In mammalian species, including humans, spinal cord in- jury （SCI） leads to permanent disability. A major cause of disability after SCI is the failure of axotomized descending axons to regenerate across the trauma z...In mammalian species, including humans, spinal cord in- jury （SCI） leads to permanent disability. A major cause of disability after SCI is the failure of axotomized descending axons to regenerate across the trauma zone and to reconnect to they appropriate targets distal to the site of injury. Cur- renfly, major research efforts are devoted to find new ways of promoting the regrowth of damaged descending axons. However, activation of axonal regrowth will depend on the survival of the axotomized descending brain neurons.展开更多
The catalyst regeneration process running under the partial oxidation mode in traditional fluid catalytic cracking(FCC)units needs a carbon monoxide(CO)boiler to burn the flue gas,resulting in a large volume of CO_(2)...The catalyst regeneration process running under the partial oxidation mode in traditional fluid catalytic cracking(FCC)units needs a carbon monoxide(CO)boiler to burn the flue gas,resulting in a large volume of CO_(2) emissions.In this study,the performance of a set of industrial serial-type FCC regenerators and the changes in flue gas composition were analyzed by establishing a model of the regenerators and the flue gas energy recovery section.Considering the value of utilizing CO,based on the simulation,this paper proposes two schemes for maximizing CO content in the flue gas of regenerators.The two sets of optimal process operating parameters were obtained using a genetic algorithm.Compared with the original process,the CO contents of flue gas in the two optimized processes increased to 6.6%and 12.5%,CO_(2) emissions were reduced by 48.4%and 96.7%,and the costs of CO production were 0.57$/m^(3) and 0.84$/m^(3),respectively.展开更多
During long-term use,the clay checker bricks for regenerators of coke ovens on gas side react with the impurities containing Fe and K20,causing foaming,softening and deformation,which is not only related with the impu...During long-term use,the clay checker bricks for regenerators of coke ovens on gas side react with the impurities containing Fe and K20,causing foaming,softening and deformation,which is not only related with the impurity content and properties of the clay checker bricks,but also related with the type and the composition of the dust in the gas.After long term use,the clay checker bricks of coke ovens on air side have relative lower impurities containing Fe and K20.The inferior clay checker bricks,with high impurity content and high porosity,are easy to pulverize and deteriorate due to the oxidationreduction reaction with the iron oxide and the gas.The gas quality shall be concerned for long service life of the coke oven regenerators.展开更多
To extend the service life of the upper checker bricks in the regenerator of glass furnaces with petroleum coke as fuel,the corrosion resistance of magnesia-chrome and alumina-chrome bricks with the similar apparent p...To extend the service life of the upper checker bricks in the regenerator of glass furnaces with petroleum coke as fuel,the corrosion resistance of magnesia-chrome and alumina-chrome bricks with the similar apparent porosity was systematically researched.The results show that the Cr2O3 content and the microstructure present significant effects on the corrosion resistance.The molten corrosion reagent forms silicate and vanadate phases with low melting points between MgO crystals in magnesia-chrome bricks,and the volume strain generated by the melting and solidification process leads to the cracking and spalling of refractories,which intensifies the corrosion process.The encapsulation of alumina particles by alumina-chrome solid solutions in alumina-chrome bricks avoids contact with the low melting point liquid phases and improves the corrosion resistance of refractories.展开更多
With the development of optical communication systems in high bandwidth fiber, various degradations affect the propagation of light signals such as polarization mode dispersion which represents a temporal pulse broade...With the development of optical communication systems in high bandwidth fiber, various degradations affect the propagation of light signals such as polarization mode dispersion which represents a temporal pulse broadening, it becomes troublesome from long and long distances for this, it is necessary to regenerate the signal optically, that is to say, the amplified （1R regeneration） , the reshaping （2R regeneration） and sometimes resynchronize to overcome the phenomenon of jitter time （3R regeneration）. In this paper we study the contribution of 2R optical regenerator self-modulation to combat the phenomenon of polarization mode dispersion. The experiment is simulated with optisystem.展开更多
Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a...Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.展开更多
Lactate serves as a key energy metabolite in the central nervous system,facilitating essential brain functions,including energy supply,signaling,and epigenetic modulation.Moreover,it links epigenetic modifications wit...Lactate serves as a key energy metabolite in the central nervous system,facilitating essential brain functions,including energy supply,signaling,and epigenetic modulation.Moreover,it links epigenetic modifications with metabolic reprogramming.Nonetheless,the specific mechanisms and roles of this connection in astrocytes remain unclear.Therefore,this review aims to explore the role and specific mechanisms of lactate in the metabolic reprogramming of astrocytes in the central nervous system.The close relationship between epigenetic modifications and metabolic reprogramming was discussed.Therapeutic strategies for targeting metabolic reprogramming in astrocytes in the central nervous system were also outlined to guide future research in central nervous system diseases.In the nervous system,lactate plays an essential role.However,its mechanism of action as a bridge between metabolic reprogramming and epigenetic modifications in the nervous system requires future investigation.The involvement of lactate in epigenetic modifications is currently a hot research topic,especially in lactylation modification,a key determinant in this process.Lactate also indirectly regulates various epigenetic modifications,such as N6-methyladenosine,acetylation,ubiquitination,and phosphorylation modifications,which are closely linked to several neurological disorders.In addition,exploring the clinical applications and potential therapeutic strategies of lactic acid provides new insights for future neurological disease treatments.展开更多
Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted t...Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.展开更多
