alleviating ischemic stroke damage through modulation of the neuronal CCR5/ERK/CREB pathway.

neuroscience↗

Fluctuating chromatin facilitates enhancer-promoter communication by regulating transcriptional clustering dynamics

AbstractEnhancers regulate gene expression by forming contacts with distant promoters. Phase-separated condensates or clusters formed by transcription factors (TFs) and co-factors are thought to facilitate these enhancer-promoter (E-P) interactions. Using polymer physics, we developed distinct coarse-grained chromatin models that produce similar ensemble-averaged Hi-C maps but with "stable" and "dynamic" characteristics. Our findings, consistent with recent experiments, reveal a multi-step E-P communication process. The dynamic model facilitates E-P proximity by enhancing TF clustering and subsequently promotes direct E-P interactions by destabilizing the TF clusters through chain flexibility. Our study promotes physical understanding of the molecular mechanisms governing E-P communication in transcriptional regulation. Graphical TOC Entry O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=86 SRC="FIGDIR/small/610578v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@114b51borg.highwire.dtl.DTLVardef@7e261forg.highwire.dtl.DTLVardef@1f8dc3forg.highwire.dtl.DTLVardef@143ecb5_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

Reciprocal regulation of m6A modification and miRNA production machineries via phase separation-dependent and -independent mechanisms

Methyltransferase complex (MTC) deposits N6-adenosine (m6A) onto RNA, whereas microprocessor produces miRNA. Whether and how these two distinct complexes cross-regulate each other has been poorly studied. Here we report that the MTC subunit B (MTB) tends to form insoluble condensates with poor activity, with its level monitored by 20S proteasome. Conversely, the microprocessor component SERRATE (SE) forms liquid-like condensates, which in turn promotes solubility and stability of MTB, leading to increased MTC activity. Consistently, the hypomorphic lines expressing SE variants, defective in MTC interaction or liquid-like phase behavior, exhibit reduced m6A level. Reciprocally, MTC can recruit microprocessor to MIRNA loci, prompting co-transcriptional cleavage of primary miRNA (pri-miRNAs) substrates. Additionally, pri-miRNAs carrying m6A modifications at their single-stranded basal regions are enriched by m6A readers, which retain microprocessor in the nucleoplasm for continuing processing. This reveals an unappreciated mechanism of phase separation in RNA modification and processing through MTC and microprocessor coordination.

plant biology↗

Co-zorbs: Motile, multispecies biofilms aid transport of diverse bacterial species

Biofilms are three-dimensional structures containing one or more bacterial species embedded in extracellular polymeric substances. Although most biofilms are stationary, Flavobacterium johnsoniae forms a motile spherical biofilm called a zorb, which is propelled by its base cells and contains a polysaccharide core. Here, we report formation of spatially organized, motile, multispecies biofilms, designated "co-zorbs," that are distinguished by a core-shell structure. F. johnsoniae forms zorbs whose cells collect other bacterial species and transport them to the zorb core, forming a co-zorb. Live imaging revealed that co-zorbs also form in zebrafish, thereby demonstrating a new type of bacterial movement in vivo. This discovery opens new avenues for understanding community behaviors, the role of biofilms in bulk bacterial transport, and collective strategies for microbial success in various environments. Significance StatementThis paper reports the discovery of co-zorbs, which are spherical aggregates of bacteria that move and transport other bacteria. Zorbs move toward other bacteria and collect them in a manner reminiscent of phagocytes. Once inside the zorb, the new species form a striking, organized core. The discovery of co-zorbs introduces an entirely new type of bacterial movement and transport involving cooperation among bacterial species. Co-zorbs have potential for engineering microbial systems for biotechnology applications and for managing spread of bacterial pathogens in their hosts.

microbiology↗

Gain-of-function study reveals the pleiotropic roles of serine protease HtrA in Borrelia burgdorferi

