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Applied Mathematics and Mechanics(English Edition) 2025年第1期46卷 25-36页

作者： Jue ZhU Longyuan li Ningtao ZhU Zhejiang Provincial Engineering Research Center for the safety of Pressure Vessel and Pipeline Key Laboratory of Impact and safety Engineering (Ningbo University) Ministry of Education school of Engineering Computing and Mathematics University of Plymouth Xi'an Zhanshi Testing & Engineering Co.Ltd.

Carbon nanotubes(CNTs) have garnered great attention in recent years due to their outstanding electrical, thermal, and mechanical properties. The incorporation of small amounts of CNTs in polymers can substantially improve the sensitivity of the polymer's electrical conductivity. This paper presents a modified Maxwell model to evaluate the electrical conductivity of CNTs-filled polymer composites by introducing a transition zone to account for the tunneling effect. In this modified Maxwell model, the CNTs-filled polymer composite is modeled as a three-phase composite, consisting of a matrix(polymer), inclusions(CNTs), and a transition zone(tunneling zone). The effective electrical conductivity(EEC) of the composite is calculated based on the volume fractions and electrical conductivities of the matrix, inclusions, and transition zone. The model's validity is confirmed through the use of available test data, which demonstrates its capability to accurately capture the nonlinear conductivity behavior observed in CNTs-polymer composites. This study offers valuable insights into the design of high-performance conductive polymer nanocomposites, and enhances the understanding of electrical conduction mechanisms in CNT-dispersed polymer composites.

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Boosting bidirectional sulfur conversion enabled by introducing boron-doped atoms and phosphorus vacancies in Ni2P for lithium-sulfur batteries

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Journal of Energy Chemistry 2025年第1期100卷 760-769页

作者： lin Peng Yu Bai hang li Meixiu Qu Zhenhua Wang Kening sun Advanced Research Institute of Multidisciplinary science Beijing Institute of Technology Beijing Key Laboratory of Chemical Power source and Green Catalysis School of Chemistry and Chemical Engineering Beijing Institute of Technology

lithium-sulfur （li-s） batteries have gained great attention due to the high theoretical energy density and low cost,yet their further commercialization has been obstructed by the notorious shuttle effect and sluggish redox ***,we supply a strategy to optimize the electron structure of Ni2P by concurrently introducing B-doped atoms and P vacancies in Ni2P （Vp-B-Ni2P）,thereby enhancing the bidirectional sulfur *** study indicates that the simultaneous introduction of B-doped atoms and P vacancies in Ni2P causes the redistribution of electron around Ni atoms,bringing about the upward shift of d-band center of Ni atoms and effective d-p orbital hybridization between Ni atoms and sulfur species,thus strengthening the chemical anchoring for lithium polysulfides （liPss） as well as expediting the bidirectional conversion kinetics of sulfur ***,theoretical calculations reveal that the incorporation of B-doped atoms and P vacancies in Ni2P selectively promotes li2s dissolution and nucleation ***,the li-s batteries with Vp-B-Ni2P-separators present outstanding rate ability of 777 m A h g-1at 5 C and high areal capacity of 8.03 mA h cm-2under E/s of 5μL mg-1and sulfur loading of 7.20 mg *** work elucidates that introducing heteroatom and vacancy in metal phosphide collaboratively regulates the electron structure to accelerate bidirectional sulfur conversion.

