Background:This study addresses the pressing need to understand the nuanced relationship between‘mattering’—the perception of being significant to others—and problematic internet use(PIU)among university students....Background:This study addresses the pressing need to understand the nuanced relationship between‘mattering’—the perception of being significant to others—and problematic internet use(PIU)among university students.Unlike previous research that has primarily employed variable-centered approaches,this study first adopts a person-centered approach using Latent Profile Analysis(LPA)to identify distinct mattering profiles.Subsequently,through variable-centered analyses,these profiles are examined in relation to different types of PIU—specifically problematic social media use(PSMU)and problematic gaming(PG)—as well as adaptability.Methods:Data were collected from 3587 university students across 19 universities in China.Participants completed three mattering-related scales(General Mattering Scale,Anti-Mattering Scale,and Fear of Not Mattering Inventory),along with the Bergen Social Media Addiction Scale,the Internet Gaming Disorder Scale-Short Form,and the Nine-item Adaptability Scale.Results:A four-class model identified by LPA was optimally selected:Class 1(high general mattering,low anti-mattering,low fear of not mattering),Class 2(moderate levels),Class 3(moderate general mattering,high antimattering,high fear of not mattering),and Class 4(low general mattering,low fear of not mattering,moderate anti-mattering).Significant differences were found among these classes in both PIU types(PSMU:F=139.66,p<0.001;PG:F=162.96,p<0.001).The pattern of mean differences consistently showed:Class 3>Class 2>Class 4>Class 1.Class 3 participants demonstrated the highest likelihood of meeting the addiction criteria,Class 2 showed moderate probability,while Classes 1 and 4 exhibited lower probabilities(χ^(2)=113.38 to 408.87,all p<0.001).Additionally,Class 3 reported the lowest adaptability(F=131.67,p<0.001).Conclusion:This study reveals that the unique influence of three ways of assessing feelings of mattering and the fear of not mattering on university students’PIU at the personal level,concluding that these factors are integral to understanding PIU among this demographic.展开更多
Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have rev...Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis.This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury.The NACHT,LRR,and pyrin domain-containing protein 3(NLRP3)inflammasome plays a crucial role in this context.This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome.These mechanisms include metabolic pathways(involving short-chain fatty acids,lipopolysaccharides,lactic acid,bile acids,trimethylamine-N-oxide,and tryptophan),neural pathways(such as the vagus nerve and sympathetic nerve),and immune pathways(involving microglia and T cells).We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage.The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier,inducing neuroinflammation,and interfering with nerve regeneration.Finally,we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury.Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage,paving the way for exploring potential therapeutic approaches.展开更多
Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables th...Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.展开更多
Microorganisms constitute an essential component in the indoor environment,which is closely related to hu-man health.However,there is limited evidence regarding the associations between indoor airborne microbiome and ...Microorganisms constitute an essential component in the indoor environment,which is closely related to hu-man health.However,there is limited evidence regarding the associations between indoor airborne microbiome and systemic inflammation,as well as whether this association is modified by indoor particulate matter and the underlying mechanisms.In this prospective repeated-measure study among 66 participants,indoor airborne mi-crobiome was characterized using amplicon sequencing and qPCR.Indoor fine particulate matter(PM_(2.5))and inhalable particulate matter(PM10)were measured.Systemic inflammatory biomarkers were assessed,including white blood cell(WBC),neutrophil(NEUT),monocyte,eosinophil counts,and their proportions.Targeted serum amino acid metabolomics were conducted to explore the underlying mechanisms.Linear mixed-effect models re-vealed that bacterial and fungal Simpson diversity were significantly associated with decreased WBC and NEUT.For example,for each interquartile range increase in the bacterial Simpson diversity,WBC and NEUT changed by-4.53%(95%CI:-8.25%,-0.66%)and-5.95%(95%CI:-11.3%,-0.27%),respectively.Notably,increased inflammatory risks of airborne microbial exposure were observed when indoor PM_(2.5) and PM10 levels were below the WHO air quality guidelines.Mediation analyses indicated that dopamine metabolism partially mediated the anti-inflammatory effects of fungal diversity exposure.Overall,our study indicated protection from a diverse indoor microbial environment on cardiovascular health and proposed an underlying mechanism through amino acid metabolism.Additionally,health risks associated with microbial exposure deserve more attention in con-texts of low indoor particulate matter pollution.Further research is necessary to fully disentangle the complex relationships between indoor microbiome,air pollutants,and human health.展开更多
The Dongsha area,a key target for gas hydrate exploration,is influenced by multiple factors,including sedimentary processes and the paleoenvironment,which play critical roles in gas hydrate formation.To elucidate the ...The Dongsha area,a key target for gas hydrate exploration,is influenced by multiple factors,including sedimentary processes and the paleoenvironment,which play critical roles in gas hydrate formation.To elucidate the coupling among sedimentary processes,paleoenvironment,and gas hydrate accumulation,this study investigates the Site DS-W16 using particle size analysis,biological component content,and geochemistry data.Oxygen isotope data from foraminifera and biostratigraphic evidence indicate that sedimentation at the bottom of core interval from Site DS-W16 began during MIS 11(Marine isotope stage).The sedimentation dynamics of the studied layers are complex,involving gravity flows,traction currents,and suspended deposition.Organic matter shows a significant correlation with transgressive-regressive cycle.The site DS-W16 contains two distinct gas hydrate reservoirs:a shallow reservoir(10-24 mbsf)and a deep reservoir(below 182 mbsf).The paleomarine environment influences gas hydrate accumulation by altering sedimentary processes and sediment characteristics,especially the distribution of biological components.Both shallow and deep gas hydrate reservoirs formed under dynamic conditions dominated by traction currents and are characterized by a higher abundance of foraminifera.Sedimentary layers rich in foraminifera and modified by traction currents represent key intervals for preferential gas hydrate accumulation.展开更多
