miRNA-21-5p is an important contributor to the promotion of injured peripheral nerve regeneration using hypoxia-pretreated bone marrow-derived neural crest cells.

JOURNAL/nrgr/04.03/01300535-202501000-00035/figure1/v/2024-05-14T021156Z/r/image-tiff Our previous study found that rat bone marrow-derived neural crest cells (acting as Schwann cell progenitors) have the potential to promote long-distance nerve repair. Cell-based therapy can enhance peripheral nerve repair and regeneration through paracrine bioactive factors and intercellular communication. Nevertheless, the complex contributions of various types of soluble cytokines and extracellular vesicle cargos to the secretome remain unclear. To investigate the role of the secretome and extracellular vesicles in repairing damaged peripheral nerves, we collected conditioned culture medium from hypoxia-pretreated neural crest cells, and found that it significantly promoted the repair of sensory neurons damaged by oxygen-glucose deprivation. The mRNA expression of trophic factors was highly expressed in hypoxia-pretreated neural crest cells. We performed RNA sequencing and bioinformatics analysis and found that miR-21-5p was enriched in hypoxia-pretreated extracellular vesicles of neural crest cells. Subsequently, to further clarify the role of hypoxia-pretreated neural crest cell extracellular vesicles rich in miR-21-5p in axonal growth and regeneration of sensory neurons, we used a microfluidic axonal dissociation model of sensory neurons in vitro, and found that hypoxia-pretreated neural crest cell extracellular vesicles promoted axonal growth and regeneration of sensory neurons, which was greatly dependent on loaded miR-21-5p. Finally, we constructed a miR-21-5p-loaded neural conduit to repair the sciatic nerve defect in rats and found that the motor and sensory functions of injured rat hind limb, as well as muscle tissue morphology of the hind limbs, were obviously restored. These findings suggest that hypoxia-pretreated neural crest extracellular vesicles are natural nanoparticles rich in miRNA-21-5p. miRNA-21-5p is one of the main contributors to promoting nerve regeneration by the neural crest cell secretome. This helps to explain the mechanism of action of the secretome and extracellular vesicles of neural crest cells in repairing damaged peripheral nerves, and also promotes the application of miR-21-5p in tissue engineering regeneration medicine.

Innate Orientating Behavior of a Multi-Legged Robot Driven by the Neural Circuits of C. elegans.

The objective of this research is to achieve biologically autonomous control by utilizing a whole-brain network model, drawing inspiration from biological neural networks to enhance the development of bionic intelligence. Here, we constructed a whole-brain neural network model of Caenorhabditis elegans (C. elegans), which characterizes the electrochemical processes at the level of the cellular synapses. The neural network simulation integrates computational programming and the visualization of the neurons and synapse connections of C. elegans, containing the specific controllable circuits and their dynamic characteristics. To illustrate the biological neural network (BNN)'s particular intelligent control capability, we introduced an innovative methodology for applying the BNN model to a 12-legged robot's movement control. Two methods were designed, one involving orientation control and the other involving locomotion generation, to demonstrate the intelligent control performance of the BNN. Both the simulation and experimental results indicate that the robot exhibits more autonomy and a more intelligent movement performance under BNN control. The systematic approach of employing the whole-brain BNN for robot control provides biomimetic research with a framework that has been substantiated by innovative methodologies and validated through the observed positive outcomes. This method is established as follows: (1) two integrated dynamic models of the C. elegans' whole-brain network and the robot moving dynamics are built, and all of the controllable circuits are discovered and verified; (2) real-time communication is achieved between the BNN model and the robot's dynamical model, both in the simulation and the experiments, including applicable encoding and decoding algorithms, facilitating their collaborative operation; (3) the designed mechanisms using the BNN model to control the robot are shown to be effective through numerical and experimental tests, focusing on 'foraging' behavior control and locomotion control.

Adipocyte-specific FAK deletion promotes pancreatic ß-cell apoptosis via adipose inflammatory response to exacerbate diabetes mellitus.