High-temperature requirement protease A (HtrA) is a family of serine proteases degrading misfolded and damaged proteins that are toxic to bacteria. The Lyme disease agent Borrelia burgdorferi encodes a single HtrA (BbHtrA). Previous studies have shown that BbHtrA is a key virulence determinant of B. burgdorferi as a deletion mutant of htrA ({Delta}htrA) fails to establish infection in mice. However, previous complementation could only restore protein expression but not infectivity in mice. In this report, we first identify the native promoter of BbHtrA which allows us to construct a fully complemented{Delta} htrA strain. Follow up promoter activity analysis reveals that BbHtrA is likely dually regulated by the house keeping sigma factor RpoD and the alternative sigma factor RpoS. The{Delta} htrA mutant exhibits growth defect upon entering the mid-log to stationary phase especially at high temperatures. Microscopic analysis further demonstrates that the absence of htrA induces extensive cell death. Additionally, the{Delta} htrA mutant has defects in cell locomotion as the expression of several key chemotaxis proteins are significantly downregulated. Cryo-electron tomography imaging of htrA mutant further reveals that deletion of htrA disrupts flagellar homeostasis. The failure of{Delta} htrA to establish an infection in mice is likely due to repressed expression of BosR and RpoS at the transcriptional level which ultimately causes dysregulation of the RpoS-induced virulence factors. Collectively, we conclude that the expression of htrA is finely tuned which is critical for its pleiotropic roles in the regulation of motility, stress response, and virulence gene expression in B. burgdorferi. IMPORTANCELyme borreliosis is the most commonly reported vector-borne illnesses in the United States, which is caused by Borrelia burgdorferi. As the enzootic pathogen alternates between the tick vector and mammalian hosts, adaptation to drastically different growth milieu is imperative to its survival. Hence, robust alteration of gene expression and proper quality control on protein synthesis and turnover are pivotal for its fitness. The family of HtrA serine proteases is mainly responsible for the maintenance of protein homeostasis particularly under stressful conditions. The significance of this report is to decode how BbHtrA contributes to the fitness of B. burgdorferi. BbHtrA is essential for mammalian host infection but little is known about its regulatory mechanism as well as its contribution to the virulence of B. burgdorferi. By deciphering the regulatory elements involved in the expression of BbHtrA, we are one step closer to comprehending its significance in the pathophysiology of B. burgdorferi.

microbiology↗

A single-molecule nanopore sequencing platform

Nanopore sequencing, a third-generation sequencing technology, has revolutionized the gene sequencing industry with its advantages of long reads, fast speed, real-time sequencing and analysis, and potential in detecting base modifications. This technology allows researchers to sequence longer DNA fragments in a single read, providing more comprehensive genomic information compared to previous methods. Nanopore sequencing operates on electrical signals generated by a nanopore embedded in a membrane separating two electrolyte-filled chambers. When single-stranded DNA (ssDNA) passes through the nanopore, it creates variations in the current that correspond to different DNA bases. By analyzing these current fluctuations with machine learning algorithms, the DNA sequence can be determined. In this study, we introduced several improvements to nanopore sequencing, including nanopore local chemistry sequencing, novel motor and pore proteins, chip design, and basecalling algorithms. Our new nanopore sequencing platform, CycloneSEQ, demonstrated long-duration sequencing (107 hours) on a single chip with high yield (>50 Gb). In human genomic DNA sequencing, CycloneSEQ was able to produce long reads with N50 33.6 kb and modal identity 97.0%. Preliminary findings on human whole-genome de novo assembly, variant calling, metagenomics sequencing, and single-cell RNA sequencing have further highlighted CycloneSEQs potential across different areas of genomics.

genomics↗

SUV39H1 Preserves Cancer Stem Cell Chromatin State and Properties in Glioblastoma

Of the more than 100 types of brain cancer, glioblastoma (GBM) is the deadliest. As GBM stem cells (GSCs) are considered to be responsible for therapeutic resistance and tumor recurrence, effective targeting and elimination of GSCs could hold promise for preventing GBM recurrence and achieving potential cures. We show here that SUV39H1, which encodes a histone-3, lysine-9 methyltransferase, plays a critical role in GSC maintenance and GBM progression. Upregulation of SUV39H1 was observed in GBM samples compared to normal brain tissues, and knockdown of SUV39H1 in patient-derived GSCs impaired their proliferation and stemness. Single-cell RNA-seq analysis demonstrated restricted expression of SUV39H1 is in GSCs relative to non-stem GBM cells, likely due to super-enhancer-mediated transcriptional activation, while whole cell RNA-seq analysis revealed that SUV39H1 regulates G2/M cell cycle progression, stem cell maintenance, and cell death pathways in GSCs. By integrating the RNA-seq data with ATAC-seq (assay for transposase-accessible chromatin followed by sequencing), we further demonstrated altered chromatin accessibility in key genes associated with these pathways following SUV39H1 knockdown. Treatment with chaetocin, a SUV39H1 inhibitor, mimicked the functional effects of SUV39H1 knockdown in GSCs and sensitized GSCs to the GBM chemotherapy drug temozolomide. Furthermore, targeting SUV39H1 in vivo using a patient-derived xenograft model for GBM inhibited GSC-driven tumor formation. This is the first report demonstrating a critical role for SUV39H1 in GSC maintenance. SUV39H1-mediated targeting of GSCs could enhance the efficacy of existing chemotherapy, presenting a promising strategy for improving GBM treatment and patient outcomes. HighlightsO_LISUV39H1 is upregulated in GBM, especially GSCs C_LIO_LITargeting SUV39H1 disrupts GSC maintenance and sensitizes GSCs to TMZ C_LIO_LITargeting SUV39H1 alters chromatin accessibility at cell cycle and stemness genes C_LIO_LITargeting SUV39H1 suppresses GSC-driven tumors in a patient-derived xenograft model C_LI