Neurodegenerative diseases,which are characterized by progressive neuronal loss and the lack of disease-modifying therapies,are becoming a major global health challenge.The existing neuromodulation techniques,such as ...Neurodegenerative diseases,which are characterized by progressive neuronal loss and the lack of disease-modifying therapies,are becoming a major global health challenge.The existing neuromodulation techniques,such as deep brain stimulation and transcranial magnetic stimulation,show limitations such as invasiveness,restricted cortical targeting,and irreversible tissue effects.In this context,low-intensity transcranial ultrasound has emerged as a promising noninvasive alternative that can penetrate deep into the brain and modulate neuroplasticity.This review comprehensively assesses the therapeutic mechanisms,efficacy,and translational potential of low-intensity transcranial ultrasound in treating neurodegenerative diseases,with emphasis on its role in promoting neuronal regeneration,modulating neuroinflammation,and enhancing functional recovery.We summarize the findings of previous studies and systematically illustrate the potential of low-intensity transcranial ultrasound in regulating cell death mechanisms,enhancing neural repair and regeneration,and alleviating symptoms associated with neurodegenerative diseases.Preclinical findings indicate that low-intensity transcranial ultrasound can enhance the release of neurotrophic factors(e.g.,brain-derived neurotrophic factor),promote autophagy to clear protein aggregates,modulate microglial activation,and temporarily open the blood-brain barrier to facilitate targeted drug delivery.Existing clinical trial data show that low-intensity transcranial ultrasound can reduce amyloid-βplaques,improve motor and cognitive deficits,and promote remyelination in various disease models.Early clinical trials suggest that low-intensity transcranial ultrasound may enhance cognitive scores in Alzheimer’s disease and alleviate motor symptoms in Parkinson’s disease,all while demonstrating a favorable safety profile.Past studies support the notion that by integrating safety,precision,and reversibility,low-intensity transcranial ultrasound can transform the treatment landscape for neurodegenerative disease.However,more advancements are necessary for future clinical application of low-intensity transcranial ultrasound,including optimizing parameters such as frequency,intensity,and duty cycle;considering individual anatomical differences;and confirming long-term efficacy.We believe establishing standardized protocols,conducting larger trials,and investigating the underlying mechanisms to clarify dose-response relationships and refine personalized application strategies are essential in this regard.Future research should focus on translating preclinical findings into clinical practice,addressing technical challenges,and exploring combination therapies with pharmacological or gene interventions.展开更多
Contrary to the adult central nervous system,the peripheral nervous system has an intrinsic ability to regenerate that relies on the expression of regenerationassociated genes,such as some kinesin family members.Kines...Contrary to the adult central nervous system,the peripheral nervous system has an intrinsic ability to regenerate that relies on the expression of regenerationassociated genes,such as some kinesin family members.Kinesins contribute to nerve regeneration through the transport of specific cargo,such as proteins and membrane components,from the cell body towards the axon periphery.We show here that KIF4A,associated with neurodevelopmental disorders and previously believed to be only expressed during development,is also expressed in the adult vertebrate nervous system and up-regulated in injured peripheral nervous system cells.KIF4A is detected both in the cell bodies and regrowing axons of injured neurons,consistent with its function as an axonal transporter of cargoes such asβ1-integrin and L1CAM.Our study further demonstrates that KIF4A levels are greatly increased in Schwann cells from injured distal nerve stumps,particularly at a time when they are reprogrammed into an essential proliferative repair phenotype.Moreover,Kif4a m RNA levels were approximately~6-fold higher in proliferative cultured Schwann cells compared with non-proliferative ones.A hypothesized function for Kif4a in Schwann cell proliferation was further confirmed by Kif4a knockdown,as this significantly reduced Schwann cell proliferation in vitro.Our findings show that KIF4A is expressed in adult vertebrate nervous systems and is up-regulated following peripheral injury.The timing of KIF4A up-regulation,its location during regeneration,and its proliferative role,all suggest a dual role for this protein in neuroregeneration that is worth exploring in the future.展开更多
Voltage-gated sodium channels are essential ionic-conductance pathways in the nervous system,which play an irreplaceable role in modulating neuronal excitability and signal transduction.This review comprehensively ana...Voltage-gated sodium channels are essential ionic-conductance pathways in the nervous system,which play an irreplaceable role in modulating neuronal excitability and signal transduction.This review comprehensively analyzes the molecular mechanisms and pathophysiological significance of voltage-gated sodium channels,with particular emphasis on elucidating the molecular-action mechanisms of the distinct subtypes of these channels,including Nav1.1,Nav1.2,and Nav1.6,across various neurological disorders such as familial hemiplegic migraine,epilepsy,autism spectrum disorder,and retinal dysfunction.This review also provides a comprehensive overview of the pathogenic mechanisms associated with voltage-gated sodium channels,and systematically clarifies the evolutionary pathway of treatment strategies from conventional to innovative approaches.It analyzes two major categories of conventional sodium channel blockers and their applications:antiepileptic drugs(such as carbamazepine,lamotrigine,and phenytoin)and antiarrhythmic drugs(such as lidocaine,flecainide,and quinidine).However,these conventional blockers show limitations because of the lack of selectivity,driving research toward more precise therapeutic directions.Additionally,this review evaluates gabapentin,cannabidiol,and calcium channel blockers with different mechanisms of action.These drugs modulate neuronal excitability from multiple perspectives,providing diverse options for symptom relief.This review also highlights advances in gene therapy for specific diseases,such as STK-001,which promotes effective splicing of the sodium channel voltage-gated type 1 alpha subunit(SCN1A)gene,and ETX101,which utilizes adeno-associated virus 9 vectors to deliver engineered transcription factors.These two agents provide targeted therapeutic solutions for Dravet syndrome.Furthermore,this review summarizes some innovative therapeutic agents in clinical trials,including PRAX-222(for SCN2A gain-offunction mutation-related epilepsy),which has received Food and Drug Administration orphan drug designation,and the selective Nav1.6 inhibitor NBI-921352(for SCN8A-related epilepsy).Collectively,this review comprehensively compares the advantages and disadvantages of conventional drugs and gene therapy and envisions future treatment strategies that integrate the strengths of both approaches,facilitating personalized precision medicine to provide more accurate and effective treatment options for patients with ion channel diseases.展开更多
Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability...Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.展开更多
