Perspectives in human brain plasticity sparked by glioma invasion:from intraoperative(re)mappings to neural reconfigurations

Exploring the aptitude of the human brain to compensate functional consequences of a lesion damaging its structural architecture is a key challenge to improve patient care in various neurological diseases,to optimize neuroscientifically-informed strategies of postlesional rehabilitation,and ultimately to develop innovative neuro-regenerative therapies.The term‘plasticity’,initially referring to the intrinsic propensity of neurons to modulate their synaptic transmission in a learning situation,was progressively transposed to brain injury research and clinical neurosciences.Indeed,in the event of brain damage,adaptive mechanisms of compensation allow a partial reshaping of the structure and activities of the central nervous system,thus permitting to some extent the maintenance of brain functions.

Mitochondrial recruitment in myelin:an anchor for myelin dynamics and plasticity?

Optimal propagation of neuronal electrical impulses depends on the insulation of axons by myelin,produced in the central nervous system by oligodendrocytes.Myelin is an extension of the oligodendrocyte plasma membrane,which wraps around an axon to form a compact multi-layered sheath.Myelin is composed of a substantially higher proportion of lipids compared to other biological membranes and enriched in a small number of specialized proteins.

Glial progenitor heterogeneity and plasticity in the adult spinal cord

Glial progenitor cells were reported to have the capacity to generate various types of cells in both the central nervous system(CNS)and peripheral nervous system.Glial progenitor cells can respond to diverse environmental signals and transform into distinct populations,each serving specific functions.Notably,the adult spinal cord hosts various populations of glial progenitors,a region integral to the central nervous system.During development,glial progenitors express glial fibrillary acidic protein(GFAP;Dimou and Gotz,2014).However,the specific identities of GFAP-expressing progenitors in the adult spinal cord were not thoroughly investigated.

From mice to humans:a need for comparable results in mammalian neuroplasticity

Brain plasticity-A universal tool with many variations:The study of brain plasticity has been gaining interest since almost a century and has now reached a huge amount of information(>80,000 results in PubMed).Overall,different types of plasticity,including stem cell-driven genesis of new neurons(adult neurogenesis),cells in arrested maturation(dormant neurons),neuro-glial and synaptic plasticity,can coexist and contribute to grant plastic changes in the brain,from a cellular to system level(Benedetti and Couillard-Despres,2022;Bonfanti et al.,2023).

Age-related differences in long-term potentiation-like plasticity and shortlatency afferent inhibition and their association with cognitive function

Background The neurophysiological differences in cortical plasticity and cholinergic system function due to ageing and their correlation with cognitive function remain poorly understood.Aims To reveal the differences in long-term potentiation(LTP)-like plasticity and short-latency afferent inhibition(SAl)between older and younger individuals,alongside their correlation with cognitive function using transcranial magnetic stimulation(TMS).Methods The cross-sectional study involved 31 younger adults aged 18-30 and 46 older adults aged 60-80.All participants underwent comprehensive cognitive assessments and a neurophysiological evaluation based on TMS.Cognitive function assessments included evaluations of global cognitive function,language,memory and executive function.The neurophysiological assessment included LTP-like plasticity and SAl.Results The findings of this study revealed a decline in LTP among the older adults compared with the younger adults(wald χ^(2)=3.98,p=0.046).Subgroup analysis further demonstrated a significant reduction in SAl level among individuals aged 70-80 years in comparison to both the younger adults(SAI(N20)):(t=-3.37,p=0.018);SAl(N20+4):(t=-3.13,p=0.038)and those aged 60-70(SAl(N20)):(t=3.26,p=0.025);SAl(N20+4):(t=-3.69,p=0.006).Conversely,there was no notable difference in SAl level between those aged 60-70 years and the younger group.Furthermore,after employing the Bonferroni correction,the correlation analysis revealed that only the positive correlation between LTP-like plasticity and language function(r=0.61,p<0.001)in the younger group remained statistically significant.Conclusions During the normal ageing process,a decline in synaptic plasticity may precede cholinergic system dysfunction.In individuals over 60 years of age,there is a reduction in LTP-like plasticity,while a decline in cholinergic system function is observed in those over 70.Thus,the cholinergic system may play a vital role in preventing cognitive decline during normal ageing.In younger individuals,LTP-like plasticity might represent a potential neurophysiological marker for language function.