β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano ...β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano et al.,2024).GBA is a membrane-bound lysosomalenzyme responsible for glucosylceramide and glucosylsphingosine hydrolysis.When this enzyme is mutated and dysfunctional,its substrates progressively accumulate within cells.展开更多
Particulate matter(PM)emitted by power machinery severely harms air quality and ecological balance,making the development of efficient and green PM-removal technologies a key global environmental challenge.This work b...Particulate matter(PM)emitted by power machinery severely harms air quality and ecological balance,making the development of efficient and green PM-removal technologies a key global environmental challenge.This work built a visualization system for diesel engine PM decomposition via non-thermal plasma(NTP),conducting multi-stage NTP oxidation at 120℃to clarify reaction pathways.The results demonstrate that NTP significantly influences the microcrystalline reconstruction and chemical evolution of PM.Early oxidation removes surface short crystallites,increasing crystallite length,reducing tortuosity,narrowing D1 peak,and boosting graphitization.Mid-stage sees NTP active substances penetrate inside,shortening crystallites and regularizing structure.Late-stage primary particles form“hollow shells”with few long crystallites,and order/graphitization rises again.Chemically,NTP reduces high-carbon components while increasing lowcarbon ones in PM soluble organics,decomposes C=C bonds to form oxygen-containing groups,enhances PM oxidation activity,weakensπ^(*)peaks,and strengthensσ^(*)peaks,clearly confirmed by the carbon K-edge electron energy loss spectra.This study clarifies the mechanistic pathways of NTP-driven PM decomposition,supporting clean energy advancement and atmospheric governance.展开更多
Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an i...Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.展开更多
Interfacial superconductivity(IS)has been a topic of intense interest in condensed matter physics,due to its unique properties and exotic photoelectrical performance.However,there are few reports about IS systems cons...Interfacial superconductivity(IS)has been a topic of intense interest in condensed matter physics,due to its unique properties and exotic photoelectrical performance.However,there are few reports about IS systems consisting of two insulators.Here,motivated by the emergence of an insulator-metal transition in type-Ⅲ heterostructures and the superconductivity in some“special”two-dimensional(2D)semiconductors via electron doping,we predict that the 2D heterostructure SnSe_(2)/PtTe_(2) is a model system for realizing IS by using firstprinciples calculations.Our results show that due to slight but crucial interlayer charge transfer,SnSe_(2)/PtTe_(2) turns to be a type-Ⅲ heterostructure with metallic properties and shows a superconducting transition with the critical temperature(T_(c))of 3.73 K.Similar to the enhanced electron–phonon coupling(EPC)in the electrondoped SnSe_(2) monolayer,the IS in the SnSe_(2)/PtTe_(2) heterostructure mainly originates from the metallized SnSe_(2) layer.Furthermore,we find that its superconductivity is sensitive to tensile lattice strain,forming a domeshaped superconducting phase diagram.Remarkably,at 7%biaxial tensile strain,the superconducting T_(c) can increase more than twofold(8.80 K),resulting from softened acoustic phonons at the𝑀point and enhanced EPC strength.Our study provides a concrete example for realizing IS in type-Ⅲ heterostructures,which waits for future experimental verification.展开更多
The accurate segmentation of deep gray matter nuclei is critical for neuropathological research,disease diagnosis and treatment.Existing methods employ the supervised learning training approach,which requires large la...The accurate segmentation of deep gray matter nuclei is critical for neuropathological research,disease diagnosis and treatment.Existing methods employ the supervised learning training approach,which requires large labeled datasets.It is challenging and time-consuming to obtain such datasets for medical image analysis.In addition,these methods based on convolutional neural networks(CNNs)only achieve suboptimal performance due to the locality of convolutional operations.Vision Transformers(ViTs)efficiently model long-range dependencies and thus have the potentiality to outperform these methods in segmentation tasks.To address these issues,we propose a novel hybrid network based on self-supervised pre-training for deep gray matter nuclei segmentation.Specifically,we present a CNN-Transformer hybrid network(CTNet),whose encoder consists of 3D CNN and ViT to learn local spatial-detailed features and global semantic information.A self-supervised learning(SSL)approach that integrates rotation prediction and masked feature reconstruction is proposed to pre-train the CTNet,enabling the model to learn valuable visual representations from unlabeled data.We evaluate the effectiveness of our method on 3T and 7T human brain MRI datasets.The results demonstrate that our CTNet achieves better performance than other comparison models and our pre-training strategy outperforms other advanced self-supervised methods.When the training set has only one sample,our pre-trained CTNet enhances segmentation performance,showing an 8.4%improvement in Dice similarity coefficient(DSC)compared to the randomly initialized CTNet.展开更多
Tunable plasmonic structures provide the possibility to actively modify the radiation from atoms through electromagnetic coupling.In this paper,we investigate the decay and radiation behavior of an atom near a dielect...Tunable plasmonic structures provide the possibility to actively modify the radiation from atoms through electromagnetic coupling.In this paper,we investigate the decay and radiation behavior of an atom near a dielectric nanosphere with conductive surface within the framework of macroscopic quantum electrodynamics.The electromagnetic fields including the losses in the materials can be taken as fundamental excitations which interact with the atom through a transition dipole.Both weak and strong coupling regimes have been investigated.The decay rate and the angle-dependent light intensities indeed strongly depend on the parameters of the system,i.e.,the position and orientation of the dipole,the geometric size,and the surface conductivity,providing the opportunity of artificial control over these quantities.Generalizing the formalism in this paper to other systems,like metamaterials,is straightforward,which we believe may pave a way for future active quantum nanophotonic devices.展开更多
Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In th...Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In this study,we investigated the potential therapeutic effects of MCC950,a selective NOD-like receptor family pyrin domain-containing protein 3 inhibitor,on cerebral small vessel disease pathogenesis and cognitive decline in spontaneously hypertensive rats.Our results showed that chronic administration of MCC950(10 mg/kg)to spontaneously hypertensive rats inhibited NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation,thereby considerably suppressing the production of pyroptosis executive protein gasdermin D and pro-inflammatory factors,including interleukin-1βand-18.A decrease in astrocytic and microglial activation was also observed.We also found that MCC950 significantly inhibited autophagy.More importantly,behavioral assessment indicated that MCC950 administration ameliorated impaired neurocognitive function,which was associated with improvements in neuropathological hallmarks in the cerebral small vessel disease brain,such as blood‒brain barrier breakdown,white matter damage,and endothelial dysfunction.Thus,our findings revealed that the NOD-like receptor family pyrin domain-containing protein 3 inflammasome is a key contributor to the onset or progression of cerebral small vessel disease and suggested the potential of NOD-like receptor family pyrin domain-containing protein 3-based therapy as a potential novel strategy for treating cerebral small vessel disease.展开更多
Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune respons...Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune responses and promote tissue repair.This review thoroughly examines the dynamic changes in the number and function of regulatory T cells and highlights their distinct roles at various stages of stroke progression.In the acute phase(within 5-7 days),regulatory T cells exert neuroprotective effects primarily by reducing inflammation.In the chronic phase(7 days post-onset),these cells support neuroregeneration and functional recovery.The review also explores the emerging role of regulatory T cells in the brain-gut axis,a key mediator of the systemic immune responses following stroke,and discusses its relevance in modulating post-stroke inflammation and repair.Various strategies aimed at enhancing regulatory T cell responses include adoptive transfer of regulatory T cells,administration of pharmacological agents,and induction of mucosal tolerance.All these approaches can potentially enhance the immunomodulatory and repair functions of regulatory T cells.Nevertheless,despite the promising preclinical results,the translation of regulatory T cell-based therapies into clinical practice is associated with challenges related to optimal timing,dosage,and long-term efficacy.Overall,targeting regulatory T cells is a novel and promising immunoregulatory approach for mitigating stroke-induced injury and promoting neural repair.展开更多
Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury respons...Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury response,including inflammation and repair.Although colony-stimulating factor 1 receptor inhibitors such as PLX5622 enable the selective depletion of microglia,their therapeutic potential in neonatal germinal matrix hemorrhage remains underexplored.Here,we used a collagenase-induced germinal matrix hemorrhage model in postnatal day 5 mice,and intraperitoneally administered PLX562272 hours post-germinal matrix hemorrhage to achieve targeted,temporary microglial depletion during the peak injury response.We then assessed the effects of this delayed intervention on oligodendrocyte lineage cell maturation,white matter integrity,and neurobehavioral outcomes.Additionally,RNA sequencing data from a germinal matrix hemorrhage rat model were analyzed using weighted gene co-expression network analysis to identify the critical phases for interventions.RNA sequencing data revealed a critical period in which key synaptic functions declined while immune responses intensified post-germinal matrix hemorrhage,thus pinpointing the critical response phases for potential interventions.Delayed PLX5622 treatment effectively depleted activated microglia,protecting against white matter injury and enhancing oligodendrocyte lineage cell maturation and myelination in subcortical white matter regions.Moreover,magnetic resonance imaging analysis revealed reduced brain lesion volumes in treated mice.Behaviorally,PLX5622-treated mice exhibited significant improvements in motor coordination and reduced hyperactivity compared with vehicle-treated germinal matrix hemorrhage model mice.These findings suggest that,when timed to avoid interference with initial oligodendrocyte lineage cell proliferation,targeted microglial depletion with PLX5622 significantly mitigates white matter damage and improves neurobehavioral outcomes in neonatal germinal matrix hemorrhage.The present study highlights the therapeutic potential of selectively modulating microglial reactivity to support neurodevelopment in preterm infants with brain injury.展开更多
Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provid...Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.展开更多
White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet li...White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet little is known about the underlying mechanism.To examine this,we established a transient middle cerebral artery occlusion male mouse model.We found that physical exercise elevated brain Treg cells,thereby enhancing neurological recovery,reducing neuroinflammation,promoting myelin debris clearance,and accelerating white matter repair.Depletion of Treg cells caused a decrease in these positive effects of physical exercise.Mechanistically,the rise in osteopontin triggered by physical exercise is dampened when Treg cells are depleted.In addition,Treg-conditioned medium reduced oxygen-glucose deprivation/re-oxygenation-induced microglial inflammation and enhanced phagocytosis,which could be blocked by osteopontin antibodies.Importantly,although Treg infusion could mimic the protective effects of physical exercise,osteopontin blockade partially countered the effects of physical exercise and Treg cells.Finally,our sequencing data revealed a marked upregulation of C-X-C motif chemokine ligand 12(CXCL12)mRNA expression subsequent to physical exercise,which was confirmed at the protein level.Stimulation of Treg cells with stroke brain lysates increased C-X-C motif chemokine receptor 4(CXCR4)expression,indicating a potential role for the CXCL12-CXCR4 axis in recruiting Treg cells.These findings suggest that physical exercise promotes white matter repair after ischemic stroke by Treg cells.展开更多
Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are...Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are incomplete and spare supraspinal pathways,especially those located within the peripheral white matter of the spinal cord,which includes reticulospinal pathways originating from the medullary reticular formation.Whereas there is abundant literature about the motor cortex,its corticospinal pathway,and its capacity to modulate functional recovery after SCI,less is known about the medullary reticular formation and its reticulospinal pathway.展开更多