Economical and sustainable wastewater treatment techniques are highly demanded to alleviate the issues of clearwater scarcity globally.In this work,the acetic acid/H_(2)O_(2) (AHP) was leveraged to enrich oxygenated f...Economical and sustainable wastewater treatment techniques are highly demanded to alleviate the issues of clearwater scarcity globally.In this work,the acetic acid/H_(2)O_(2) (AHP) was leveraged to enrich oxygenated functional groups on the biochar surface for efficient ciprofloxacin (CIP) adsorption and biochar regeneration (In situ degradation of CIP in the spent AHP solution).The AHP-modified biochar exhibited significantly enhanced CIP adsorption capacity,about 22 times that of the pristine biochar.The optimized modification condition (acetic acid/H_(2)O_(2):2.11,temperature:45 ℃,and time:12 h) was screened by the response surface method,reaching the highest CIP adsorption capacity of 86.26 mg·g^(−1).Characterization results revealed that the content of carboxyl —C=O—O was enhanced in AHP-modified biochar,which contributed to efficient CIP adsorption by the electrostatic interaction,hydrogen bonding,and hydrophobic interaction.The adsorption of modified biochar to CIP molecules was a spontaneous endothermic process,and in line with the pseudo-second-order model and the Langmuir isotherm model.Moreover,the biochar modification process enabled the spent AHP solution with a strong oxidizing agent of peracetic acid (PAA),which can be employed to degrade adsorbed CIP for biochar in-situ generation.This work tailored a closed-loop strategy for biochar oxidation,contaminant adsorption,and biochar regeneration,highlighting a viable route for sustainable wastewater treatment.展开更多
Wound management continues to present major clinical challenges,often necessitating therapeutic strategies that extend beyond conventional dressings,which provide only passive protection.Magnesium(Mg),a biologically i...Wound management continues to present major clinical challenges,often necessitating therapeutic strategies that extend beyond conventional dressings,which provide only passive protection.Magnesium(Mg),a biologically indispensable element,has attracted considerable attention for its multifaceted role in wound repair,including modulation of inflammatory responses,stimulation of fibroblast and keratinocyte proliferation,promotion of angiogenesis,and enhancement of collagen synthesis.However,the direct application of Mg formulations is limited by uncontrolled Mg ion(Mg^(2+))release,localized cytotoxicity at elevated concentrations,and inadequate mechanical stability at the wound site.To address these challenges,Mg-incorporated polymeric scaffolds have been developed as advanced delivery platforms.These systems integrate the regenerative capacity of Mg with the tunable properties of polymers,enabling controlled degradation,mechanical reinforcement,and sustained Mg^(2+)release to establish a favorable microenvironment for tissue repair.This review critically examines the role of Mg in wound healing and the effectiveness of polymeric matrices for controlled Mg^(2+)delivery.It further provides a comprehensive evaluation of recent advances in Mg-incorporated polymeric scaffolds,including nanofibers,hydrogels,and sponges,with emphasis on fabrication strategies,structural characteristics,and therapeutic efficacy.Key challenges,such as optimizing ion release kinetics,enhancing scaffold stability,and facilitating clinical translation,are also discussed.Collectively,this work underscores the potential of Mg-polymeric scaffolds as a next-generation platform for advanced wound care and highlights perspectives for future research and development.展开更多
Spinal cord injury is a severe neurological condition characterized by the permanent loss of nerve cell function and a failure in neural circuit reconstruction-key factors contributing to disability.Therefore,explorin...Spinal cord injury is a severe neurological condition characterized by the permanent loss of nerve cell function and a failure in neural circuit reconstruction-key factors contributing to disability.Therefore,exploring effective strategies to promote the repair and regeneration of nerve cells after spinal cord injury is crucial for optimizing patient prognosis.The purpose of this paper is to conduct an in-depth review of the pathological changes in nerve cells after spinal cord injury and to present the state of research on the role of exercise training in promoting the repair and regeneration of nerve cells after spinal cord injury.In terms of the intrinsic growth capacity of neurons,disruptions in the dynamic balance between growth cones and the cytoskeleton,the dysregulation of transcription factors,abnormal protein signaling transduction,and altered epigenetic modifications collectively hinder axonal regeneration.Additionally,the microenvironment of neurons undergoes a series of complex changes,initially manifesting as edema,which may be exacerbated by spinal cord ischemia-reperfusion injury,further increasing the extent of nerve cell damage.The abnormal proliferation of astrocytes leads to the formation of glial scars,creating a physical barrier to nerve regeneration.The inflammatory response triggered by the excessive activation of microglia negatively impacts the process of nerve repair.Non-invasive interventions involving exercise training have shown significant potential in promoting nerve repair as part of a comprehensive treatment strategy for spinal cord injury.Specifically,exercise training can reshape the growth cone and cytoskeletal structures of neurons,regulate transcription factor activity,modulate protein signaling pathways,and influence epigenetic modifications,thereby activating the intrinsic repair mechanisms of neurons.Moreover,exercise training can regulate the activation state of astrocytes,optimize the inflammatory response and metabolic processes,promote astrocyte polarization,enhance angiogenesis,reduce glial scar formation,and modulate the expression levels of nerve growth factors.It also effectively helps regulate microglial activation,promotes axonal regeneration,and improves phagocytic function,thereby optimizing the microenvironment for nerve repair.In terms of clinical translation,we summarize the preliminary results of new drug research and development efforts,the development of innovative devices,and the use of exercise training in promoting clinical advancements in nerve repair following spinal cord injury,while considering their limitations and future application prospects.In summary,this review systematically analyzes findings relating to the pathological changes occurring in nerve cells after spinal cord injury and emphasizes the critical role of exercise training in facilitating the repair and regeneration of nerve cells.This work is expected to provide new ideas and methods for the rehabilitation of patients with spinal cord injury.展开更多
The growing volume of end-of-life lithium-ion batteries(LIBs)represents both an urgent environmental challenge and a critical resource opportunity,especially for cathode materials.Among commercial cathodes,LiFePO4(LFP...The growing volume of end-of-life lithium-ion batteries(LIBs)represents both an urgent environmental challenge and a critical resource opportunity,especially for cathode materials.Among commercial cathodes,LiFePO4(LFP)dominates the market due to its favorable properties;thus,a substantial amount of LFP cathode materials is expected to retire in the near future.The conventional hydrometallurgical method suffers from high costs and serious pollution.Direct regeneration technologies,especially solid-state sintering,provide a more efficient and environmentally benign alternative by repairing cathode structures through high-temperature solid-phase reactions without extra chemical reagents.Traditional solid-state sintering faces challenges in processing spent LFP from diverse sources,struggling to achieve the homogenization of physical–chemical properties and electrochemical performance.To address the limitations above,phase homogenization with a lattice reconstruction strategy has been investigated,which can enable effective lattice reconstruction and microstructural homogenization,demonstrating robust adaptability to spent samples from variable sources.This review systematically summarizes the mechanisms,detailed steps,characterization techniques,and advances in pre-oxidation optimization(including ion-doping and coated carbon layer modification),as well as future research directions for sustainable LFP recycling.Given this,this review is expected to offer theoretical guidance for achieving homogeneous regeneration of LFP cathode.展开更多