BACKGROUND: White adipose tissue (WAT) has a key role in maintaining energy balance throughout the body, and their dysfunction take part in the regulation of diabetes mellitus. However, the internal regulatory mechanisms underlying are still unknown. METHODS AND RESULTS: We generated adipocyte-specific FAK KO (FAK-AKO) mice and investigated their phenotype. The cascade of adipocyte, macrophage in adipocyte tissues, and pancreatic ß-cells were proposed in FAK-AKO mice and validated by cell line studies using 3T3-L1, Raw264.7 and Min6. The FAK-AKO mice exhibited glucose intolerance, reduced adipose tissue mass and increased apoptosis, lipolysis and inflammatory response in adipose tissue. We further demonstrate that adipocyte FAK deletion increases ß cell apoptosis and inflammatory infiltrates into islets, which is potentiated if mice were treated with STZ. In the STZ-induced diabetes model, FAK AKO mice exhibit less serum insulin content and pancreatic ß cell area. Moreover, serum pro-inflammatory factors increased and insulin levels decreased after glucose stimulation in FAK AKO mice. In a parallel vitro experiment, knockdown or inhibition of FAK during differentiation also increased apoptosis, lipolysis and inflammatory in 3T3-L1 adipocytes, whereas the opposite was observed upon overexpression of FAK. Moreover, coculturing LPS-treated RAW264.7 macrophages with knockdown FAK of 3T3-L1 adipocytes increased macrophage pro-inflammatory response. Furthermore, conditioned medium from above stimulated Min6 cells apoptosis (with or without STZ), whereas the opposite was observed upon overexpression of FAK. Mechanistically, FAK protein interact with TRAF6 in adipocytes and knockdown or inhibition of FAK activated TRAF6/TAK1/NF-κB signaling, which exacerbates inflammation of adipocytes themselves. CONCLUSION: Adipocyte FAK deletion promotes both adipocyte apoptosis and adipose tissue inflammation. Pro-inflammatory factors released by the FAK-null adipose tissue further trigger apoptosis in pancreatic islets induced by the administration of STZ, thereby exacerbating the diabetes mellitus. This study reveals a link between FAK-mediated adipose inflammation and diabetes mellitus, a mechanism that has not been previously recognized.

Multihierarchical Regulation To Achieve Quantum Dot Nanospheres with a Photoluminescence Quantum Yield Close to 100.

Quantum dots (QDs) exhibit superior brightness and photochemical stability, making them the preferred option for highly sensitive single-molecule detection compared with fluorescent dyes or proteins. Nevertheless, their high surface energy leads to nonspecific adsorption and poor colloidal stability. In the past decades, we have found that QD-based fluorescent nanoparticles (FNs) can not only address these limitations but also enhance detection sensitivity. However, the photoluminescence quantum yield (PLQY) of FNs is significantly lower compared with that of original QDs. It is urgent to develop a strategy to solve the issue, aiming to further enhance detection sensitivity. In this study, we found that the decrease of PLQY of FNs prepared by free radical polymerization was attributed to two factors: (1) generation of defects that can cause nonradiative transitions resulting from QD-ligands desorption and QD-shell oxidation induced by free radicals; (2) self-absorption resulting from aggregation caused by incompatibility of QDs with polymers. Based on these, we proposed a multihierarchical regulation strategy that includes: (1) regulating QD-ligands; (2) precisely controlling free radical concentration; and (3) constructing cross-linked structures of polymer to improve compatibility and to reduce the formation of surface defects. It is crucial to emphasize that the simultaneous coordination of multiple factors is essential. Consequently, a world-record PLQY of 97.6% for FNs was achieved, breaking through the current bottleneck at 65%. The flexible application of this regulatory concept paves the way for the large-scale production of high-brightness QD-polymer complexes, enhancing their potential applications in sensitive biomedical detection.

Rice body synovitis in pediatrics: three different case reports.

Rice body synovitis (RBS) is a rare disease, especially in children. Rheumatoid disorders and tuberculosis are the first two reasons for the formation of the RB. The diagnosis is mainly based on imaging and histopathological features. Herein, we report three cases of RBS in children diagnosed with congenital synovial chondromatosis, tuberculosis (unconfirmed), and ANA -positive juvenile idiopathic arthritis. Clinical features, radiographic findings, pathophysiology, treatment process, and prognosis were reviewed and documented meticulously to enhance cognition in this population and provide some references for clinicians in diagnosing and treating the disease.