To elucidate the geographical differentiation characteristics and driving mechanisms of Dissolved Organic Matter(DOM)in typical rivers,this study conducted a multi-spectral investigation on three representative river ...To elucidate the geographical differentiation characteristics and driving mechanisms of Dissolved Organic Matter(DOM)in typical rivers,this study conducted a multi-spectral investigation on three representative river types within Shandong Province:The mountainous Dawen River,the plain Tuhai River,and the artificial East Grand Canal.The DOM composition was analyzed using Ultraviolet-Visible(UV-Vis)absorption spectroscopy,Excitation-Emission Matrix(EEM)fluorescence spectroscopy,and parallel factor analysis(PARAFAC),while Principal Component Analysis(PCA)was employed to quantify the synergistic effects of natural processes and anthropogenic activities.Results revealed significant spatial heterogeneity in DOM composition and sources.The plain river exhibited the highest aromaticity(humic-like components:43.3%)due to long-term agricultural non-point source inputs and urban wastewater discharge.The mountain stream,shaped by complex terrain and relatively intact ecosystems,was dominated by autochthonous DOM derived from microbial metabolism,with higher Fluorescence Index(FI=2.12)and biological index(BIX=1.35)than other river types.The artificial canal retained protein-like components(64.2%),largely attributed to winter hydrological stagnation and disturbances from shipping activities.Further analysis demonstrated that geographical settings(e.g.,mountain terrain)and anthropogenic activities(e.g.,agriculture,shipping)jointly regulated DOM composition by altering the balance between input and transformation processes.Integrated fluorescence parameters and PCA results suggested differentiated management strategies:protecting ecological integrity in mountain streams to sustain selfpurification,enhancing non-point source interception in plain rivers,and mitigating shipping pollution in canals.This study systematically reveals the natural-anthropogenic coupling mechanisms driving DOM dynamics in northern China rivers,providing critical insights for precision water environment management at the watershed scale.展开更多
The brain atlas,or parcellation-delineating spatial partitions,organizes the brain's structure and function[1].The spatial arrangements of highly heterogeneous landscapes represent specialized functional regions f...The brain atlas,or parcellation-delineating spatial partitions,organizes the brain's structure and function[1].The spatial arrangements of highly heterogeneous landscapes represent specialized functional regions for investigating their interactions.Early efforts to parcellate the mammalian brain,using histological cytoarchitecture and myeloarchitecture,as well as recent in vivo magnetic resonance imaging(MRl)[2,3],have primarily involved cortical areas,subcortical structures,and cerebellar nuclei.Human brain parcellations primarily focus on grey matter(GM),which purposefully excludes white matter(WM),hindering the development of next-generation brain atlases.展开更多
The inter-related pathological cascades following a traumatic spinal cord injury(tSCI)disrupt multiple cell types and physiological processes.Subsequently,motor and sensory functions are disrupted by breakdowns in cel...The inter-related pathological cascades following a traumatic spinal cord injury(tSCI)disrupt multiple cell types and physiological processes.Subsequently,motor and sensory functions are disrupted by breakdowns in cellular interactions and circuitry.Therapeutic interventions seek to modify some aspects of the injury course to enable the re-establishment of functional circuitry.Interventions often target one cell type(e.g.,promoting neuroprotection or neural regeneration)or one process(e.g.,modulating inflammation,affecting astrocytic,microglial,or macrophage responses.)Many axons in the spinal cord are myelinated,and after injury oligodendrocyte death causes demyelination.Promoting remyelination of spared or new axons to re-establish conduction seems a logical choice as a therapeutic target.展开更多
基金supported by a special grant from the Taishan Scholars Project(Project No.tsqn202211130).
文摘Background:This study addresses the pressing need to understand the nuanced relationship between‘mattering’—the perception of being significant to others—and problematic internet use(PIU)among university students.Unlike previous research that has primarily employed variable-centered approaches,this study first adopts a person-centered approach using Latent Profile Analysis(LPA)to identify distinct mattering profiles.Subsequently,through variable-centered analyses,these profiles are examined in relation to different types of PIU—specifically problematic social media use(PSMU)and problematic gaming(PG)—as well as adaptability.Methods:Data were collected from 3587 university students across 19 universities in China.Participants completed three mattering-related scales(General Mattering Scale,Anti-Mattering Scale,and Fear of Not Mattering Inventory),along with the Bergen Social Media Addiction Scale,the Internet Gaming Disorder Scale-Short Form,and the Nine-item Adaptability Scale.Results:A four-class model identified by LPA was optimally selected:Class 1(high general mattering,low anti-mattering,low fear of not mattering),Class 2(moderate levels),Class 3(moderate general mattering,high antimattering,high fear of not mattering),and Class 4(low general mattering,low fear of not mattering,moderate anti-mattering).Significant differences were found among these classes in both PIU types(PSMU:F=139.66,p<0.001;PG:F=162.96,p<0.001).The pattern of mean differences consistently showed:Class 3>Class 2>Class 4>Class 1.Class 3 participants demonstrated the highest likelihood of meeting the addiction criteria,Class 2 showed moderate probability,while Classes 1 and 4 exhibited lower probabilities(χ^(2)=113.38 to 408.87,all p<0.001).Additionally,Class 3 reported the lowest adaptability(F=131.67,p<0.001).Conclusion:This study reveals that the unique influence of three ways of assessing feelings of mattering and the fear of not mattering on university students’PIU at the personal level,concluding that these factors are integral to understanding PIU among this demographic.
基金supported by the Guangdong Basic and Applied Basic Research Foundation,No.2023A1515030045(to HS)Presidential Foundation of Zhujiang Hospital of Southern Medical University,No.yzjj2022ms4(to HS)。
文摘Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis.This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury.The NACHT,LRR,and pyrin domain-containing protein 3(NLRP3)inflammasome plays a crucial role in this context.This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome.These mechanisms include metabolic pathways(involving short-chain fatty acids,lipopolysaccharides,lactic acid,bile acids,trimethylamine-N-oxide,and tryptophan),neural pathways(such as the vagus nerve and sympathetic nerve),and immune pathways(involving microglia and T cells).We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage.The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier,inducing neuroinflammation,and interfering with nerve regeneration.Finally,we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury.Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage,paving the way for exploring potential therapeutic approaches.