cancer biology↗

SegFinder: an automated tool for identifying RNA virus genome segments through co-occurrence in multiple sequenced samples

Metagenomic sequencing has expanded the RNA virosphere, but many identified viral genomes remain incomplete, especially for segmented viruses. Traditional methods relying on sequence homology struggle to identify highly divergent segments and group them confidently within a single virus species. To address this, we developed a new bioinformatic tool - SegFinder - that identifies virus genome segments based on their common co-occurrence at similar abundance within segmented viruses. SegFinder successfully re-discovered all segments from a test data set of individual mosquito transcriptomes, which was also used to establish parameter thresholds for reliable segment identification. Using these optimal parameters, we applied SegFinder to 858 libraries from eight metagenomic sequencing projects, including vertebrates, invertebrates, plants, and environmental samples. Furthermore, we identified 108 (excluding RdRP) unique viral genome segments, of which 55 were novel and 32 showed no recognizable sequence homology to known sequences but which were verified by the presence of conserved sequences at the genome termini. SegFinder is also able to identify segmented genome structures in viruses previously considered to be predominantly unsegmented, and in doing so expanded the number of known families and orders of segmented RNA viruses, making it a valuable tool in an era of large-scale parallel sequencing.

bioinformatics↗

Calcium tunneling through the entoplasmic reticulum and transfer to other organelles for optimal signaling in Toxoplasma gondii

Ca2+ signaling in cells begins with the opening of Ca2+ channels in either the plasma membrane (PM) or endoplasmic reticulum (ER), leading to a sharp increase of the physiologically low (<100 nM) cytosolic Ca2+ level. The temporal and spatial regulation of Ca{superscript 2} is crucial for the precise activation of key biological processes. In the apicomplexan parasite Toxoplasma gondii, which infects approximately one-third of the global population, Ca{superscript 2} signaling governs essential aspects of the parasites infection cycle. T. gondii relies on Ca{superscript 2} signals to regulate pathogenic traits, with several Ca{superscript 2}-signaling components playing critical roles. Ca2+ entry from the extracellular environment has been demonstrated in T. gondii for both, extracellular parasites, exposed to high Ca2+, and intracellular parasites, which acquire Ca{superscript 2} from host cells during host Ca{superscript 2} signaling events. Active egress, an essential step of the parasites infection cycle, is preceded by a large increase in cytosolic Ca2+, most likely initiated by release from intracellular stores. However, extracellular Ca2+ is also necessary to reach a cytosolic Ca2+ threshold required for timely egress. In this study, we investigated the mechanism of Ca{superscript 2} intracellular store replenishment and identified a central role for the SERCA-Ca2+-ATPase in maintaining Ca{superscript 2} homeostasis not only within the ER but also in other organelles. We demonstrate mitochondrial Ca2+ uptake, which occurs by transfer of Ca2+ from the ER, likely through membrane contact sites. Our findings suggest that the T. gondii ER plays a key role in sequestering and redistributing Ca{superscript 2} to intracellular organelles following Ca{superscript 2} influx at the PM. HIGHLIGHTSThe T. gondii ER takes up Ca2+ that enters the cytosol from the extracellular milieu. Filling of acidic stores in T. gondii depends on ER Ca{superscript 2} content. The mitochondrion of T. gondii has no direct access to extracellular Ca{superscript 2} but can take it up via transfer from the ER and/or acidic stores. The absence of SERCA activity results in reduced Ca{superscript 2} levels in the ER as well as in other organelles

cell biology↗

Heterogeny in cages: Age-structure and timing of attractant availability impacts fertile egg production in the black soldier fly, Hermetia illucens