The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well define...The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well defined.We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6,24,and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.To understand the changes that these oligodendrocytes undergo during regeneration,we used Sox2 immunohistochemistry,a stem cell marker involved in oligodendrocyte differentiation.We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation.Before optic nerve crush,sox10:tagRFP oligodendrocytes are located in the retina,in the optic nerve head,and through all the entire optic nerve.Sox2-positive cells are present in the peripheral germinal zone,the mature retina,and the optic nerve.After optic nerve crush,sox10:tagRFP cells disappeared from the optic nerve crush zone,suggesting that they died,although they were not TUNEL positive.Concomitantly,the number of Sox2-positive cells increased around the crushed area,the optic nerve head,and the retina.Then,between 24 hours post-lesion and 14 days post-lesion,double sox10:tagRFP/Sox2-positive cells were detected in the retina,optic nerve head,and whole optic nerve,together with a proliferation response at 72 hours post-lesion.Our results confirm that a degenerating process may occur prior to regeneration.First,sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them,change their“myelinating oligodendrocyte”morphology to a“nonmyelinating oligodendrocyte”morphology,and die.Then,residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination.As new axons arise from the surviving retinal ganglion cells,new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide,nourish and myelinate them.Thus,oligodendrocytes play an active role in zebrafish axon regeneration and remyelination.展开更多
The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular rec...The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular recanalization treatments such as thrombolysis and mechanical thrombectomy have achieved some success,reperfusion injury remains a significant contributor to the exacerbation of brain injury.This emphasizes the need for developing neuroprotective strategies to mitigate this type of injury.The purpose of this review was to examine the application of nanotechnology in the treatment of ischemic stroke,covering research progress in nanoparticlebased drug delivery,targeted therapy,and antioxidant and anti-inflammatory applications.Nanobased drug delivery systems offer several advantages compared to traditional therapies,including enhanced blood–brain barrier penetration,prolonged drug circulation time,improved drug stability,and targeted delivery.For example,inorganic nanoparticles,such as those based on CeO_(2),have been widely studied for their strong antioxidant capabilities.Biomimetic nanoparticles,such as those coated with cell membranes,have garnered significant attention owing to their excellent biocompatibility and targeting abilities.Nanoparticles can be used to deliver a wide range of neuroprotective agents,such as antioxidants(e.g.,edaravone),anti-inflammatory drugs(e.g.,curcumin),and neurotrophic factors.Nanotechnology significantly enhances the efficacy of these drugs while minimizing adverse reactions.Although nanotechnology has demonstrated great potential in animal studies,its clinical application still faces several challenges,including the long-term safety of nanoparticles,the feasibility of large-scale production,quality control,and the ability to predict therapeutic effects in humans.In summary,nanotechnology holds significant promise for the treatment of ischemic stroke.Future research should focus on further exploring the mechanisms of action of nanoparticles,developing multifunctional nanoparticles,and validating their safety and efficacy through rigorous clinical trials.Moreover,interdisciplinary collaboration is essential for advancing the use of nanotechnology in stroke treatment.展开更多
To address the problems with catalytic degradation,such as poisoning and inactivation,a simple and efficient gas purging regeneration technique was developed for iron-based catalyst in-situ regeneration.Specifically,t...To address the problems with catalytic degradation,such as poisoning and inactivation,a simple and efficient gas purging regeneration technique was developed for iron-based catalyst in-situ regeneration.Specifically,the effects of carrier gas types,regeneration temperatures,and granular activated carbon(GAC)addition on iron-based catalyst regeneration were investigated.The Fe_(3)O_(4)/𝛾-Al_(2)O_(3) regenerated at 550°C with additional GAC and 15%water vapor exhibited the optimal degradation efficiency towards polychlorinated biphenyls(PCBs),with an increase from 41.2%to 93.5%,compared with non-regenerated Fe_(3)O_(4)/𝛾-Al_(2)O_(3).In addition,the 60-hour stability test revealed a well-recovered catalytic activity.During the Fe_(3)O_(4)/𝛾-Al_(2)O_(3) regeneration,the coke on the catalyst surface was oxidized and removed in the form of CO_(2),and meanwhile the oxidized Fe(III)was reduced into Fe(II)in the catalyst.This study provides a safe and efficient iron-based catalyst regeneration technology for PCB off-gas degradation and reveals the catalytic activity recovery mechanism during catalyst regeneration.展开更多
文摘In mammalian species, including humans, spinal cord in- jury （SCI） leads to permanent disability. A major cause of disability after SCI is the failure of axotomized descending axons to regenerate across the trauma zone and to reconnect to they appropriate targets distal to the site of injury. Cur- renfly, major research efforts are devoted to find new ways of promoting the regrowth of damaged descending axons. However, activation of axonal regrowth will depend on the survival of the axotomized descending brain neurons.
文摘The catalyst regeneration process running under the partial oxidation mode in traditional fluid catalytic cracking(FCC)units needs a carbon monoxide(CO)boiler to burn the flue gas,resulting in a large volume of CO_(2) emissions.In this study,the performance of a set of industrial serial-type FCC regenerators and the changes in flue gas composition were analyzed by establishing a model of the regenerators and the flue gas energy recovery section.Considering the value of utilizing CO,based on the simulation,this paper proposes two schemes for maximizing CO content in the flue gas of regenerators.The two sets of optimal process operating parameters were obtained using a genetic algorithm.Compared with the original process,the CO contents of flue gas in the two optimized processes increased to 6.6%and 12.5%,CO_(2) emissions were reduced by 48.4%and 96.7%,and the costs of CO production were 0.57$/m^(3) and 0.84$/m^(3),respectively.
文摘During long-term use,the clay checker bricks for regenerators of coke ovens on gas side react with the impurities containing Fe and K20,causing foaming,softening and deformation,which is not only related with the impurity content and properties of the clay checker bricks,but also related with the type and the composition of the dust in the gas.After long term use,the clay checker bricks of coke ovens on air side have relative lower impurities containing Fe and K20.The inferior clay checker bricks,with high impurity content and high porosity,are easy to pulverize and deteriorate due to the oxidationreduction reaction with the iron oxide and the gas.The gas quality shall be concerned for long service life of the coke oven regenerators.