Timing effect of high temperature exposure on the plasticity of internode and plant architecture in maize

The occurrence of high temperature(HT)in crop production is becoming more frequent and unpredictable with global warming,severely threatening food security.The state of an organ’s growth and development is largely determined by the temperature conditions it is exposed to over time.Maize is the main cereal crop,and its stem growth and plant architecture are closely related to lodging resistance,and especially sensitive to temperature.However,systematic research on the timing effect of HT on the sequentially developing internode and stem is currently lacking.To identify the timing effect of HT on the morphology and plasticity of the stem in maize,two hybrids(Zhengdan 958(ZD958),Xianyu 335(XY335))characterized by distinct morphological traits in the stem were exposed to a 7-day HT treatment from the V6 to V17 stages(Vn presents the vegetative stage with n leaves fully expanded)in 2019-2020.The results demonstrated that exposure to HT during V6-V12 accelerated the rapid elongation of stems.For instance,HT occurring at V7 and V12 specifically promoted the lengths and weights of the 3rd-5th and 9th-11th internodes,respectively.Meanwhile,HT slowed the growth of internodes adjacent to the promoted internodes.Interestingly,compared with control,the plant height was significantly increased soon after HT treatment,but the promotion effect became narrower at the subsequent flowering stage,demonstrating a self-adjusting mechanism in the maize plant in response to HT.Importantly,HT altered the plant architectures,including a rising of the ear position and increase in the ear position coefficient.XY335 exhibited greater sensitivity in stem development than ZD958 under HT treatment.These findings improve our systematic understanding of the plasticity of internode and plant architecture in response to the timing of HT exposure.

Superplasticity of fine-grained Mg-10Li alloy prepared by severe plastic deformation and understanding its deformation mechanisms

The superplastic behavior and associated deformation mechanisms of a fine-grained Mg-10.1 Li-0.8Al-0.6Zn alloy(LAZ1011)with a grain size of 3.2μm,primarily composed of the BCCβphase and a small amount of the HCPαphase,were examined in a temperature range of 473 K to 623 K.The microstructural refinement of this alloy was achieved by employing high-ratio differential speed rolling.The best superplasticity was achieved at 523 K and at strain rates of 10^(-4)-5×10^(-4)s^(-1),where tensile elongations of 550±600%were obtained.During the heating and holding stage of the tensile samples prior to tensile loading,a significant increase in grain size was observed at temperatures above 573 K.Therefore,it was important to consider this effect when analyzing and understanding the superplastic deformation behavior and mechanisms.In the investigated strain rate range,the superplastic flow at low strain rates was governed by lattice diffusion-controlled grain boundary sliding,while at high strain rates,lattice diffusion-controlled dislocation climb creep was the rate-controlling deformation mechanism.It was concluded that solute drag creep is unlikely to occur.During the late stages of deformation at 523 K,it was observed that grain boundary sliding led to the agglomeration of theαphase,resulting in significant strain hardening.Deformation mechanism maps were constructed forβ-Mg-Li alloys in the form of 2D and 3D formats as a function of strain rate,stress,temperature,and grain size,using the constitutive equations for various deformation mechanisms derived based on the data of the current tests.