文摘Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.
基金supported by the National Key Research and Development Program of China(No.2022YFC3702704)the National Natural Science Foundation of China(Nos.22376005,22076006 and 82073506).
文摘Microorganisms constitute an essential component in the indoor environment,which is closely related to hu-man health.However,there is limited evidence regarding the associations between indoor airborne microbiome and systemic inflammation,as well as whether this association is modified by indoor particulate matter and the underlying mechanisms.In this prospective repeated-measure study among 66 participants,indoor airborne mi-crobiome was characterized using amplicon sequencing and qPCR.Indoor fine particulate matter(PM_(2.5))and inhalable particulate matter(PM10)were measured.Systemic inflammatory biomarkers were assessed,including white blood cell(WBC),neutrophil(NEUT),monocyte,eosinophil counts,and their proportions.Targeted serum amino acid metabolomics were conducted to explore the underlying mechanisms.Linear mixed-effect models re-vealed that bacterial and fungal Simpson diversity were significantly associated with decreased WBC and NEUT.For example,for each interquartile range increase in the bacterial Simpson diversity,WBC and NEUT changed by-4.53%(95%CI:-8.25%,-0.66%)and-5.95%(95%CI:-11.3%,-0.27%),respectively.Notably,increased inflammatory risks of airborne microbial exposure were observed when indoor PM_(2.5) and PM10 levels were below the WHO air quality guidelines.Mediation analyses indicated that dopamine metabolism partially mediated the anti-inflammatory effects of fungal diversity exposure.Overall,our study indicated protection from a diverse indoor microbial environment on cardiovascular health and proposed an underlying mechanism through amino acid metabolism.Additionally,health risks associated with microbial exposure deserve more attention in con-texts of low indoor particulate matter pollution.Further research is necessary to fully disentangle the complex relationships between indoor microbiome,air pollutants,and human health.
基金supported by National Natural Science Foundation of China(No.42376217)Fundamental Research Funds for the Central Universities of China(No.3-7-10-2025-03)National Key Research and Development Program of China(No.2024YFC2814702).
文摘The Dongsha area,a key target for gas hydrate exploration,is influenced by multiple factors,including sedimentary processes and the paleoenvironment,which play critical roles in gas hydrate formation.To elucidate the coupling among sedimentary processes,paleoenvironment,and gas hydrate accumulation,this study investigates the Site DS-W16 using particle size analysis,biological component content,and geochemistry data.Oxygen isotope data from foraminifera and biostratigraphic evidence indicate that sedimentation at the bottom of core interval from Site DS-W16 began during MIS 11(Marine isotope stage).The sedimentation dynamics of the studied layers are complex,involving gravity flows,traction currents,and suspended deposition.Organic matter shows a significant correlation with transgressive-regressive cycle.The site DS-W16 contains two distinct gas hydrate reservoirs:a shallow reservoir(10-24 mbsf)and a deep reservoir(below 182 mbsf).The paleomarine environment influences gas hydrate accumulation by altering sedimentary processes and sediment characteristics,especially the distribution of biological components.Both shallow and deep gas hydrate reservoirs formed under dynamic conditions dominated by traction currents and are characterized by a higher abundance of foraminifera.Sedimentary layers rich in foraminifera and modified by traction currents represent key intervals for preferential gas hydrate accumulation.
基金funded by the AFM-Telethon Foundation (#28703)by the Italian Ministry of Education, University and Research (Grant P2022Y2A3L funded in the framework of NRRP, Mission 4.2, Investment 1.1 “progetti di ricerca di Rilevante Interesse Nazionale - PRIN”, funded by the European Union Next Generation EU, CUP C53D23007520001+2 种基金Grant P20227YB93, CUP C53D23003030001) (to MC)the activities of the National Center for Gene Therapy and Drugs based on RNA Technology, funded in the framework of the National Recovery and Resilience Plan (NRRP), Mission 4 “Education and Research”, Component 2 “From Research to Business”, Investment 1.4 “Strengthening research structures for supporting the creation of National Centres, national R&D leaders on some Key Enabling Technologies”funded by the European Union-Next Generation EU, Project CN00000041, CUP B93D21010860004, Spoke n. 5 “Inflammatory and infectious diseases” (to MC)
文摘β-glucocerebrosidase in health and disease:Mutations in theβ-glucocerebrosidase(GBA)gene do cause the rare lysosomal storage disorder Gaucher’s disease(GD)with an estimated global prevalence of 1:200,000(Imbalzano et al.,2024).GBA is a membrane-bound lysosomalenzyme responsible for glucosylceramide and glucosylsphingosine hydrolysis.When this enzyme is mutated and dysfunctional,its substrates progressively accumulate within cells.