Circular photonic crystal grating design for charge-tunable quantum light sources in the telecom C-band.

Efficient generation of entangled photon pairs at telecom wavelengths is a key ingredient for long-range quantum networks. While embedding semiconductor quantum dots into hybrid circular Bragg gratings has proven effective, it conflicts with p-i-n diode heterostructures which offer superior coherence. We propose and analyze hybrid circular photonic crystal gratings, incorporating air holes to facilitate charge carrier transport without compromising optical properties. Through numerical simulations, a broad cavity mode with a Purcell factor of 23 enhancing both exciton and biexciton transitions, and exceptional collection efficiency of 92.4% into an objective with numerical aperture of 0.7 are achieved. Furthermore, our design demonstrates direct coupling efficiency over 90.5% into a single-mode fiber over the entire telecom C-band. The hybrid circular photonic crystal grating thereby emerges as a promising solution for the efficient generation of highly coherent, polarization-entangled photon pairs.

Promotive effect of skin precursor-derived Schwann cells on brachial plexus neurotomy and motor neuron damage repair through milieu-regulating secretome.

Brachial plexus injury (BPI) with motor neurons (MNs) damage still remain poor recovery in preclinical research and clinical therapy, while cell-based therapy approaches emerged as novel strategies. Previous work of rat skin precursor-derived Schwann cells (SKP-SCs) provided substantial foundation for repairing peripheral nerve injury (PNI). Given that, our present work focused on exploring the repair efficacy and possible mechanisms of SKP-SCs implantation on rat BPI combined with neurorrhaphy post-neurotomy. Results indicated the significant locomotive and sensory function recovery, with improved morphological remodeling of regenerated nerves and angiogenesis, as well as amelioration of target muscles atrophy and motor endplate degeneration. Besides, MNs could restore from oxygen-glucose-deprivation (OGD) injury upon SKP-SCs-sourced secretome treatment, implying the underlying paracrine mechanisms. Moreover, rat cytokine array assay detected 67 cytokines from SKP-SC-secretome, and bioinformatic analyses of screened 32 cytokines presented multiple functional clusters covering diverse cell types, including inflammatory cells, Schwann cells, vascular endothelial cells (VECs), neurons, and SKP-SCs themselves, relating distinct biological processes to nerve regeneration. Especially, a panel of hypoxia-responsive cytokines (HRCK), can participate into multicellular biological process regulation for permissive regeneration milieu, which underscored the benefits of SKP-SCs and sourced secretome, facilitating the chorus of nerve regenerative microenvironment. Furthermore, platelet-derived growth factor-AA (PDGF-AA) and vascular endothelial growth factor-A (VEGF-A) were outstanding cytokines involved with nerve regenerative microenvironment regulating, with significantly elevated mRNA expression level in hypoxia-responsive SKP-SCs. Altogether, through recapitulating the implanted SKP-SCs and derived secretome as niche sensor and paracrine transmitters respectively, HRCK would be further excavated as molecular underpinning of the neural recuperative mechanizations for efficient cell therapy; meanwhile, the analysis paradigm in this study validated and anticipated the actions and mechanisms of SKP-SCs on traumatic BPI repair, and was beneficial to identify promising bioactive molecule cocktail and signaling targets for cell-free therapy strategy on neural repair and regeneration.

Correction: Expanded graphite incorporated with Li4Ti5O12 nanoparticles as a high-rate lithium-ion battery anode.

[This corrects the article DOI: 10.1039/D4RA00832D.].

Exogenous Functional Mitochondria Derived from Bone Mesenchymal Stem Cells That Respond to ROS Can Rescue Neural Cells Following Ischemic Stroke.