Anelasticity to plasticity transition in a model two-dimensional amorphous solid

Anelasticity, as an intrinsic property of amorphous solids, plays a significant role in understanding their relaxation and deformation mechanism. However, due to the lack of long-range order in amorphous solids, the structural origin of anelasticity and its distinction from plasticity remain elusive. In this work, using frozen matrix method, we study the transition from anelasticity to plasticity in a two-dimensional model glass. Three distinct mechanical behaviors, namely,elasticity, anelasticity, and plasticity, are identified with control parameters in the amorphous solid. Through the study of finite size effects on these mechanical behaviors, it is revealed that anelasticity can be distinguished from plasticity.Anelasticity serves as an intrinsic bridge connecting the elasticity and plasticity of amorphous solids. Additionally, it is observed that anelastic events are localized, while plastic events are subextensive. The transition from anelasticity to plasticity is found to resemble the entanglement of long-range interactions between element excitations. This study sheds light on the fundamental nature of anelasticity as a key property of element excitations in amorphous solids.

The interaction between KIF21A and KANK1 regulates dendritic morphology and synapse plasticity in neurons

Morphological alterations in dendritic spines have been linked to changes in functional communication between neurons that affect learning and memory.Kinesin-4 KIF21A helps organize the microtubule-actin network at the cell cortex by interacting with KANK1;however,whether KIF21A modulates dendritic structure and function in neurons remains unknown.In this study,we found that KIF21A was distributed in a subset of dendritic spines,and that these KIF21A-positive spines were larger and more structurally plastic than KIF21A-negative spines.Furthermore,the interaction between KIF21A and KANK1 was found to be critical for dendritic spine morphogenesis and synaptic plasticity.Knockdown of either KIF21A or KANK1 inhibited dendritic spine morphogenesis and dendritic branching,and these deficits were fully rescued by coexpressing full-length KIF21A or KANK1,but not by proteins with mutations disrupting direct binding between KIF21A and KANK1 or binding between KANK1 and talin1.Knocking down KIF21A in the hippocampus of rats inhibited the amplitudes of long-term potentiation induced by high-frequency stimulation and negatively impacted the animals’cognitive abilities.Taken together,our findings demonstrate the function of KIF21A in modulating spine morphology and provide insight into its role in synaptic function.

Neural stem cells promote neuroplasticity: a promising therapeutic strategy for the treatment of Alzheimer’s disease

Recent studies have demonstrated that neuroplasticity,such as synaptic plasticity and neurogenesis,exists throughout the normal lifespan but declines with age and is significantly impaired in individuals with Alzheimer’s disease.Hence,promoting neuroplasticity may represent an effective strategy with which Alzheimer’s disease can be alleviated.Due to their significant ability to self-renew,differentiate,and migrate,neural stem cells play an essential role in reversing synaptic and neuronal damage,reducing the pathology of Alzheimer’s disease,including amyloid-β,tau protein,and neuroinflammation,and secreting neurotrophic factors and growth factors that are related to plasticity.These events can promote synaptic plasticity and neurogenesis to repair the microenvironment of the mammalian brain.Consequently,neural stem cells are considered to represent a potential regenerative therapy with which to improve Alzheimer’s disease and other neurodegenerative diseases.In this review,we discuss how neural stem cells regulate neuroplasticity and optimize their effects to enhance their potential for treating Alzheimer’s disease in the clinic.

3'-Deoxyadenosin alleviates methamphetamine-induced aberrant synaptic plasticity and seeking behavior by inhibiting the NLRP3 inflammasome

