Water-blown polyurethane rigid foams are getting more and more attention,because the traditional blowing agent HCFC141b has already been abolished to prevent the ozone layer from destruction.However,the polyurethane r...Water-blown polyurethane rigid foams are getting more and more attention,because the traditional blowing agent HCFC141b has already been abolished to prevent the ozone layer from destruction.However,the polyurethane rigid foams blown by water have serious defects,i.e.friability and resulting lower adhesion strength.Thus,the purpose of this study is to resolve the problems by chemical plastication.The maleate was added to polyol-premix containing water or to polyisocyanate,with both of which maleate does not react.To prove the reaction when polyol-premix and polyisocyanate were mixed,the model composite was synthesized and analyzed by IR,NMR and ESI(MS).Furthermore,a series of water-blown polyurethane rigid foams added different amount maleate were successfully prepared.By testing impact strength and adhesion strength of the foams,the actual effect of adding maleate was obtained.展开更多
The dentate gyrus of the hippocampus is a plastic structure that displays modifications at different levels in response to positive stimuli as well as to negative conditions such as brain damage.The latter involves gl...The dentate gyrus of the hippocampus is a plastic structure that displays modifications at different levels in response to positive stimuli as well as to negative conditions such as brain damage.The latter involves global alterations,making understanding plastic responses triggered by local damage difficult.One key feature of the dentate gyrus is that it contains a well-defined neurogenic niche,the subgranular zone,and beyond neurogenesis,newly born granule cells may maintain a“young”phenotype throughout life,adding to the plastic nature of the structure.Here,we present a novel experimental model of local brain damage in organotypic entorhino-hippocampal cultures that results in the activation of adjacent newly born granule cells.A small piece of filter paper was placed on the surface of the granule cell layer of the dentate gyrus,which evoked a foreign body reaction of astrocytes,along with the activation of local young neurons expressing doublecortin.Forty-eight hours after foreign body placement,the number of doublecortin-immunoreactive cells increased in the subgranular zone in the direct vicinity of the foreign body,whereas overall increased doublecortin immunoreactivity was observed in the granule cell layer and molecular layer of the dentate gyrus.Foreign body placement in the pyramidal layer of the CA1 region evoked a comparable local astroglial reaction but did not lead to an increase in doublecortin-immunoreactive in either the CA1 region or the adjacent dentate gyrus.Seven days after foreign body placement in the dentate gyrus,the increase in doublecortin-immunoreactivity was no longer observed,indicating the transient activation of young cells.However,7 days after foreign body placement,the number of doublecortin-immunoreactive granule cells coimmunoreactive for calbindin was lower than that under the control conditions.As calbindin is a marker for mature granule cells,this result suggests that activated young cells remain at a more immature stage following foreign body placement.Live imaging of retrovirally green fluorescent protein-labeled newly born granule cells revealed the orientation and growth of their dendrites toward the foreign body placement.This novel experimental model of foreign body placement in organotypic entorhino-hippocampal cultures could serve as a valuable tool for studying both glial reactivity and neuronal plasticity,specifically of newly born neurons under controlled in vitro conditions.展开更多
Neuronal plasticity,the brain's ability to adapt structurally and functionally,is essential for learning,memory,and recovery from injuries.In neurodegenerative diseases such as Alzheimer's disease and Parkinso...Neuronal plasticity,the brain's ability to adapt structurally and functionally,is essential for learning,memory,and recovery from injuries.In neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease,this plasticity is disrupted,leading to cognitive and motor deficits.This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer's disease and Parkinson's disease.Alzheimer's disease features amyloid-beta plaques and tau tangles that impair synaptic function,while Parkinson's disease involves the loss of dopaminergic neurons affecting motor control.Enhancing neuronal plasticity offers therapeutic potential for these diseases.A systematic literature review was conducted using databases such as PubMed,Scopus,and Google Scholar,focusing on studies of neuronal plasticity in Alzheimer's disease and Parkinson's disease.Data synthesis identified key themes such as synaptic mechanisms,neurogenesis,and therapeutic strategies,linking molecular insights to clinical applications.Results highlight that targeting synaptic plasticity mechanisms,such as long-term potentiation and long-term depression,shows promise.Neurotrophic factors,advanced imaging techniques,and molecular tools(e.g.,clustered regularly interspaced short palindromic repeats and optogenetics)are crucial in understanding and enhancing plasticity.Current therapies,including dopamine replacement,deep brain stimulation,and lifestyle interventions,demonstrate the potential to alleviate symptoms and improve outcomes.In conclusion,enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases.Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer's disease and Parkinson's disease.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
The capacity of the central nervous system for structural plasticity and regeneration is commonly believed to show a decreasing progression from“small and simple”brains to the larger,more complex brains of mammals.H...The capacity of the central nervous system for structural plasticity and regeneration is commonly believed to show a decreasing progression from“small and simple”brains to the larger,more complex brains of mammals.However,recent findings revealed that some forms of neural plasticity can show a reverse trend.Although plasticity is a well-preserved,transversal feature across the animal world,a variety of cell populations and mechanisms seem to have evolved to enable structural modifications to take place in widely different brains,likely as adaptations to selective pressures.Increasing evidence now indicates that a trade-off has occurred between regenerative(mostly stem cell–driven)plasticity and developmental(mostly juvenile)remodeling,with the latter primarily aimed not at brain repair but rather at“sculpting”the neural circuits based on experience.In particular,an evolutionary trade-off has occurred between neurogenic processes intended to support the possibility of recruiting new neurons throughout life and the different ways of obtaining new neurons,and between the different brain locations in which plasticity occurs.This review first briefly surveys the different types of plasticity and the complexity of their possible outcomes and then focuses on recent findings showing that the mammalian brain has a stem cell–independent integration of new neurons into pre-existing(mature)neural circuits.This process is still largely unknown but involves neuronal cells that have been blocked in arrested maturation since their embryonic origin(also termed“immature”or“dormant”neurons).These cells can then restart maturation throughout the animal's lifespan to become functional neurons in brain regions,such as the cerebral cortex and amygdala,that are relevant to high-order cognition and emotions.Unlike stem cell–driven postnatal/adult neurogenesis,which significantly decreases from small-brained,short-living species to large-brained ones,immature neurons are particularly abundant in large-brained,long-living mammals,including humans.The immature neural cell populations hosted in these complex brains are an interesting example of an“enlarged road”in the phylogenetic trend of plastic potential decreases commonly observed in the animal world.The topic of dormant neurons that covary with brain size and gyrencephaly represents a prospective turning point in the field of neuroplasticity,with important translational outcomes.These cells can represent a reservoir of undifferentiated neurons,potentially granting plasticity within the high-order circuits subserving the most sophisticated cognitive skills that are important in the growing brains of young,healthy individuals and are frequently affected by debilitating neurodevelopmental and degenerative disorders.展开更多
Regenerative capacity of the central nervous system(CNS)is unevenly distributed among vertebrates.While most mammalian species including humans elicit limited repair following CNS injury or disease,highly regenerative...Regenerative capacity of the central nervous system(CNS)is unevenly distributed among vertebrates.While most mammalian species including humans elicit limited repair following CNS injury or disease,highly regenerative vertebrates including urodele amphibians and teleost fish spontaneously reverse CNS damage.Teletost zebrafish(danio rerio)are tropical freshwater fish that proved to be an excellent vertebrate model of successful CNS regeneration.Differential neuronal,glial,and immune injury responses underlie disparate injury outcomes between highly regenerative zebrafish and poorly regenerative mammals.This article describes complications associated with neuronal repair following spinal cord injury(SCI)in poorly regenerative mammals and highlights intersecting modes of plasticity and regeneration in highly regenerative zebrafish(Figures 1 and 2).Comparative approaches evaluating immunoglial SCI responses were recently reviewed elsewhere(Reyes and Mokalled,2024).展开更多
Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease.Glaucoma directly impairs retinal ganglio...Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease.Glaucoma directly impairs retinal ganglion cells and their axons,leading to axonal transport dysfuntion,subsequently causing secondary damage to anterior or posterior ends of the visual system.Accordingly,recent evidence indicates that glaucoma is a degenerative disease of the central nervous system that causes damage throughout the visual pathway.However,the effects of glaucoma on synaptic plasticity in the primary visual cortex remain unclear.In this study,we established a mouse model of unilateral chronic ocular hypertension by injecting magnetic microbeads into the anterior chamber of one eye.We found that,after 4 weeks of chronic ocular hypertension,the neuronal somas were smaller in the superior colliculus and lateral geniculate body regions of the brain contralateral to the affected eye.This was accompanied by glial cell activation and increased expression of inflammatory factors.After 8 weeks of ocular hypertension,we observed a reduction in the number of excitatory and inhibitory synapses,dendritic spines,and activation of glial cells in the primary visual cortex contralateral to the affected eye.These findings suggest that glaucoma not only directly damages the retina but also induces alterations in synapses and dendritic spines in the primary visual cortex,providing new insights into the pathogenesis of glaucoma.展开更多
The remodeling of axonal connections following injury is an important feature driving functional recovery.The reticulospinal tract is an interesting descending motor tract that contains both excitatory and inhibitory ...The remodeling of axonal connections following injury is an important feature driving functional recovery.The reticulospinal tract is an interesting descending motor tract that contains both excitatory and inhibitory fibers.While the reticulospinal tract has been shown to be particularly prone to axonal growth and plasticity following injuries of the spinal cord,the differential capacities of excitatory and inhibitory fibers for plasticity remain unclear.As adaptive axonal plasticity involves a sophisticated interplay between excitatory and inhibitory input,we investigated in this study the plastic potential of glutamatergic(vGlut2)and GABAergic(vGat)fibers originating from the gigantocellular nucleus and the lateral paragigantocellular nucleus,two nuclei important for locomotor function.Using a combination of viral tracing,chemogenetic silencing,and AI-based kinematic analysis,we investigated plasticity and its impact on functional recovery within the first 3 weeks following injury,a period prone to neuronal remodeling.We demonstrate that,in this time frame,while vGlut2-positive fibers within the gigantocellular and lateral paragigantocellular nuclei rewire significantly following cervical spinal cord injury,vGat-positive fibers are rather unresponsive to injury.We also show that the acute silencing of excitatory axonal fibers which rewire in response to lesions of the spinal cord triggers a worsening of the functional recovery.Using kinematic analysis,we also pinpoint the locomotion features associated with the gigantocellular nucleus or lateral paragigantocellular nucleus during functional recovery.Overall,our study increases the understanding of the role of the gigantocellular and lateral paragigantocellular nuclei during functional recovery following spinal cord injury.展开更多
目的基于贝叶斯网状Meta分析系统评价不同血管化骨瓣在下颌骨缺损修复重建中的存活率。方法计算机检索PubMed、EBSCO、Scopus、Web of Science、Cochrane Library、WanFang Data和CNKI数据库,搜集与研究目的相关的临床研究,检索时限均...目的基于贝叶斯网状Meta分析系统评价不同血管化骨瓣在下颌骨缺损修复重建中的存活率。方法计算机检索PubMed、EBSCO、Scopus、Web of Science、Cochrane Library、WanFang Data和CNKI数据库,搜集与研究目的相关的临床研究,检索时限均从建库至2024年2月。由2名研究者独立筛选文献、提取资料并评价纳入研究的偏倚风险后,采用R软件进行贝叶斯网状Meta分析。结果共纳入24项研究,包括1615名患者。Meta分析结果显示腓骨游离瓣、旋髂深动脉髂骨瓣、肩胛骨瓣及携带桡骨的前臂桡侧皮瓣用于下颌骨重建的术后存活率分别为95.62%、94.09%、98.16%和93.75%。网状Meta分析结果显示各组织瓣术后存活率之间的差异均无统计学意义。结论当前证据表明,不同血管化骨瓣在下颌骨缺损修复重建中的存活率相似。受纳入研究数量和质量的限制,上述结论尚待更多高质量研究予以验证。展开更多
文摘Water-blown polyurethane rigid foams are getting more and more attention,because the traditional blowing agent HCFC141b has already been abolished to prevent the ozone layer from destruction.However,the polyurethane rigid foams blown by water have serious defects,i.e.friability and resulting lower adhesion strength.Thus,the purpose of this study is to resolve the problems by chemical plastication.The maleate was added to polyol-premix containing water or to polyisocyanate,with both of which maleate does not react.To prove the reaction when polyol-premix and polyisocyanate were mixed,the model composite was synthesized and analyzed by IR,NMR and ESI(MS).Furthermore,a series of water-blown polyurethane rigid foams added different amount maleate were successfully prepared.By testing impact strength and adhesion strength of the foams,the actual effect of adding maleate was obtained.