Background: Upon uptake by stressed cells, functional mitochondria can perform their normal functions, ultimately enhancing the survival of host cells. However, despite the promising results of this approach, there is still a lack of understanding of the specific relationship between nerve cells and functional mitochondria. Methods: Functional mitochondria (F-Mito) were isolated from bone marrow-derived mesenchymal stem cells (BMSCs). The ability of microglia cells to internalize F-Mito was evaluated using a middle cerebral artery occlusion (MCAO) model in C57BL/6J mice and an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model. After OGD/R and F-Mito treatment, the temporal dynamics of intracellular reactive oxygen species (ROS) levels were examined.The relationship between ROS levels and F-Mito uptake was assessed at the individual cell level using MitoSOX, Mitotracker, and HIF-1α labeling. Results: Our findings indicate that microglia cells exhibit enhanced mitochondrial uptake compared to astrocytes. Furthermore, internalized F-Mito reduced ROS levels and HIF-1α levels. Importantly, we found that the ROS response in microglia cells following ischemia is a critical regulator of F-Mito internalization, and promoting autophagy in microglia cells might reduce the uptake of ROS and HIF-1α levels. Conclusion: It is verified that F-Mito derived from BMSCs play a protective role in ischemia-reperfusion injury, as their weakening reduces microglial cell activation and alleviates neuroinflammation.

Optic Neuritis in a Pediatric Patient with Kikuchi-Fujimoto Disease: A Case Report and Review of the Literature.

Kikuchi-Fujimoto disease (KFD), also known as histiocytic necrotizing lymphadenitis, is a rare, benign, and self-limiting condition characterized by lymph node inflammation. While KFD is rarely associated with ocular manifestations, our case report highlights bilateral optic neuritis in a 13-year-old male patient with KFD. We also provide a comprehensive review of similar cases in the literature.

A Review of Weak Gel Fracturing Fluids for Deep Shale Gas Reservoirs.

Low-viscosity slickwater fracturing fluids are a crucial technology for the commercial development of shallow shale gas. However, in deep shale gas formations with high pressure, a higher sand concentration is required to support fractures. Linear gel fracturing fluids and crosslinked gel fracturing fluids have a strong sand-carrying capacity, but the drag reduction effect is poor, and it needs to be pre-prepared to decrease the fracturing cost. Slick water fracturing fluids have a strong drag reduction effect and low cost, but their sand-carrying capacity is poor and the fracturing fluid sand ratio is low. The research and development of viscous slick water fracturing fluids solves this problem. It can be switched on-line between a low-viscosity slick water fracturing fluid and high-viscosity weak gel fracturing fluid, which significantly reduces the cost of single-well fracturing. A polyacrylamide drag reducer is the core additive of slick water fracturing fluids. By adjusting its concentration, the control of the on-line viscosity of fracturing fluid can be realized, that is, 'low viscosity for drag reduction, high viscosity for sand-carrying'. Therefore, this article introduces the research and application status of a linear gel fracturing fluid, crosslinked gel fracturing fluid, and slick water fracturing fluid for deep shale gas reservoirs, and focuses on the research status of a viscous slick water fracturing fluid and viscosity-controllable polyacrylamide drag reducer, with the aim of providing valuable insights for the research on water-based fracturing fluids in the stimulation of deep shale gas reservoirs.

Expanded graphite incorporated with Li4Ti5O12 nanoparticles as a high-rate lithium-ion battery anode.

Due to their small interlayer spacing and a low lithiation potential close to Li+ deposition, current graphite anodes suffer from weak kinetics, and lithium deposition in a fast-charging process, hindering their practical application in high-power lithium-ion batteries (LIBs). In this work, expanded graphite incorporated with Li4Ti5O12 nanoparticles (EG/LTO) was synthesized via moderate oxidization of artificial graphite following a solution coating process. The EG/LTO has sufficient porosity for fast Li+ diffusion and a dense Li4Ti5O12 layer for decreased interface reaction resistance, resulting in excellent fast-charging properties. EG/LTO presented a high reversible capacity of 272.8 mA h g-1 at 3.74 A g-1 (10C), much higher than that of the original commercial graphite (50.1 mA h g-1 at 10C) and even superior to that of hard carbon. In addition, EG/LTO exhibited capacity retention rate of 98.4% after 500 cycles at 10C, demonstrating high structural stability during a long cycling process. This study provides a protocol for a solution chemistry method to prepare fast-charging graphite anode materials with high stability for high-power LIBs.