基金support from the National Natural Science Foundation of China(U20A20239)the Key Research and Development Project of Hubei Province,China(2022BAA032).
文摘To extend the service life of the upper checker bricks in the regenerator of glass furnaces with petroleum coke as fuel,the corrosion resistance of magnesia-chrome and alumina-chrome bricks with the similar apparent porosity was systematically researched.The results show that the Cr2O3 content and the microstructure present significant effects on the corrosion resistance.The molten corrosion reagent forms silicate and vanadate phases with low melting points between MgO crystals in magnesia-chrome bricks,and the volume strain generated by the melting and solidification process leads to the cracking and spalling of refractories,which intensifies the corrosion process.The encapsulation of alumina particles by alumina-chrome solid solutions in alumina-chrome bricks avoids contact with the low melting point liquid phases and improves the corrosion resistance of refractories.
文摘With the development of optical communication systems in high bandwidth fiber, various degradations affect the propagation of light signals such as polarization mode dispersion which represents a temporal pulse broadening, it becomes troublesome from long and long distances for this, it is necessary to regenerate the signal optically, that is to say, the amplified （1R regeneration） , the reshaping （2R regeneration） and sometimes resynchronize to overcome the phenomenon of jitter time （3R regeneration）. In this paper we study the contribution of 2R optical regenerator self-modulation to combat the phenomenon of polarization mode dispersion. The experiment is simulated with optisystem.
基金supported by the National Natural Science Foundation of China,82471345(to LC)the Key Research and Development Program for Social Development by the Jiangsu Provincial Department of Science and Technology.No.BE2022668(to LC).
文摘Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.
基金supported by the National Natural Science Foundation of China,Nos.82071383,82371392(to BN)the Natural Science Foundation of Shandong Province of China(Key Project),No.ZR2020KH007(to BN)+1 种基金“Taishan Scholar Distinguished Expert Program”of Shandong Province,No.tstp20231257(to BN)Health Commission Science and Technology Plan Project of Jinan,No.2023-1-8(to YZ).
文摘Lactate serves as a key energy metabolite in the central nervous system,facilitating essential brain functions,including energy supply,signaling,and epigenetic modulation.Moreover,it links epigenetic modifications with metabolic reprogramming.Nonetheless,the specific mechanisms and roles of this connection in astrocytes remain unclear.Therefore,this review aims to explore the role and specific mechanisms of lactate in the metabolic reprogramming of astrocytes in the central nervous system.The close relationship between epigenetic modifications and metabolic reprogramming was discussed.Therapeutic strategies for targeting metabolic reprogramming in astrocytes in the central nervous system were also outlined to guide future research in central nervous system diseases.In the nervous system,lactate plays an essential role.However,its mechanism of action as a bridge between metabolic reprogramming and epigenetic modifications in the nervous system requires future investigation.The involvement of lactate in epigenetic modifications is currently a hot research topic,especially in lactylation modification,a key determinant in this process.Lactate also indirectly regulates various epigenetic modifications,such as N6-methyladenosine,acetylation,ubiquitination,and phosphorylation modifications,which are closely linked to several neurological disorders.In addition,exploring the clinical applications and potential therapeutic strategies of lactic acid provides new insights for future neurological disease treatments.
基金supported by the National Natural Science Foundation of China,Nos.32271389,31900987(both to PY)the Natural Science Foundation of Jiangsu Province,No.BK20230608(to JJ)。
文摘Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.
基金supported by STI2030-Major Project,No,2021ZD0204200(to LX).
文摘Neurodegenerative diseases,which are characterized by progressive neuronal loss and the lack of disease-modifying therapies,are becoming a major global health challenge.The existing neuromodulation techniques,such as deep brain stimulation and transcranial magnetic stimulation,show limitations such as invasiveness,restricted cortical targeting,and irreversible tissue effects.In this context,low-intensity transcranial ultrasound has emerged as a promising noninvasive alternative that can penetrate deep into the brain and modulate neuroplasticity.This review comprehensively assesses the therapeutic mechanisms,efficacy,and translational potential of low-intensity transcranial ultrasound in treating neurodegenerative diseases,with emphasis on its role in promoting neuronal regeneration,modulating neuroinflammation,and enhancing functional recovery.We summarize the findings of previous studies and systematically illustrate the potential of low-intensity transcranial ultrasound in regulating cell death mechanisms,enhancing neural repair and regeneration,and alleviating symptoms associated with neurodegenerative diseases.Preclinical findings indicate that low-intensity transcranial ultrasound can enhance the release of neurotrophic factors(e.g.,brain-derived neurotrophic factor),promote autophagy to clear protein aggregates,modulate microglial activation,and temporarily open the blood-brain barrier to facilitate targeted drug delivery.Existing clinical trial data show that low-intensity transcranial ultrasound can reduce amyloid-βplaques,improve motor and cognitive deficits,and promote remyelination in various disease models.Early clinical trials suggest that low-intensity transcranial ultrasound may enhance cognitive scores in Alzheimer’s disease and alleviate motor symptoms in Parkinson’s disease,all while demonstrating a favorable safety profile.Past studies support the notion that by integrating safety,precision,and reversibility,low-intensity transcranial ultrasound can transform the treatment landscape for neurodegenerative disease.However,more advancements are necessary for future clinical application of low-intensity transcranial ultrasound,including optimizing parameters such as frequency,intensity,and duty cycle;considering individual anatomical differences;and confirming long-term efficacy.We believe establishing standardized protocols,conducting larger trials,and investigating the underlying mechanisms to clarify dose-response relationships and refine personalized application strategies are essential in this regard.Future research should focus on translating preclinical findings into clinical practice,addressing technical challenges,and exploring combination therapies with pharmacological or gene interventions.