基金funded by the Alexander von Humboldt Stiftungsupported by DFG (SCH W534/6-1 to SWS)
文摘The dentate gyrus of the hippocampus is a plastic structure that displays modifications at different levels in response to positive stimuli as well as to negative conditions such as brain damage.The latter involves global alterations,making understanding plastic responses triggered by local damage difficult.One key feature of the dentate gyrus is that it contains a well-defined neurogenic niche,the subgranular zone,and beyond neurogenesis,newly born granule cells may maintain a“young”phenotype throughout life,adding to the plastic nature of the structure.Here,we present a novel experimental model of local brain damage in organotypic entorhino-hippocampal cultures that results in the activation of adjacent newly born granule cells.A small piece of filter paper was placed on the surface of the granule cell layer of the dentate gyrus,which evoked a foreign body reaction of astrocytes,along with the activation of local young neurons expressing doublecortin.Forty-eight hours after foreign body placement,the number of doublecortin-immunoreactive cells increased in the subgranular zone in the direct vicinity of the foreign body,whereas overall increased doublecortin immunoreactivity was observed in the granule cell layer and molecular layer of the dentate gyrus.Foreign body placement in the pyramidal layer of the CA1 region evoked a comparable local astroglial reaction but did not lead to an increase in doublecortin-immunoreactive in either the CA1 region or the adjacent dentate gyrus.Seven days after foreign body placement in the dentate gyrus,the increase in doublecortin-immunoreactivity was no longer observed,indicating the transient activation of young cells.However,7 days after foreign body placement,the number of doublecortin-immunoreactive granule cells coimmunoreactive for calbindin was lower than that under the control conditions.As calbindin is a marker for mature granule cells,this result suggests that activated young cells remain at a more immature stage following foreign body placement.Live imaging of retrovirally green fluorescent protein-labeled newly born granule cells revealed the orientation and growth of their dendrites toward the foreign body placement.This novel experimental model of foreign body placement in organotypic entorhino-hippocampal cultures could serve as a valuable tool for studying both glial reactivity and neuronal plasticity,specifically of newly born neurons under controlled in vitro conditions.
基金financially supported by King Abdulaziz University,Deanship of Scientific Research(DSR)。
文摘Neuronal plasticity,the brain's ability to adapt structurally and functionally,is essential for learning,memory,and recovery from injuries.In neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease,this plasticity is disrupted,leading to cognitive and motor deficits.This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer's disease and Parkinson's disease.Alzheimer's disease features amyloid-beta plaques and tau tangles that impair synaptic function,while Parkinson's disease involves the loss of dopaminergic neurons affecting motor control.Enhancing neuronal plasticity offers therapeutic potential for these diseases.A systematic literature review was conducted using databases such as PubMed,Scopus,and Google Scholar,focusing on studies of neuronal plasticity in Alzheimer's disease and Parkinson's disease.Data synthesis identified key themes such as synaptic mechanisms,neurogenesis,and therapeutic strategies,linking molecular insights to clinical applications.Results highlight that targeting synaptic plasticity mechanisms,such as long-term potentiation and long-term depression,shows promise.Neurotrophic factors,advanced imaging techniques,and molecular tools(e.g.,clustered regularly interspaced short palindromic repeats and optogenetics)are crucial in understanding and enhancing plasticity.Current therapies,including dopamine replacement,deep brain stimulation,and lifestyle interventions,demonstrate the potential to alleviate symptoms and improve outcomes.In conclusion,enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases.Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer's disease and Parkinson's disease.