Jasmonates Promote ß-Amylase-Mediated Starch Degradation to Confer Cold Tolerance in Tomato Plants.

Cold stress severely restricts growth and development, reduces yields, and impairs quality in tomatoes (Solanum lycopersicum). Amylase-associated starch degradation and soluble sugar accumulation have been implicated in adaptation and resistance to abiotic stress. Here, we report a ß-amylase (BAM) gene, SlBAM3, which plays a central role in tomato cold tolerance. The expression of SlBAM3 was triggered by cold stress. SlBAM3 knockout using the CRISPR/Cas9 system retarded starch degradation and reduced soluble sugar accumulation in tomato plants, eventually attenuating cold tolerance. Expression analysis revealed that the SlBAM3 transcript level was boosted by MeJA. Furthermore, MYC2, an essential component of the JA signaling pathway, could bind to the SlBAM3 promoter and directly activate SlBAM3 transcription, as revealed by yeast one-hybrid and dual LUC assays. In addition, the suppression of MYC2 resulted in increased starch accumulation, decreased soluble sugar content, and reduced tolerance to cold stress in tomato plants. Taken together, these findings demonstrate that JA positively regulates ß-amylase-associated starch degradation through the MYC2-SlBAM3 module in tomato during cold stress. The results of the present work expand our understanding of the mechanisms underlying BAM gene activation and starch catabolism under cold stress. The regulatory module of SlBAM3 can be further utilized to breed tomato cultivars with enhanced cold tolerance.

Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson's disease.

The pathogenesis of Parkinson's disease (PD) is strongly associated with neuroinflammation, and type I interferons (IFN-I) play a crucial role in regulating immune and inflammatory responses. However, the specific features of IFN in different cell types and the underlying mechanisms of PD have yet to be fully described. In this study, we analyzed the GSE157783 dataset, which includes 39,024 single-cell RNA sequencing results for five PD patients and six healthy controls from the Gene Expression Omnibus database. After cell type annotation, we intersected differentially expressed genes in each cell subcluster with genes collected in The Interferome database to generate an IFN-I-stimulated gene set (ISGs). Based on this gene set, we used the R package AUCell to score each cell, representing the IFN-I activity. Additionally, we performed monocle trajectory analysis, and single-cell regulatory network inference and clustering (SCENIC) to uncover the underlying mechanisms. In silico gene perturbation and subsequent experiments confirm NFATc2 regulation of type I interferon response and neuroinflammation. Our analysis revealed that microglia, endothelial cells, and pericytes exhibited the highest activity of IFN-I. Furthermore, single-cell trajectory detection demonstrated that microglia in the midbrain of PD patients were in a pro-inflammatory activation state, which was validated in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model as well. We identified transcription factors NFATc2, which was significantly up-regulated and involved in the expression of ISGs and activation of microglia in PD. In the 1-Methyl-4-phenylpyridinium (MPP+)-induced BV2 cell model, the suppression of NFATc2 resulted in a reduction in IFN-ß levels, impeding the phosphorylation of STAT1, and attenuating the activation of the NF-κB pathway. Furthermore, the downregulation of NFATc2 mitigated the detrimental effects on SH-SY5Y cells co-cultured in conditioned medium. Our study highlights the critical role of microglia in type I interferon responses in PD. Additionally, we identified transcription factors NFATc2 as key regulators of aberrant type I interferon responses and microglial pro-inflammatory activation in PD. These findings provide new insights into the pathogenesis of PD and may have implications for the development of novel therapeutic strategies.

MircoRNA-25-3p in skin precursor cell-induced Schwann cell-derived extracellular vesicles promotes axon regeneration by targeting Tgif1.