基金supported by the Portuguese Foundation for Science and Technology(FCT),Centro 2020 and Portugol2020 and the EU FEDER program,via the project GoBack to SIV(PTDC/CVT-CVT/32261/2017,CENTRO-01-0145-FEDER-032261)the doctoral grants of PDC(SFRH/BD/139974/2018)and BMS(2020.06525.BD and DOI 10.54499/2020.06525.BD)+5 种基金the post-doctoral grant to JPF(SFRH/BPD/113359/2015-program-contract described in paragraphs 4,5,6 of art.23 of Law no.100157/2016,of August 29,as amended by Law no.57/2017 of July 2019),the project PTDC/MED-NEU/1677/2021 to JBRthe Institute of Biomedicine iBiMED(UIDB/04501/2020 and DOI 10.54499/UIDB/04501/2020,UIDP/04501/2020 and DOI 10.54499/UIDP/04501/2020)its LiM Bioimaging Facility-a PPBI node(POCI-01-0145-FEDER-022122)supported by the Research Commission of the Medical Faculty of the Heinrich-Heine-University(HHU)Düsseldorf,of the Biologisch-Medizinisches Forschungszentrum(BMFZ)of HHUfinanced by the Spanish"Plan Nacional de Investigacion Cientifica,Desarrollo e Innovacion Tecnologica,Ministerio de Economia y Competitividad(Instituto de Salud CarlosⅢ)",co-financed by the European Union(FEDER program),(grant FIS P/20/00318 and FIS P23/00337 to VC)grant CPP2021-009070 to VC by the"Proyectos de colaboracion publico-privada,Plan de Investigacion Cientifica,Tecnica y de inovacion 2021-2023,Ministerio de Ciencia e Innovacion,Union Europea,Agencia Estatal de Investigacion,Espana"。
文摘Contrary to the adult central nervous system,the peripheral nervous system has an intrinsic ability to regenerate that relies on the expression of regenerationassociated genes,such as some kinesin family members.Kinesins contribute to nerve regeneration through the transport of specific cargo,such as proteins and membrane components,from the cell body towards the axon periphery.We show here that KIF4A,associated with neurodevelopmental disorders and previously believed to be only expressed during development,is also expressed in the adult vertebrate nervous system and up-regulated in injured peripheral nervous system cells.KIF4A is detected both in the cell bodies and regrowing axons of injured neurons,consistent with its function as an axonal transporter of cargoes such asβ1-integrin and L1CAM.Our study further demonstrates that KIF4A levels are greatly increased in Schwann cells from injured distal nerve stumps,particularly at a time when they are reprogrammed into an essential proliferative repair phenotype.Moreover,Kif4a m RNA levels were approximately~6-fold higher in proliferative cultured Schwann cells compared with non-proliferative ones.A hypothesized function for Kif4a in Schwann cell proliferation was further confirmed by Kif4a knockdown,as this significantly reduced Schwann cell proliferation in vitro.Our findings show that KIF4A is expressed in adult vertebrate nervous systems and is up-regulated following peripheral injury.The timing of KIF4A up-regulation,its location during regeneration,and its proliferative role,all suggest a dual role for this protein in neuroregeneration that is worth exploring in the future.
基金supported by the National Natural Science Foundation of China,Nos.82471107,31970930(both to KY)the National Key Research and Development Program of China,No.2024YFA1108701(to KY)+1 种基金the Natural Science Foundation of Hubei Province,Nos.2020CFA069(to KY),2018CFB434(to KY),2025AFB042(to HQ)the Neuroscience Team Development Project of Wuhan University of Science and Technology,Nos.1180002,1180030(both to KY)。
文摘Voltage-gated sodium channels are essential ionic-conductance pathways in the nervous system,which play an irreplaceable role in modulating neuronal excitability and signal transduction.This review comprehensively analyzes the molecular mechanisms and pathophysiological significance of voltage-gated sodium channels,with particular emphasis on elucidating the molecular-action mechanisms of the distinct subtypes of these channels,including Nav1.1,Nav1.2,and Nav1.6,across various neurological disorders such as familial hemiplegic migraine,epilepsy,autism spectrum disorder,and retinal dysfunction.This review also provides a comprehensive overview of the pathogenic mechanisms associated with voltage-gated sodium channels,and systematically clarifies the evolutionary pathway of treatment strategies from conventional to innovative approaches.It analyzes two major categories of conventional sodium channel blockers and their applications:antiepileptic drugs(such as carbamazepine,lamotrigine,and phenytoin)and antiarrhythmic drugs(such as lidocaine,flecainide,and quinidine).However,these conventional blockers show limitations because of the lack of selectivity,driving research toward more precise therapeutic directions.Additionally,this review evaluates gabapentin,cannabidiol,and calcium channel blockers with different mechanisms of action.These drugs modulate neuronal excitability from multiple perspectives,providing diverse options for symptom relief.This review also highlights advances in gene therapy for specific diseases,such as STK-001,which promotes effective splicing of the sodium channel voltage-gated type 1 alpha subunit(SCN1A)gene,and ETX101,which utilizes adeno-associated virus 9 vectors to deliver engineered transcription factors.These two agents provide targeted therapeutic solutions for Dravet syndrome.Furthermore,this review summarizes some innovative therapeutic agents in clinical trials,including PRAX-222(for SCN2A gain-offunction mutation-related epilepsy),which has received Food and Drug Administration orphan drug designation,and the selective Nav1.6 inhibitor NBI-921352(for SCN8A-related epilepsy).Collectively,this review comprehensively compares the advantages and disadvantages of conventional drugs and gene therapy and envisions future treatment strategies that integrate the strengths of both approaches,facilitating personalized precision medicine to provide more accurate and effective treatment options for patients with ion channel diseases.
文摘Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of proinflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of plateletrich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.
基金supported by the National Natural Science Foundation of China(22478266 and 32472027)the National Key Research&Development Program of China(2022YFE0207100)the Department of Science and Technology of Sichuan Province(2024ZYD0080 and 2022YFN0027).
文摘Economical and sustainable wastewater treatment techniques are highly demanded to alleviate the issues of clearwater scarcity globally.In this work,the acetic acid/H_(2)O_(2) (AHP) was leveraged to enrich oxygenated functional groups on the biochar surface for efficient ciprofloxacin (CIP) adsorption and biochar regeneration (In situ degradation of CIP in the spent AHP solution).The AHP-modified biochar exhibited significantly enhanced CIP adsorption capacity,about 22 times that of the pristine biochar.The optimized modification condition (acetic acid/H_(2)O_(2):2.11,temperature:45 ℃,and time:12 h) was screened by the response surface method,reaching the highest CIP adsorption capacity of 86.26 mg·g^(−1).Characterization results revealed that the content of carboxyl —C=O—O was enhanced in AHP-modified biochar,which contributed to efficient CIP adsorption by the electrostatic interaction,hydrogen bonding,and hydrophobic interaction.The adsorption of modified biochar to CIP molecules was a spontaneous endothermic process,and in line with the pseudo-second-order model and the Langmuir isotherm model.Moreover,the biochar modification process enabled the spent AHP solution with a strong oxidizing agent of peracetic acid (PAA),which can be employed to degrade adsorbed CIP for biochar in-situ generation.This work tailored a closed-loop strategy for biochar oxidation,contaminant adsorption,and biochar regeneration,highlighting a viable route for sustainable wastewater treatment.