Adult behavior is a growing area of interest for those researching the black soldier fly, Hermetia illucens (L.) (Diptera: Stratiomyidae), which is affected by underlying demography and spatiotemporal patterns. This greenhouse experiment examined the interaction of age-related effects that can accrue within heterogeneous breeding populations and the potential benefits of delaying an oviposition attractant in concert with restricting mean cohort age. The impetus for this investigation was because if flies are introduced into a mating-cage before old flies are removed or culled, this creates a population of mixed-age and mating-status. We hypothesized this potentially reduces quality among available mate choices, especially in small cages where flies might not be able to spatially segregate. Metrics for fitness included copulation frequency, oviposition frequency, weight of eggs produced, and hatch percentage. "Same"-aged cohorts (maximum 4-d-old at introduction) performed better than highly heterogeneous (1-16-d-old) "mixed" cohorts by mating 2.32-times more frequently and laying 6.58-times more eggs that were 1.17-times more fertile, despite 1.41 fewer observed oviposition events. Delaying the attractant had a significant effect on egg collection weight and led to 1.25-times higher egg yields for same- age populations compared to mixed-aged cohorts where the delaying the attractant had no significant effect. These results are likely due in part to an immediate desire to lay eggs by older females as well as haphazard egg laying in cage material, which was 2.09-times higher for mixed cohorts. The results highlight the importance of constraining the age of breeding populations and removing old adults from cages to improve yields and better manipulate behavior. For those for whom this is logistically unfeasible, providing an attractant box initially and continuously may be the preferred method to trap more eggs from heterogeneous populations.

ecology↗

Biomolecular condensates and biogeomorphological systems exhibit a phase-separation behavior unified by a mass-conserving model

Phase separation is crucial in biological processes and ecological resilience, yet experimental evidence supporting validity of mass-conserving reaction-diffusion (MCRD) models in describing phase separation remains rare. Here, we identified one type of biomolecular condensates - double-stranded DNA (dsDNA) and the human transcription factor p53 as forming dsDNA-protein interactive co-condensates (DPICs) as an experimental model, where dynamic DPICs evolve into droplet-like patterns through reversible autocatalytic biochemical reactions. Thus, we can use the MCRD model to describe this experimental system. The pattern formation depends on concentration of protein and dsDNA and their local nonlinear interactions, which were experimentally tested at meso-scale and integrated into an MCRD model. Our results provide direct evidence that the experimental data-driven MCRD models can reproduce the observed phase diagram and scaling-invariance coarsening patterns, thus, providing a compelling mechanism for phase-separation pattern in other systems.

biophysics↗

Heat Shock Factor Regulation of Antimicrobial Peptides Expression Suggests a Conserved Defense Mechanism Induced by Febrile Temperature in Arthropods

Temperature is a critical factor influencing the outbreak and progression of viral diseases in organisms. Febrile temperatures have been shown to enhance immune competence and reduce viral replication in various species. However, the underlying mechanisms remain largely unknown. In this study, we investigate the molecular mechanisms by which elevated temperatures confer resistance to viral infections, focusing on the role of heat shock factor 1 (HSF1) in regulating antimicrobial effectors rather than the traditional target genes molecular chaperones. Using shrimp Litopenaeus vannamei as a model, we demonstrate that febrile temperatures induce HSF1, which in turn upregulates antimicrobial peptides (AMPs) that target viral envelope proteins and inhibit viral replication. Importantly, this is the first to show that HSF1 directly binds to the heat shock elements (HSE) motifs of AMPs both in shrimp and Drosophila S2 cells, suggesting this may be a conserved regulatory mechanism in arthropods. Additionally, our findings highlight the role of HSF1 beyond the classical heat shock response, revealing its critical function in modulating innate immunity. These insights provide new avenues for managing viral infections in aquaculture and other settings by leveraging environmental temperature control.

immunology↗

A biodegradable and restorative peripheral neural interface for the interrogation of neuropathic injuries

Monitoring the early-stage healing of severe traumatic nerve injuries is essential to gather physiological and pathological information for timely interventions and optimal clinical outcomes. While implantable peripheral nerve interfaces provide direct access to nerve fibers for precise interrogation and modulation, conventional non-degradable designs pose limited utilization in nerve injury rehabilitation. Here, we introduce a biodegradable and restorative neural interface for wireless real-time tracking and recovery of long-gap nerve injuries. Leveraging machine learning techniques, this electronic platform deciphers nerve recovery status and identifies traumatic neuroma formation at the early phase, enabling timely intervention and significantly improved therapeutic outcomes. The biodegradable nature of the device eliminates the need for retrieval procedures, reducing infection risks and secondary tissue damage. This research sheds light on bioresorbable multifunctional peripheral nerve interfaces for probing neuropathic injuries, offering vital information for early diagnosis and therapeutic intervention.

bioengineering↗