关键词： lithium sulfur batteries

Brain endothelial cyclic GMP-AMP synthase(cGAs)-stimulator of interferon genes(sTING)signaling pathway in aging and neurodegeneration

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Neural Regeneration Research 2025年第7期20卷 2005-2007页

作者： Bryan sun Lulin li Jian Luo Palo Alto Veterans Institute for Research VA Palo Alto Health Care SystemPalo AltoCAUSA Polytrauma system of Care VA Palo Alto Health Care SystemPalo AltoCAUSA

The cyclic GMP-AMP synthase(cGAs)-stimulator of interferon genes(sTING)signaling pathway has emerged as a key mediator of *** current studies primarily attribute its effects to neurons and glial cells,emerging research suggests that cGAs-sTING signaling may play a critical role in cerebral vasculature,particularly in brain endothelial ***,studying the role 7of inflammation caused by the cGAs-sTING pathway in brain endothelial cells could provide a more comprehensive understanding of neuroinflammatory disease and new avenues for therapeutic ***,we review the multifaceted role of global cGAs-sTING signaling in various neurological and neuroinflammatory diseases and the potential contribution of cGAs-sTING in brain endothelial cells.

关键词： stimulator interferon inflammation

CNKsR2 interactome analysis indicates its association with the centrosome/microtubule system

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Neural Regeneration Research 2025年第8期20卷 2420-2432页

作者： lin Yin Yalan Xu Jie Mu Yu Leng Lei Ma Yu Zheng Ruizhi li Yin Wang Peifeng li hai Zhu Dong Wang Jing li Institute for Translational Medicine The Affiliated Hospital of Qingdao UniversityMedical CollegeQingdao UniversityQingdaoShandong ProvinceChina school of Basic Medicine Qingdao UniversityQingdaoShandong ProvinceChina College of life sciences and School of PharmacyMedical CollegeQingdao UniversityQingdaoShandong ProvinceChina Department of Urology Qingdao Municipal Hospital Affiliated to Qingdao UniversityQingdaoShandong ProvinceChina

The protein connector enhancer of kinase suppressor of Ras 2(CNKsR2),present in both the postsynaptic density and cytoplasm of neurons,is a scaffolding protein with several protein-binding *** of the CNKsR2 gene have been implicated in neurodevelopmental disorders,particularly intellectual disability,although the precise mechanism involved has not yet been fully *** has demonstrated that CNKsR2 plays a role in facilitating the localization of postsynaptic density protein complexes to the membrane,thereby influencing synaptic signaling and the morphogenesis of dendritic ***,the function of CNKsR2 in the cytoplasm remains to be *** this study,we used immunoprecipitation and high-resolution liquid chromatography-mass spectrometry to identify the interactors of *** a combination of bioinformatic analysis and cytological experiments,we found that the CNKsR2 interactors were significantly enriched in the proteome of the *** also showed that CNKsR2 interacted with the microtubule protein DYNC1h1 and with the centrosome marker *** colocalization analysis confirmed the centrosomal localization of *** we downregulated CNKsR2 expression in mouse neuroblastoma cells(Neuro 2A),we observed significant changes in the expression of numerous centrosomal *** manipulation also affected centrosome-related functions,including cell size and shape,cell proliferation,and ***,we found that CNKsR2 interactors were highly enriched in de novo variants associated with intellectual disability and autism spectrum *** findings establish a connection between CNKsR2 and the centrosome,and offer new insights into the underlying mechanisms of neurodevelopmental disorders.

关键词： autism spectrum disorder centrosome CNKsR2 intellectual disability interactome mass spectrometry microtubule neurodevelopmental disease protein complexes protein-protein interactions

Exosomes originating from neural stem cells undergoing necroptosis participate in cellular communication by inducing TsC2 upregulation of recipient cells following spinal cord injury

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Neural Regeneration Research 2025年第11期20卷 3273-3286页

作者： shiming li Jianfeng li Guoliang Chen Tao lin Penghui Zhang Kuileung Tong Ningning Chen shaoyu liu shenzhen Key Laboratory of Bone Tissue Repair and Translational Research Department of Orthopedic SurgeryThe Seventh Affiliated HospitalSun Yat-sen UniversityShenzhenGuangdong ProvinceChina Department of Orthopedic surgery The First Affiliated Hospital of Jinan UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedics and Traumatology Zhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedic surgery The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedic surgery The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina

We previously demonstrated that inhibiting neural stem cells necroptosis enhances functional recovery after spinal cord *** exosomes are recognized as playing a pivotal role in neural stem cells exocrine function,their precise function in spinal cord injury remains *** investigate the role of exosomes generated following neural stem cells necroptosis after spinal cord injury,we conducted singlecell RNA sequencing and validated that neural stem cells originate from ependymal cells and undergo necroptosis in response to spinal cord ***,we established an in vitro necroptosis model using neural stem cells isolated from embryonic mice aged 16-17 days and extracted *** results showed that necroptosis did not significantly impact the fundamental characteristics or number of *** sequencing of exosomes in necroptosis group identified 108 differentially expressed messenger RNAs,104 long non-coding RNAs,720 circular RNAs,and 14 microRNAs compared with the control *** of a competing endogenous RNA network identified the following hub genes:tuberous sclerosis 2(Tsc2),solute carrier family 16 member 3(slc16a3),and forkhead box protein P1(Foxp1).Notably,a significant elevation in TsC2 expression was observed in spinal cord tissues following spinal cord ***2-positive cells were localized around sRY-box transcription factor 2-positive cells within the injury ***,in vitro analysis revealed increased TsC2 expression in exosomal receptor cells compared with other *** assessment of cellular communication following spinal cord injury showed that Tsc2 was involved in ependymal cellular communication at 1 and 3 days post-injury through the epidermal growth factor and midkine signaling *** addition,slc16a3 participated in cellular communication in ependymal cells at 7 days post-injury via the vascular endothelial growth factor and macrophage migration inhibitory factor signaling

关键词： cellular communication competing endogenous RNA exosomes Foxp1 necroptosis neural stem cells slc16a3 spinal cord injury transcriptome sequencing Tsc2

Peripheral blood RNA biomarkers can predict lesion severity in degenerative cervical myelopathy

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Neural Regeneration Research 2025年第6期20卷 1764-1775页

作者： Zhenzhong Zheng Jialin Chen Jinghong Xu Bin Jiang Lei li Yawei li Yuliang Dai Bing Wang Department of spine surgery The Second Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina

Degenerative cervical myelopathy is a common cause of spinal cord injury,with longer symptom duration and higher myelopathy severity indicating a worse *** numerous studies have investigated serological biomarkers for acute spinal cord injury,few studies have explored such biomarkers for diagnosing degenerative cervical *** study involved 30 patients with degenerative cervical myelopathy(51.3±7.3 years old,12 women and 18 men),seven healthy controls(25.7±1.7 years old,one woman and six men),and nine patients with cervical spondylotic radiculopathy(51.9±8.6 years old,three women and six men).Analysis of blood samples from the three groups showed clear differences in transcriptomic *** analysis identified 128 differentially expressed genes that were enriched in patients with neurological *** least absolute shrinkage and selection operator analysis,we constructed a five-gene model(TBCD,TPM2,PNKD,EIF4G2,and AP5Z1)to diagnose degenerative cervical myelopathy with an accuracy of 93.5%.One-gene models(TCAP and sDhA)identified mild and severe degenerative cervical myelopathy with accuracies of 83.3%and 76.7%,*** of two immune cell types(memory B cells and memory-activated CD4^(+)T cells)predicted levels of lesions in degenerative cervical myelopathy with 80%*** results suggest that peripheral blood RNA biomarkers could be used to predict lesion severity in degenerative cervical myelopathy.