Nerve injury often leads to severe dysfunction because of the lack of axon regeneration in adult mammal. Intriguingly a series of extracellular vesicles (EVs) have the obvious ability to accelerate the nerve repair. However, the detailed molecular mechanisms to describe that EVs switch neuron from a transmitter to a regenerative state have not been elucidated. This study elucidated the microRNA (miRNA) expression profiles of two types of EVs that promote nerve regeneration. The functions of these miRNAs were screened in vitro. Among the 12 overlapping miRNAs, miR-25-3p was selected for further analysis as it markedly promoted axon regeneration both in vivo and in vitro. Furthermore, knockdown experiments confirmed that PTEN and Klf4, which are the major inhibitors of axon regeneration, were the direct targets of miR-25-3p in dorsal root ganglion (DRG) neurons. The utilization of luciferase reporter assays and functional tests provided evidence that miR-25-3p enhances axon regeneration by targeting Tgif1. Additionally, miR-25-3p upregulated the phosphorylation of Erk. Furthermore, Rapamycin modulated the expression of miR-25-3p in DRG neurons. Finally, the pro-axon regeneration effects of EVs were confirmed by overexpressing miR-25-3p and Tgif1 knockdown in the optic nerve crush model. Thus, the enrichment of miR-25-3p in EVs suggests that it regulates axon regeneration, proving a potential cell-free treatment strategy for nerve injury.

Intracavity spatially modulated metasurfaces for a wavelength-tunable figure-9 vortex fiber laser.

Intracavity optical metasurfaces with compact and flexible light manipulation capabilities, effectively enrich the implementation of miniaturized and user-friendly orbital angular momentum (OAM) laser sources. Here we demonstrate a wavelength-tunable figure-9 Yb-doped vortex fiber laser solely with standard non-polarization-maintaining single-mode fibers, which utilizes a gap-surface plasmon (GSP) metasurface as the intracavity mode regulation component to generate OAM beams, extending the avenues and related applications for cost-effective OAM laser sources. Gained by the broadband operation range of the metasurface, the figure-9 fiber laser could emit OAM light with center wavelength tunable from 1020 nm to 1060 nm and of high mode purity (about 90%). OAM beams with different topological charges such as l = ±1 have been obtained by changing the metasurface design. The proposed fiber laser with the intracavity GSP metasurface provides a reliable and customized output of OAM beams at the laser source, holding great promise for a wide range of applications in optical communications, sensing, and super-resolution imaging.

Exploring the neurotoxicity of chiral dinotefuran towards nicotinic acetylcholine receptors: Enantioselective insights into species selectivity.

Dinotefuran is a chiral neonicotinoid that is widely distributed in environmental matrices, but its health risks to different organisms are poorly understood. This study investigated the neurotoxic responses of honeybee/cotton aphid nicotinic acetylcholine receptors (nAChRs) to chiral dinotefuran at the enantiomeric scale and demonstrated the microscopic mechanism of species selectivity in nAChR-mediated enantioselective neurotoxicity. The findings indicated that (S)-dinotefuran had a higher affinity for honeybee nAChR than (R)-dinotefuran whereas both enantiomers exhibited similar bioactivity toward cotton aphid nAChR. The results of dynamic neurotoxic processes indicated the association of conformational changes induced by chiral dinotefuran with its macroscopic neurotoxicity, and (R)-dinotefuran, which exhibit low toxicity to honeybee, was found to induce significant conformational changes in the enantioselective neurotoxic reaction, as supported by the average root-mean-square fluctuation (0.35 nm). Energy decomposition results indicated that electrostatic contribution (ΔGele) is the critical energy term that leads to substantial enantioselectivity, and both Trp-51 (－2.57 kcal mol-1) and Arg-75 (－4.86 kcal mol-1), which form a hydrogen-bond network, are crucial residues in mediating the species selectivity for enantioselective neurotoxic responses. Clearly, this study provides experimental evidence for a comprehensive assessment of the health hazards of chiral dinotefuran.

Burkitt's lymphoma in a young boy progressing to systemic lupus erythematosus during follow-up: a case report and literature review.