基金supported by the National Natural Science Foundation of China(Grant Nos.52276115,62004143)the Open Fund for Anhui Provincial Key Laboratory of Advanced Internal Combustion Engines,the Key R&D Program of Hubei Province(Grant No.2022BAA084)+2 种基金the Key Project of Scientific Research Plan of Hubei Provincial Department of Education(Grant No.D20241501)the National College Students Innovation and Entrepreneurship Training Program(Grant No.202410299069Z)the Innovation Project of Engineering Research Center of Phosphorus Resources Development and Utilization of Ministry of Education(Grant No.LCX202404)。
文摘Particulate matter(PM)emitted by power machinery severely harms air quality and ecological balance,making the development of efficient and green PM-removal technologies a key global environmental challenge.This work built a visualization system for diesel engine PM decomposition via non-thermal plasma(NTP),conducting multi-stage NTP oxidation at 120℃to clarify reaction pathways.The results demonstrate that NTP significantly influences the microcrystalline reconstruction and chemical evolution of PM.Early oxidation removes surface short crystallites,increasing crystallite length,reducing tortuosity,narrowing D1 peak,and boosting graphitization.Mid-stage sees NTP active substances penetrate inside,shortening crystallites and regularizing structure.Late-stage primary particles form“hollow shells”with few long crystallites,and order/graphitization rises again.Chemically,NTP reduces high-carbon components while increasing lowcarbon ones in PM soluble organics,decomposes C=C bonds to form oxygen-containing groups,enhances PM oxidation activity,weakensπ^(*)peaks,and strengthensσ^(*)peaks,clearly confirmed by the carbon K-edge electron energy loss spectra.This study clarifies the mechanistic pathways of NTP-driven PM decomposition,supporting clean energy advancement and atmospheric governance.
基金supported by the Natural Science Foundation of Beijing,No.7232279(to XW)the National Natural Science Foundation of China,No.U21A20400(to QW)Key Project of Beijing University of Chinese Medicine,Nos.2022-JYB-JBZR-004(to XW),2024-JYB-JBZD-043(to CL).
文摘Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.
基金supported by the National Key R&D Program of China (Grant Nos.2022YFA1403103 and 2019YFA0308603)the National Natural Science Foundation of China (Grant No.12304167)the Shandong Provincial Natural Science Foundation of China (Grant No.ZR2023QA020)。
文摘Interfacial superconductivity(IS)has been a topic of intense interest in condensed matter physics,due to its unique properties and exotic photoelectrical performance.However,there are few reports about IS systems consisting of two insulators.Here,motivated by the emergence of an insulator-metal transition in type-Ⅲ heterostructures and the superconductivity in some“special”two-dimensional(2D)semiconductors via electron doping,we predict that the 2D heterostructure SnSe_(2)/PtTe_(2) is a model system for realizing IS by using firstprinciples calculations.Our results show that due to slight but crucial interlayer charge transfer,SnSe_(2)/PtTe_(2) turns to be a type-Ⅲ heterostructure with metallic properties and shows a superconducting transition with the critical temperature(T_(c))of 3.73 K.Similar to the enhanced electron–phonon coupling(EPC)in the electrondoped SnSe_(2) monolayer,the IS in the SnSe_(2)/PtTe_(2) heterostructure mainly originates from the metallized SnSe_(2) layer.Furthermore,we find that its superconductivity is sensitive to tensile lattice strain,forming a domeshaped superconducting phase diagram.Remarkably,at 7%biaxial tensile strain,the superconducting T_(c) can increase more than twofold(8.80 K),resulting from softened acoustic phonons at the𝑀point and enhanced EPC strength.Our study provides a concrete example for realizing IS in type-Ⅲ heterostructures,which waits for future experimental verification.
基金supported in part by the National Natural Science Foundation of China under Grant 62071405the National Natural Science Foundation of China under Grant 12175189.
文摘The accurate segmentation of deep gray matter nuclei is critical for neuropathological research,disease diagnosis and treatment.Existing methods employ the supervised learning training approach,which requires large labeled datasets.It is challenging and time-consuming to obtain such datasets for medical image analysis.In addition,these methods based on convolutional neural networks(CNNs)only achieve suboptimal performance due to the locality of convolutional operations.Vision Transformers(ViTs)efficiently model long-range dependencies and thus have the potentiality to outperform these methods in segmentation tasks.To address these issues,we propose a novel hybrid network based on self-supervised pre-training for deep gray matter nuclei segmentation.Specifically,we present a CNN-Transformer hybrid network(CTNet),whose encoder consists of 3D CNN and ViT to learn local spatial-detailed features and global semantic information.A self-supervised learning(SSL)approach that integrates rotation prediction and masked feature reconstruction is proposed to pre-train the CTNet,enabling the model to learn valuable visual representations from unlabeled data.We evaluate the effectiveness of our method on 3T and 7T human brain MRI datasets.The results demonstrate that our CTNet achieves better performance than other comparison models and our pre-training strategy outperforms other advanced self-supervised methods.When the training set has only one sample,our pre-trained CTNet enhances segmentation performance,showing an 8.4%improvement in Dice similarity coefficient(DSC)compared to the randomly initialized CTNet.
基金supported by Hangzhou Dianzi University(Grant No.KYS075621018)supported by the Natural Science Foundation of Zhejiang Province(Grant No.LY24A050004)。
文摘Tunable plasmonic structures provide the possibility to actively modify the radiation from atoms through electromagnetic coupling.In this paper,we investigate the decay and radiation behavior of an atom near a dielectric nanosphere with conductive surface within the framework of macroscopic quantum electrodynamics.The electromagnetic fields including the losses in the materials can be taken as fundamental excitations which interact with the atom through a transition dipole.Both weak and strong coupling regimes have been investigated.The decay rate and the angle-dependent light intensities indeed strongly depend on the parameters of the system,i.e.,the position and orientation of the dipole,the geometric size,and the surface conductivity,providing the opportunity of artificial control over these quantities.Generalizing the formalism in this paper to other systems,like metamaterials,is straightforward,which we believe may pave a way for future active quantum nanophotonic devices.
基金supported by the National Natural Science Foundation of China,No.82201626(to CC)the Natural Science Foundation of LiaoningProvince,No.2022-MS-442(to CC)the Dalian Municipal Medical Key Specialty Climbing Project,No.2024ZZ040(to MZ).