关键词： biomarkers candidate genes degenerative cervical myelopathy gene expression analysis immune cell types neurological disabilities peripheral blood RNA profiles spinal cord injury

hypidone hydrochloride(YL-0919)ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation

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Neural Regeneration Research 2025年第8期20卷 2325-2336页

作者： Yafan Bai hui Ma Yue Zhang Jinfeng li Xiaojuan hou Yixin Yang Guyan Wang Yunfeng li Department of Anesthesiology Beijing Tongren HospitalCapital Medical UniversityBeijingChina Beijing Institute of Basic Medical sciences BeijingChina hebei North University ZhangjiakouHebei ProvinceChina Beijing Institute of Pharmacology and Toxicology State Key Laboratory of Toxicology and Medical CountermeasuresBeijing Key Laboratory of NeuropsychopharmacologyBeijingChina

Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary *** this study,we evaluated hypidone hydrochloride(YL-0919),a self-developed antidepressant with selective sigma-1 receptor agonist properties,and its associated mechanisms and targets in traumatic brain *** experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain ***,we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in hT22 ***,the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist(BD-1047).Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury,while also decreasing neuronal mortality and reversing blood-brain barrier disruption and brain ***,YL-0919 effectively combated oxidative stress both in vivo and in *** protective effects of YL-0919 were partially inhibited by *** results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress,a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist ***-0919 may have potential as a new treatment for traumatic brain injury.

关键词： antidepressant drug blood-brain barrier cognitive function hypidone hydrochloride(YL-0919) neurological function nuclear factor-erythroid 2 related factor 2 oxidative stress sigma-1 receptor superoxide dismutase traumatic brain injury

Transforming growth factor-beta 1 enhances discharge activity of cortical neurons

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Neural Regeneration Research 2025年第2期20卷 548-556页

作者： Zhihui Ren Tian li Xueer liu Zelin Zhang Xiaoxuan Chen Weiqiang Chen Kangsheng li Jiangtao sheng Department of Microbiology and Immunology Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular ImmunopathologyShantou University Medical CollegeShantouGuangdong ProvinceChina Department of Neurosurgery First Affiliated Hospital of Shantou University Medical CollegeShantouGuangdong ProvinceChina

Transforming growth factor-beta 1(TGF-β1)has been extensively studied for its pleiotropic effects on central nervous system *** neuroprotective or neurotoxic effects of TGF-β1 in specific brain areas may depend on the pathological process and cell types ***-gated sodium channels(VGsCs)are essential ion channels for the generation of action potentials in neurons,and are involved in various neuroexcitation-related ***,the effects of TGF-β1 on the functional properties of VGsCs and firing properties in cortical neurons remain *** this study,we investigated the effects of TGF-β1 on VGsC function and firing properties in primary cortical neurons from *** found that TGF-β1 increased VGsC current density in a dose-and time-dependent manner,which was attributable to the upregulation of Nav1.3 *** VGsC current density and Nav1.3 expression were significantly abolished by preincubation with inhibitors of mitogen-activated protein kinase kinase(PD98059),p38 mitogen-activated protein kinase(sB203580),and Jun Nh2-terminal kinase 1/2 inhibitor(sP600125).Interestingly,TGF-β1 significantly increased the firing threshold of action potentials but did not change their firing rate in cortical *** findings suggest that TGF-β1 can increase Nav1.3 expression through activation of the ERK1/2-JNK-MAPK pathway,which leads to a decrease in the firing threshold of action potentials in cortical neurons under pathological ***,this contributes to the occurrence and progression of neuroexcitatory-related diseases of the central nervous system.

关键词： central nervous system cortical neurons ERK firing properties JNK Nav1.3 p38 transforming growth factor-beta 1 traumatic brain injury voltage-gated sodium currents

Plasmon-induced local electric field improved hydrogen evolution reaction on Ag/Mo_(2)C nanosheets

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Nano Research 2025年第1期18卷 270-277页

作者： huangJingWei li Xin Zi Jun Wu Xinli Wang li Zhu Qiyou Wang Jianfu han Junwei Fu hongmei li Kai huang Yu Chen Min liu school of Physics State Key Laboratory of Powder MetallurgyHunan Joint International Research Center for Carbon Dioxide Resource UtilizationCentral South UniversityChangsha 410083China school of Metallurgy and Environment Central South UniversityChangsha 410083China Institute of high Energy Physics Chinese Academy of Sciences(CAS)Beijing 100049China Nano-Institute Munich Faculty of PhysicsLudwig-Maxilimians-Universität MünchenMünchen 80539Germany hunan Institute of Advanced sensing and Information Technology Xiangtan UniversityXiangtan 411105China