Introduction: Patients with systemic lupus erythematosus (SLE) are at a higher risk of developing cancer, particularly hematological malignancies such as lymphoma and leukemia. However, existing studies on this topic that assess cancer incidence following SLE diagnosis are limited. In addition, SLE can be diagnosed after cancer, although such cases in children have been rarely reported. Case report: We present the case of a 2.6-year-old boy who presented to our institute with fever and abdominal pain. His physical examination revealed a periumbilical mass, which was pathologically diagnosed as Burkitt's lymphoma. Autologous stem cell transplantation was performed to consolidate the effect of chemotherapy and reduce the risk of cancer relapse. He was diagnosed with SLE 5 years later, following the presentation of a fever with rash, positive autoantibodies, decreased complement, and kidney involvement. At the final follow-up, the patient was still alive and showed no recurrence of Burkitt's lymphoma or disease activity of SLE. Conclusion: Despite the low frequency of SLE in children with lymphoma, cancer and SLE may be induced by a common mechanism involving B-cell cloning and proliferation. Therefore, hematologists and rheumatologists should be aware of the occurrence of these two conditions during patient follow-up.

Electrically tunable topological phase transition in non-Hermitian optical MEMS metasurfaces.

Exceptional points (EPs), unique junctures in non-Hermitian open systems where eigenvalues and eigenstates simultaneously coalesce, have gained notable attention in photonics because of their enthralling physical principles and unique properties. Nonetheless, the experimental observation of EPs, particularly within the optical domain, has proven rather challenging because of the grueling demand for precise and comprehensive control over the parameter space, further compounded by the necessity for dynamic tunability. Here, we demonstrate the occurrence of optical EPs when operating with an electrically tunable non-Hermitian metasurface platform that synergizes chiral metasurfaces with piezoelectric MEMS mirrors. Moreover, we show that, with a carefully constructed metasurface, a voltage-controlled spectral space can be finely tuned to access not only the chiral EP but also the diabolic point characterized by degenerate eigenvalues and orthogonal eigenstates, thereby allowing for dynamic topological phase transition. Our work paves the way for developing cutting-edge optical devices rooted in EP physics and opening uncharted vistas in dynamic topological photonics.

Anisotropic microtopography surface of chitosan scaffold regulating skin precursor-derived Schwann cells towards repair phenotype promotes neural regeneration.

For repairing peripheral nerve and spinal cord defects, biomaterial scaffold-based cell-therapy was emerged as an effective strategy, requiring the positive response of seed cells to biomaterial substrate and environment signals. Previous work highlighted that the imposed surface properties of scaffold could provide important guidance cues to adhered cells for polarization. However, the insufficiency of native Schwann cells and unclear cellular response mechanisms remained to be addressed. Given that, this study aimed to illuminate the micropatterned chitosan-film action on the rat skin precursor-derived Schwann cells (SKP-SCs). Chitosan-film with different ridge/groove size was fabricated and applied for the SKP-SCs induction. Results indicated that SKP-SCs cultured on 30 µm size microgroove surface showed better oriented alignment phenotype. Induced SKP-SCs presented similar genic phenotype as repair Schwann cells, increasing expression of c-Jun, neural cell adhesion molecule, and neurotrophic receptor p75. Moreover, SKP-SC-secretome was subjected to cytokine array GS67 assay, data indicated the regulation of paracrine phenotype, a panel of cytokines was verified up-regulated at secreted level and gene expression level in induced SKP-SCs. These up-regulated cytokines exhibit a series of promotive neural regeneration functions, including cell survival, cell migration, cell proliferation, angiogenesis, axon growth, and cellular organization etc. through bioinformatics analysis. Furthermore, the effectively polarized SKP-SCs-sourced secretome, promoted the proliferation and migration capacity of the primarily cultured native rat Schwann cells, and augmented neurites growth of the cultured motoneurons, as well as boosted axonal regrowth of the axotomy-injured motoneurons. Taken together, SKP-SCs obtained pro-neuroregeneration phenotype in adaptive response to the anisotropic topography surface of chitosan-film, displayed the oriented parallel growth, the transition towards repair Schwann cell genic phenotype, and the enhanced paracrine effect on neural regeneration. This study provided novel insights into the potency of anisotropic microtopography surface to Schwann-like cells phenotype regulation, that facilitating to provide promising engineered cell-scaffold in neural injury therapies.