文摘Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.However,there remains a lack of effective preventative or therapeutic regimens for cerebral small vessel disease.In this study,we investigated the potential therapeutic effects of MCC950,a selective NOD-like receptor family pyrin domain-containing protein 3 inhibitor,on cerebral small vessel disease pathogenesis and cognitive decline in spontaneously hypertensive rats.Our results showed that chronic administration of MCC950(10 mg/kg)to spontaneously hypertensive rats inhibited NOD-like receptor family pyrin domain-containing protein 3 inflammasome activation,thereby considerably suppressing the production of pyroptosis executive protein gasdermin D and pro-inflammatory factors,including interleukin-1βand-18.A decrease in astrocytic and microglial activation was also observed.We also found that MCC950 significantly inhibited autophagy.More importantly,behavioral assessment indicated that MCC950 administration ameliorated impaired neurocognitive function,which was associated with improvements in neuropathological hallmarks in the cerebral small vessel disease brain,such as blood‒brain barrier breakdown,white matter damage,and endothelial dysfunction.Thus,our findings revealed that the NOD-like receptor family pyrin domain-containing protein 3 inflammasome is a key contributor to the onset or progression of cerebral small vessel disease and suggested the potential of NOD-like receptor family pyrin domain-containing protein 3-based therapy as a potential novel strategy for treating cerebral small vessel disease.
基金supported by National Key R&D Program:Key Special Project on Research for the Prevention and Treatment of Common Diseases-2022 Annual Project,Nos.2022YFC2504900,2022YFC2504902(both to ZL).
文摘Regulatory T cells are crucial immunomodulatory cells that play essential roles in both ischemic stroke and intracerebral hemorrhage.These cells are vital in post-stroke inflammation since they suppress immune responses and promote tissue repair.This review thoroughly examines the dynamic changes in the number and function of regulatory T cells and highlights their distinct roles at various stages of stroke progression.In the acute phase(within 5-7 days),regulatory T cells exert neuroprotective effects primarily by reducing inflammation.In the chronic phase(7 days post-onset),these cells support neuroregeneration and functional recovery.The review also explores the emerging role of regulatory T cells in the brain-gut axis,a key mediator of the systemic immune responses following stroke,and discusses its relevance in modulating post-stroke inflammation and repair.Various strategies aimed at enhancing regulatory T cell responses include adoptive transfer of regulatory T cells,administration of pharmacological agents,and induction of mucosal tolerance.All these approaches can potentially enhance the immunomodulatory and repair functions of regulatory T cells.Nevertheless,despite the promising preclinical results,the translation of regulatory T cell-based therapies into clinical practice is associated with challenges related to optimal timing,dosage,and long-term efficacy.Overall,targeting regulatory T cells is a novel and promising immunoregulatory approach for mitigating stroke-induced injury and promoting neural repair.
基金supported by the National Key Research and Development Program of China,No.2022YFC2704801(to CZhu)the National Natural Science Foundation of China,Nos.U21A20347(to CZhu),82203969(to YX),82371472(to XZ)+3 种基金Health Commission of Henan Province,Nos.SBGJ202303039(to XZ),SBGJ202301009(to CZhu),YQRC2024018(to XZ),YQRC2024019(to YX)Henan Science and Technology Department,Nos.242102311054(to XZ),241111521300(to CZhu),GZS2023003(to XW)Swedish Research Council,Nos.2022-01019(to CZhu),2021-01950(to XW)Swedish Governmental Grants to Scientists Working in Healthcare,Nos.ALFGBG-1005209(to CZhu),ALFBG-1005257(to XW),ALFGBG-965197(to CZhu).
文摘Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury response,including inflammation and repair.Although colony-stimulating factor 1 receptor inhibitors such as PLX5622 enable the selective depletion of microglia,their therapeutic potential in neonatal germinal matrix hemorrhage remains underexplored.Here,we used a collagenase-induced germinal matrix hemorrhage model in postnatal day 5 mice,and intraperitoneally administered PLX562272 hours post-germinal matrix hemorrhage to achieve targeted,temporary microglial depletion during the peak injury response.We then assessed the effects of this delayed intervention on oligodendrocyte lineage cell maturation,white matter integrity,and neurobehavioral outcomes.Additionally,RNA sequencing data from a germinal matrix hemorrhage rat model were analyzed using weighted gene co-expression network analysis to identify the critical phases for interventions.RNA sequencing data revealed a critical period in which key synaptic functions declined while immune responses intensified post-germinal matrix hemorrhage,thus pinpointing the critical response phases for potential interventions.Delayed PLX5622 treatment effectively depleted activated microglia,protecting against white matter injury and enhancing oligodendrocyte lineage cell maturation and myelination in subcortical white matter regions.Moreover,magnetic resonance imaging analysis revealed reduced brain lesion volumes in treated mice.Behaviorally,PLX5622-treated mice exhibited significant improvements in motor coordination and reduced hyperactivity compared with vehicle-treated germinal matrix hemorrhage model mice.These findings suggest that,when timed to avoid interference with initial oligodendrocyte lineage cell proliferation,targeted microglial depletion with PLX5622 significantly mitigates white matter damage and improves neurobehavioral outcomes in neonatal germinal matrix hemorrhage.The present study highlights the therapeutic potential of selectively modulating microglial reactivity to support neurodevelopment in preterm infants with brain injury.
基金supported by grants from Guangdong Basic and Applied Basic Research Foundation,No.2021A1515110801(to SW)the National Natural Science Foundation of China,No.82301511(to SW)+1 种基金“Double First-Class”Construction Project of NPU,Nos.0515023GH0202320(to JC),0515023SH0201320(to JC)973 Program,No.2011CB504100(to JC).
文摘Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.
基金supported by the National Natural Science Foundation of China,Nos.82172546(to XH),82172547(to ZZ)the Natural ScienceFoundation of Guangdong Province,Nos.2023A1515012695(to XH),2024A1515010419(to ZZ)the Science and Technology Plan Project of Guangzhou,Nos.202201020413(to ZZ),2023A04J1099(to ZZ).