Electrocatalytic water splitting offers a promising way for hydrogen production with near-zero ***,such as molybdenum carbides(Mo_(2)C),are promising materials for hydrogen evolution reaction(hER)but still suffer from poor intrinsic water activation ***,we developed a plasmon-induced local electric field(PILEF)strategy to solve this ***(Ag)nanoparticles decorated Mo_(2)C nanosheets(Ag/Mo_(2)C)were successfully prepared by electrostatic *** visible light excited the PILEF on Ag/Mo_(2)C remarkably reducing the activation energy by 92.7 kJ·mol^(-1)from 147.3 kJ·mol^(-1)of Mo_(2)C to 54.6 kJ·mol^(-1).As a result,the plasmonic Ag/Mo_(2)C significantly enhances~2.3-fold of the current density from 2.8 mA·cm^(-2)of Mo_(2)C to 6.5 mA·cm^(-2)at-3 V *** and reduces the overpotential by 104 mV from 403 mV of dark state to 299 mV of light state at the current density of 10 mA·cm^(-2),achieving better performance than reported *** research demonstrates that PILEF enhances hER activities,offering a potential strategy for boosting the intrinsic activities of catalysts.

关键词： sliver particles plasmon effect field effect hydrogen evolution reaction(hER) electrocatalysis

FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

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Neural Regeneration Research 2025年第7期20卷 2068-2083页

作者： Jing Yao Yuan li Xi liu Wenping liang Yu li liyong Wu Zhe Wang Weihong song The National Clinical Research Center for Geriatric Disease Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Department of Neurosurgery Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Pediatrics The Second Affiliated Hospital and Yuying Children’s HospitalKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceInstitute of AgingWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Oujiang Laboratory(Zhejiang Laboratory for Regenerative Medicine Visionand Brain Health)WenzhouZhejiang ProvinceChina

Alzheimer's disease is characterized by deposition of amyloid-β,which forms extracellular neuritic plaques,and accumulation of hyperphosphorylated tau,which aggregates to form intraneuronal neurofibrillary tangles,in the *** NLRP3 inflammasome may play a role in the transition from amyloid-βdeposition to tau phosphorylation and *** NLRP3 is primarily found in brain microglia,and tau is predominantly located in neurons,it has been suggested that NLRP3 expressed by microglia indirectly triggers tau phosphorylation by upregulating the expression of pro-inflammatory ***,we found that neurons also express NLRP3 in vitro and in vivo,and that neuronal NLRP3 regulates tau *** biochemical methods,we mapped the minimal NLRP3 promoter and identified FUBP3 as a transcription factor regulating NLRP3 expression in *** primary neurons and the neuroblastoma cell line Neuro2A,FUBP3 is required for endogenous NLRP3 expression and tau phosphorylation only when amyloid-βis *** the brains of aged wild-type mice and a mouse model of Alzheimer's disease,FUBP3 expression was markedly increased in cortical *** analysis suggested that FUBP3 plays a role in neuron-mediated immune *** also found that FUBP3 trimmed the 5′end of DNA fragments that it bound,implying that FUBP3 functions in stress-induced *** findings suggest that neuronal NLRP3 may be more directly involved in the amyloid-β-to–phospho-tau transition than microglial NLRP3,and that amyloid-βfundamentally alters the regulatory mechanism of NLRP3 expression in *** that FUBP3 was only expressed at low levels in young wild-type mice and was strongly upregulated in the brains of aged mice and Alzheimer's disease mice,FUBP3 could be a safe therapeutic target for preventing Alzheimer's disease progression.

关键词： 5′end trimming Alzheimer's disease amyloid-beta amyloid-β-dependent transcription FUBP3 inflammasome inflammation neuron NLRP3 tau transcription factor