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 Progetto Trapezio,Compagnia di San Paolo(67935-2021.2174),to LBFondazione CRT(Cassa di Risparmio di Torino,RF=2022.0618),to LBPRIN2022(grant 2022LB4X3N),to LB。
文摘The capacity of the central nervous system for structural plasticity and regeneration is commonly believed to show a decreasing progression from“small and simple”brains to the larger,more complex brains of mammals.However,recent findings revealed that some forms of neural plasticity can show a reverse trend.Although plasticity is a well-preserved,transversal feature across the animal world,a variety of cell populations and mechanisms seem to have evolved to enable structural modifications to take place in widely different brains,likely as adaptations to selective pressures.Increasing evidence now indicates that a trade-off has occurred between regenerative(mostly stem cell–driven)plasticity and developmental(mostly juvenile)remodeling,with the latter primarily aimed not at brain repair but rather at“sculpting”the neural circuits based on experience.In particular,an evolutionary trade-off has occurred between neurogenic processes intended to support the possibility of recruiting new neurons throughout life and the different ways of obtaining new neurons,and between the different brain locations in which plasticity occurs.This review first briefly surveys the different types of plasticity and the complexity of their possible outcomes and then focuses on recent findings showing that the mammalian brain has a stem cell–independent integration of new neurons into pre-existing(mature)neural circuits.This process is still largely unknown but involves neuronal cells that have been blocked in arrested maturation since their embryonic origin(also termed“immature”or“dormant”neurons).These cells can then restart maturation throughout the animal's lifespan to become functional neurons in brain regions,such as the cerebral cortex and amygdala,that are relevant to high-order cognition and emotions.Unlike stem cell–driven postnatal/adult neurogenesis,which significantly decreases from small-brained,short-living species to large-brained ones,immature neurons are particularly abundant in large-brained,long-living mammals,including humans.The immature neural cell populations hosted in these complex brains are an interesting example of an“enlarged road”in the phylogenetic trend of plastic potential decreases commonly observed in the animal world.The topic of dormant neurons that covary with brain size and gyrencephaly represents a prospective turning point in the field of neuroplasticity,with important translational outcomes.These cells can represent a reservoir of undifferentiated neurons,potentially granting plasticity within the high-order circuits subserving the most sophisticated cognitive skills that are important in the growing brains of young,healthy individuals and are frequently affected by debilitating neurodevelopmental and degenerative disorders.
文摘Regenerative capacity of the central nervous system(CNS)is unevenly distributed among vertebrates.While most mammalian species including humans elicit limited repair following CNS injury or disease,highly regenerative vertebrates including urodele amphibians and teleost fish spontaneously reverse CNS damage.Teletost zebrafish(danio rerio)are tropical freshwater fish that proved to be an excellent vertebrate model of successful CNS regeneration.Differential neuronal,glial,and immune injury responses underlie disparate injury outcomes between highly regenerative zebrafish and poorly regenerative mammals.This article describes complications associated with neuronal repair following spinal cord injury(SCI)in poorly regenerative mammals and highlights intersecting modes of plasticity and regeneration in highly regenerative zebrafish(Figures 1 and 2).Comparative approaches evaluating immunoglial SCI responses were recently reviewed elsewhere(Reyes and Mokalled,2024).