基金supported by Health and Medical Research Fund(18190481)Research Impact Fund(R4034-23F)+6 种基金Areas of Excellence(AoE/M-402/20)General Research Fund(14120924)Co-funding Mechanism on Joint Laboratories with the CAS(JLFS/M-401/24)the Knowledge Transfer Project Fund(KPF24GWP05)the IdeaBooster Fund(IDBF25MED07)Natural Science Foundation of Guangdong Province(Guangdong 2021A15150112042021A1515011285).
文摘Magnesium(Mg)-based biomaterials transform inherent limitations—rapid degradation and suboptimal strength—into therapeutic advantages for orthopedic regeneration.Contrary to industrial perceptions,the moderate corrosion rate and bone-mimetic stiffness(~30 GPa)of Mg synergistically support tissue repair:degradation products activate multiple pathways to enhance functional bone regeneration.Clinical translation milestones include China’s first NMPA-approved Mg-based 3D-printed scaffold.Future advancement hinges on three pillars:biomimetic structural design,material refinement,and smart implants.By redefining the“shortcomings”of Mg as regenerative assets,this paradigm accelerates functional bone reconstruction across orthopedic scenarios.
文摘Wound management continues to present major clinical challenges,often necessitating therapeutic strategies that extend beyond conventional dressings,which provide only passive protection.Magnesium(Mg),a biologically indispensable element,has attracted considerable attention for its multifaceted role in wound repair,including modulation of inflammatory responses,stimulation of fibroblast and keratinocyte proliferation,promotion of angiogenesis,and enhancement of collagen synthesis.However,the direct application of Mg formulations is limited by uncontrolled Mg ion(Mg^(2+))release,localized cytotoxicity at elevated concentrations,and inadequate mechanical stability at the wound site.To address these challenges,Mg-incorporated polymeric scaffolds have been developed as advanced delivery platforms.These systems integrate the regenerative capacity of Mg with the tunable properties of polymers,enabling controlled degradation,mechanical reinforcement,and sustained Mg^(2+)release to establish a favorable microenvironment for tissue repair.This review critically examines the role of Mg in wound healing and the effectiveness of polymeric matrices for controlled Mg^(2+)delivery.It further provides a comprehensive evaluation of recent advances in Mg-incorporated polymeric scaffolds,including nanofibers,hydrogels,and sponges,with emphasis on fabrication strategies,structural characteristics,and therapeutic efficacy.Key challenges,such as optimizing ion release kinetics,enhancing scaffold stability,and facilitating clinical translation,are also discussed.Collectively,this work underscores the potential of Mg-polymeric scaffolds as a next-generation platform for advanced wound care and highlights perspectives for future research and development.
基金supported by the National Natural Science Foundation of China,No.81641048Research Project of Yan’an University,No.2023JBZR-011(both to LZ).
文摘Spinal cord injury is a severe neurological condition characterized by the permanent loss of nerve cell function and a failure in neural circuit reconstruction-key factors contributing to disability.Therefore,exploring effective strategies to promote the repair and regeneration of nerve cells after spinal cord injury is crucial for optimizing patient prognosis.The purpose of this paper is to conduct an in-depth review of the pathological changes in nerve cells after spinal cord injury and to present the state of research on the role of exercise training in promoting the repair and regeneration of nerve cells after spinal cord injury.In terms of the intrinsic growth capacity of neurons,disruptions in the dynamic balance between growth cones and the cytoskeleton,the dysregulation of transcription factors,abnormal protein signaling transduction,and altered epigenetic modifications collectively hinder axonal regeneration.Additionally,the microenvironment of neurons undergoes a series of complex changes,initially manifesting as edema,which may be exacerbated by spinal cord ischemia-reperfusion injury,further increasing the extent of nerve cell damage.The abnormal proliferation of astrocytes leads to the formation of glial scars,creating a physical barrier to nerve regeneration.The inflammatory response triggered by the excessive activation of microglia negatively impacts the process of nerve repair.Non-invasive interventions involving exercise training have shown significant potential in promoting nerve repair as part of a comprehensive treatment strategy for spinal cord injury.Specifically,exercise training can reshape the growth cone and cytoskeletal structures of neurons,regulate transcription factor activity,modulate protein signaling pathways,and influence epigenetic modifications,thereby activating the intrinsic repair mechanisms of neurons.Moreover,exercise training can regulate the activation state of astrocytes,optimize the inflammatory response and metabolic processes,promote astrocyte polarization,enhance angiogenesis,reduce glial scar formation,and modulate the expression levels of nerve growth factors.It also effectively helps regulate microglial activation,promotes axonal regeneration,and improves phagocytic function,thereby optimizing the microenvironment for nerve repair.In terms of clinical translation,we summarize the preliminary results of new drug research and development efforts,the development of innovative devices,and the use of exercise training in promoting clinical advancements in nerve repair following spinal cord injury,while considering their limitations and future application prospects.In summary,this review systematically analyzes findings relating to the pathological changes occurring in nerve cells after spinal cord injury and emphasizes the critical role of exercise training in facilitating the repair and regeneration of nerve cells.This work is expected to provide new ideas and methods for the rehabilitation of patients with spinal cord injury.
基金financially supported by National Natural Science Key Foundation of China(52534010)National Natural Science Foundation of China(52374288,52204298)+2 种基金Young Elite Scientists Sponsorship Program by China Association for Science and Technology(2022QNRC001)National Key Research and Development Program of China(2022YFC3900805-4/7)Collaborative Innovation Centre for Clean and Efficient Utilization of Strategic Metal Mineral Resources,Found of State Key Laboratory of Mineral Processing(BGRIMM-KJSKL-2017-13).