文摘White matter injury is a key factor impacting stroke recovery.Physical exercise can promote white matter repair.Immune cells,especially regulatory T(Treg)cells,contribute to strengthening white matter integrity,yet little is known about the underlying mechanism.To examine this,we established a transient middle cerebral artery occlusion male mouse model.We found that physical exercise elevated brain Treg cells,thereby enhancing neurological recovery,reducing neuroinflammation,promoting myelin debris clearance,and accelerating white matter repair.Depletion of Treg cells caused a decrease in these positive effects of physical exercise.Mechanistically,the rise in osteopontin triggered by physical exercise is dampened when Treg cells are depleted.In addition,Treg-conditioned medium reduced oxygen-glucose deprivation/re-oxygenation-induced microglial inflammation and enhanced phagocytosis,which could be blocked by osteopontin antibodies.Importantly,although Treg infusion could mimic the protective effects of physical exercise,osteopontin blockade partially countered the effects of physical exercise and Treg cells.Finally,our sequencing data revealed a marked upregulation of C-X-C motif chemokine ligand 12(CXCL12)mRNA expression subsequent to physical exercise,which was confirmed at the protein level.Stimulation of Treg cells with stroke brain lysates increased C-X-C motif chemokine receptor 4(CXCR4)expression,indicating a potential role for the CXCL12-CXCR4 axis in recruiting Treg cells.These findings suggest that physical exercise promotes white matter repair after ischemic stroke by Treg cells.
基金supported by Craig H.Neilsen Foundation,Wings for Life Foundation,Canadian Institutes of Health Research,and Fonds de Recherche Québec-Santé(to FB).
文摘Spinal cord injury(SCI)interrupts the flow of information between the brain and the spinal cord,thus leading to a loss of sensory information and motor paralysis of the body below the lesion.Surprisingly,most SCIs are incomplete and spare supraspinal pathways,especially those located within the peripheral white matter of the spinal cord,which includes reticulospinal pathways originating from the medullary reticular formation.Whereas there is abundant literature about the motor cortex,its corticospinal pathway,and its capacity to modulate functional recovery after SCI,less is known about the medullary reticular formation and its reticulospinal pathway.
基金supported by the National Natural Science Foundation(42472325)the Fundamental Research Funds of Chinese Academy of Geological Science(SK202103).
文摘To elucidate the geographical differentiation characteristics and driving mechanisms of Dissolved Organic Matter(DOM)in typical rivers,this study conducted a multi-spectral investigation on three representative river types within Shandong Province:The mountainous Dawen River,the plain Tuhai River,and the artificial East Grand Canal.The DOM composition was analyzed using Ultraviolet-Visible(UV-Vis)absorption spectroscopy,Excitation-Emission Matrix(EEM)fluorescence spectroscopy,and parallel factor analysis(PARAFAC),while Principal Component Analysis(PCA)was employed to quantify the synergistic effects of natural processes and anthropogenic activities.Results revealed significant spatial heterogeneity in DOM composition and sources.The plain river exhibited the highest aromaticity(humic-like components:43.3%)due to long-term agricultural non-point source inputs and urban wastewater discharge.The mountain stream,shaped by complex terrain and relatively intact ecosystems,was dominated by autochthonous DOM derived from microbial metabolism,with higher Fluorescence Index(FI=2.12)and biological index(BIX=1.35)than other river types.The artificial canal retained protein-like components(64.2%),largely attributed to winter hydrological stagnation and disturbances from shipping activities.Further analysis demonstrated that geographical settings(e.g.,mountain terrain)and anthropogenic activities(e.g.,agriculture,shipping)jointly regulated DOM composition by altering the balance between input and transformation processes.Integrated fluorescence parameters and PCA results suggested differentiated management strategies:protecting ecological integrity in mountain streams to sustain selfpurification,enhancing non-point source interception in plain rivers,and mitigating shipping pollution in canals.This study systematically reveals the natural-anthropogenic coupling mechanisms driving DOM dynamics in northern China rivers,providing critical insights for precision water environment management at the watershed scale.
基金supported by the National Natural Science Foundation of China(62473082,82202250,82121003,62036003,and 62333003)the Fundamental Research Funds for the Central Universities(ZYGX2022YGRH008 and ZYGX2024XJ054)the Medical-Engineering Cooperation Funds from the University of Electronic Science and Technology of China(ZYGX2021YGLH201).
文摘The brain atlas,or parcellation-delineating spatial partitions,organizes the brain's structure and function[1].The spatial arrangements of highly heterogeneous landscapes represent specialized functional regions for investigating their interactions.Early efforts to parcellate the mammalian brain,using histological cytoarchitecture and myeloarchitecture,as well as recent in vivo magnetic resonance imaging(MRl)[2,3],have primarily involved cortical areas,subcortical structures,and cerebellar nuclei.Human brain parcellations primarily focus on grey matter(GM),which purposefully excludes white matter(WM),hindering the development of next-generation brain atlases.
基金supported by Grant 3195 from Paralyzed Veterans of America Research Foundation (to BRK)
文摘The inter-related pathological cascades following a traumatic spinal cord injury(tSCI)disrupt multiple cell types and physiological processes.Subsequently,motor and sensory functions are disrupted by breakdowns in cellular interactions and circuitry.Therapeutic interventions seek to modify some aspects of the injury course to enable the re-establishment of functional circuitry.Interventions often target one cell type(e.g.,promoting neuroprotection or neural regeneration)or one process(e.g.,modulating inflammation,affecting astrocytic,microglial,or macrophage responses.)Many axons in the spinal cord are myelinated,and after injury oligodendrocyte death causes demyelination.Promoting remyelination of spared or new axons to re-establish conduction seems a logical choice as a therapeutic target.