基金supported by the National Natural Science Foundation of China,No.82271115(to MY).
文摘Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease.Glaucoma directly impairs retinal ganglion cells and their axons,leading to axonal transport dysfuntion,subsequently causing secondary damage to anterior or posterior ends of the visual system.Accordingly,recent evidence indicates that glaucoma is a degenerative disease of the central nervous system that causes damage throughout the visual pathway.However,the effects of glaucoma on synaptic plasticity in the primary visual cortex remain unclear.In this study,we established a mouse model of unilateral chronic ocular hypertension by injecting magnetic microbeads into the anterior chamber of one eye.We found that,after 4 weeks of chronic ocular hypertension,the neuronal somas were smaller in the superior colliculus and lateral geniculate body regions of the brain contralateral to the affected eye.This was accompanied by glial cell activation and increased expression of inflammatory factors.After 8 weeks of ocular hypertension,we observed a reduction in the number of excitatory and inhibitory synapses,dendritic spines,and activation of glial cells in the primary visual cortex contralateral to the affected eye.These findings suggest that glaucoma not only directly damages the retina but also induces alterations in synapses and dendritic spines in the primary visual cortex,providing new insights into the pathogenesis of glaucoma.
基金supported by the Deutsche Forschungsgemeinschaft(DFG),TRR274(Project ID 408885537,Sy Nergy,EXC 2145/ID 390857198,to FMB)。
文摘The remodeling of axonal connections following injury is an important feature driving functional recovery.The reticulospinal tract is an interesting descending motor tract that contains both excitatory and inhibitory fibers.While the reticulospinal tract has been shown to be particularly prone to axonal growth and plasticity following injuries of the spinal cord,the differential capacities of excitatory and inhibitory fibers for plasticity remain unclear.As adaptive axonal plasticity involves a sophisticated interplay between excitatory and inhibitory input,we investigated in this study the plastic potential of glutamatergic(vGlut2)and GABAergic(vGat)fibers originating from the gigantocellular nucleus and the lateral paragigantocellular nucleus,two nuclei important for locomotor function.Using a combination of viral tracing,chemogenetic silencing,and AI-based kinematic analysis,we investigated plasticity and its impact on functional recovery within the first 3 weeks following injury,a period prone to neuronal remodeling.We demonstrate that,in this time frame,while vGlut2-positive fibers within the gigantocellular and lateral paragigantocellular nuclei rewire significantly following cervical spinal cord injury,vGat-positive fibers are rather unresponsive to injury.We also show that the acute silencing of excitatory axonal fibers which rewire in response to lesions of the spinal cord triggers a worsening of the functional recovery.Using kinematic analysis,we also pinpoint the locomotion features associated with the gigantocellular nucleus or lateral paragigantocellular nucleus during functional recovery.Overall,our study increases the understanding of the role of the gigantocellular and lateral paragigantocellular nuclei during functional recovery following spinal cord injury.
文摘目的基于贝叶斯网状Meta分析系统评价不同血管化骨瓣在下颌骨缺损修复重建中的存活率。方法计算机检索PubMed、EBSCO、Scopus、Web of Science、Cochrane Library、WanFang Data和CNKI数据库,搜集与研究目的相关的临床研究,检索时限均从建库至2024年2月。由2名研究者独立筛选文献、提取资料并评价纳入研究的偏倚风险后,采用R软件进行贝叶斯网状Meta分析。结果共纳入24项研究,包括1615名患者。Meta分析结果显示腓骨游离瓣、旋髂深动脉髂骨瓣、肩胛骨瓣及携带桡骨的前臂桡侧皮瓣用于下颌骨重建的术后存活率分别为95.62%、94.09%、98.16%和93.75%。网状Meta分析结果显示各组织瓣术后存活率之间的差异均无统计学意义。结论当前证据表明,不同血管化骨瓣在下颌骨缺损修复重建中的存活率相似。受纳入研究数量和质量的限制,上述结论尚待更多高质量研究予以验证。