文摘The growing volume of end-of-life lithium-ion batteries(LIBs)represents both an urgent environmental challenge and a critical resource opportunity,especially for cathode materials.Among commercial cathodes,LiFePO4(LFP)dominates the market due to its favorable properties;thus,a substantial amount of LFP cathode materials is expected to retire in the near future.The conventional hydrometallurgical method suffers from high costs and serious pollution.Direct regeneration technologies,especially solid-state sintering,provide a more efficient and environmentally benign alternative by repairing cathode structures through high-temperature solid-phase reactions without extra chemical reagents.Traditional solid-state sintering faces challenges in processing spent LFP from diverse sources,struggling to achieve the homogenization of physical–chemical properties and electrochemical performance.To address the limitations above,phase homogenization with a lattice reconstruction strategy has been investigated,which can enable effective lattice reconstruction and microstructural homogenization,demonstrating robust adaptability to spent samples from variable sources.This review systematically summarizes the mechanisms,detailed steps,characterization techniques,and advances in pre-oxidation optimization(including ion-doping and coated carbon layer modification),as well as future research directions for sustainable LFP recycling.Given this,this review is expected to offer theoretical guidance for achieving homogeneous regeneration of LFP cathode.
基金supported by the Lanzadera TCUE and C2 program(Universidad de Salamanca)(to ASL)the Spanish National Research Council(CSIC)funded by the Junta de Castilla y León and co-financed by the European Regional Development Fund(ERDF“Europe drives our growth”):Internationalization Project“CL-EI-2021-08-IBFG Unit of Excellence”,Grant(PID2022-138478OA-100)funded by MICIU/AEI/10.13039/501100011033 and,by FEDER,UE(to MGM)+3 种基金Junta de Castilla y León(SA225P23)Gerencia Regional de Salud(2701/A1/2023)(to AV)the Plan Especial Grado Medicina(USAL)(to CPM)a Ramón y Cajal researcher:Grant RYC2021-033684-I funded by MICIU/AEI/10.13039/501100011033 and,by European Union NextGenerationEU/PRTR.
文摘The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well defined.We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6,24,and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.To understand the changes that these oligodendrocytes undergo during regeneration,we used Sox2 immunohistochemistry,a stem cell marker involved in oligodendrocyte differentiation.We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation.Before optic nerve crush,sox10:tagRFP oligodendrocytes are located in the retina,in the optic nerve head,and through all the entire optic nerve.Sox2-positive cells are present in the peripheral germinal zone,the mature retina,and the optic nerve.After optic nerve crush,sox10:tagRFP cells disappeared from the optic nerve crush zone,suggesting that they died,although they were not TUNEL positive.Concomitantly,the number of Sox2-positive cells increased around the crushed area,the optic nerve head,and the retina.Then,between 24 hours post-lesion and 14 days post-lesion,double sox10:tagRFP/Sox2-positive cells were detected in the retina,optic nerve head,and whole optic nerve,together with a proliferation response at 72 hours post-lesion.Our results confirm that a degenerating process may occur prior to regeneration.First,sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them,change their“myelinating oligodendrocyte”morphology to a“nonmyelinating oligodendrocyte”morphology,and die.Then,residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination.As new axons arise from the surviving retinal ganglion cells,new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide,nourish and myelinate them.Thus,oligodendrocytes play an active role in zebrafish axon regeneration and remyelination.
基金supported by the National Natural Science Foundation of China,Nos.82301093(to QC)and 22334004(to HY)the Fuzhou University Fund for Testing Precious Equipment,No.2025T038(to QC)。
文摘The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular recanalization treatments such as thrombolysis and mechanical thrombectomy have achieved some success,reperfusion injury remains a significant contributor to the exacerbation of brain injury.This emphasizes the need for developing neuroprotective strategies to mitigate this type of injury.The purpose of this review was to examine the application of nanotechnology in the treatment of ischemic stroke,covering research progress in nanoparticlebased drug delivery,targeted therapy,and antioxidant and anti-inflammatory applications.Nanobased drug delivery systems offer several advantages compared to traditional therapies,including enhanced blood–brain barrier penetration,prolonged drug circulation time,improved drug stability,and targeted delivery.For example,inorganic nanoparticles,such as those based on CeO_(2),have been widely studied for their strong antioxidant capabilities.Biomimetic nanoparticles,such as those coated with cell membranes,have garnered significant attention owing to their excellent biocompatibility and targeting abilities.Nanoparticles can be used to deliver a wide range of neuroprotective agents,such as antioxidants(e.g.,edaravone),anti-inflammatory drugs(e.g.,curcumin),and neurotrophic factors.Nanotechnology significantly enhances the efficacy of these drugs while minimizing adverse reactions.Although nanotechnology has demonstrated great potential in animal studies,its clinical application still faces several challenges,including the long-term safety of nanoparticles,the feasibility of large-scale production,quality control,and the ability to predict therapeutic effects in humans.In summary,nanotechnology holds significant promise for the treatment of ischemic stroke.Future research should focus on further exploring the mechanisms of action of nanoparticles,developing multifunctional nanoparticles,and validating their safety and efficacy through rigorous clinical trials.Moreover,interdisciplinary collaboration is essential for advancing the use of nanotechnology in stroke treatment.
基金supported by the Fundamental Research Funds for the Central Publicinterest Scientific Institution(No.2024YSKY-44)the National Key R&D Program of China(No.2023YFC3708003).
文摘To address the problems with catalytic degradation,such as poisoning and inactivation,a simple and efficient gas purging regeneration technique was developed for iron-based catalyst in-situ regeneration.Specifically,the effects of carrier gas types,regeneration temperatures,and granular activated carbon(GAC)addition on iron-based catalyst regeneration were investigated.The Fe_(3)O_(4)/𝛾-Al_(2)O_(3) regenerated at 550°C with additional GAC and 15%water vapor exhibited the optimal degradation efficiency towards polychlorinated biphenyls(PCBs),with an increase from 41.2%to 93.5%,compared with non-regenerated Fe_(3)O_(4)/𝛾-Al_(2)O_(3).In addition,the 60-hour stability test revealed a well-recovered catalytic activity.During the Fe_(3)O_(4)/𝛾-Al_(2)O_(3) regeneration,the coke on the catalyst surface was oxidized and removed in the form of CO_(2),and meanwhile the oxidized Fe(III)was reduced into Fe(II)in the catalyst.This study provides a safe and efficient iron-based catalyst regeneration technology for PCB off-gas degradation and reveals the catalytic activity recovery mechanism during catalyst regeneration.