Methamphetamine addiction is a brain disorder characterized by persistent drug-seeking behavior, which has been linked with aberrant synaptic plasticity. An increasing body of evidence suggests that aberrant synaptic plasticity is associated with the activation of the NOD-like receptor family pyrin domain containing-3(NLRP3) inflammasome. 3′-Deoxyadenosin, an active component of the Chinese fungus Cordyceps militaris, has strong anti-inflammatory effects. However, whether 3′-deoxyadenosin attenuates methamphetamine-induced aberrant synaptic plasticity via an NLRP3-mediated inflammatory mechanism remains unclear. We first observed that 3′-deoxyadenosin attenuated conditioned place preference scores in methamphetamine-treated mice and decreased the expression of c-fos in hippocampal neurons. Furthermore, we found that 3′-deoxyadenosin reduced the aberrant potentiation of glutamatergic transmission and restored the methamphetamine-induced impairment of synaptic plasticity. We also found that 3′-deoxyadenosin decreased the expression of NLRP3 and neuronal injury. Importantly, a direct NLRP3 deficiency reduced methamphetamine-induced seeking behavior, attenuated the impaired synaptic plasticity, and prevented neuronal damage. Finally, NLRP3 activation reversed the effect of 3′-deoxyadenosin on behavior and synaptic plasticity, suggesting that the anti-neuroinflammatory mechanism of 3′-deoxyadenosin on aberrant synaptic plasticity reduces methamphetamine-induced seeking behavior. Taken together, 3′-deoxyadenosin alleviates methamphetamine-induced aberrant synaptic plasticity and seeking behavior by inhibiting the NLRP3 inflammasome.

数字金融、创业效应与实体经济高质量发展

基于2011—2021年中国省域面板数据,从五个维度对实体经济高质量发展指标体系进行构建,利用空间杜宾模型检验数字金融对实体经济高质量发展的影响。结果显示:第一,数字金融能显著促进实体经济高质量发展且存在正向空间溢出效应,发展数字金融对本省份和邻近省份实体经济高质量发展均有推动作用。第二,创业效应在数字金融助力实体经济高质量发展的过程中存在显著的传导作用,提升创业效应水平是数字金融赋能实体经济高质量发展的重要机制。第三,门槛模型检验发现,数字金融对实体经济高质量发展的积极影响呈现“边际效应递增”的非线性特点,且创业效应在其中发挥调节作用,能够增强数字金融对实体经济高质量发展的影响效果。据此提出全面建设中国数字金融体系,加强数字金融对企业创业创新活动的引导扶持,充分重视并利用数字金融的空间外溢效应,深度赋能实体经济高质量发展等政策建议。

数字经济、农业产业结构升级对农民增收的效应

【目的】数字经济作为我国经济发展的新动能,对农民增收具有重要作用。研究两者之间的关系及其作用机制,可以丰富数字经济与农民收入的研究内容,充实经济高质量发展的经验证据,为加快数字乡村战略的实施进程提供启示。【方法】基于农业产业结构升级视角,运用2012—2021年全国31个省份的面板数据,构建数字经济评价指标体系,采用熵值法测算数字经济发展水平,借助固定效应模型和最小二乘法(OLS)探究数字经济对农民增收的影响及其作用机制,并运用面板门槛模型分析数字经济对农民增收的非线性溢出特征,最后借助分位数回归等方法分析数字经济对农民增收的异质性。【结果】(1)数字经济能够促进农民增收,经过工具变量法、改变样本容量等一系列检验后,结论依然成立。其中数字经济对农民的家庭经营性收入、工资性收入、财产性收入产生显著促进效应,对农民转移性收入的影响不显著。(2)数字经济的发展提升了农业产业结构的合理化以及高级化水平,助推农业产业结构的升级,从而促进农民收入的增长。(3)数字经济的增收效应具有非线性特征,且该效应在农业产业结构合理化的调节作用下得到进一步强化。(4)数字经济会长期带动农民收入增长;数字经济对不同收入水平农民增收的影响效应呈“倒U型”,其中中等收入阶层是数字经济发展的最大受益者;数字经济发展对中、西部农民增收的推动力明显强于东部地区。【结论】数字经济、农业产业结构升级是提高农民收入水平的关键要素,基于此,提出加强数字经济建设力度、创新数字经济和农业产业结构融合发展机制、完善数字经济发展的利益分配机制以及促进区域数字经济与农业产业结构统筹联动等对策建议。

绿色技术创新对碳排放的影响效应——非线性中介效应与调节效应分析

绿色技术创新是解决环境污染和实现碳减排目标的重要手段。基于2011—2021年中国内地271个地级及以上城市面板数据,使用参数与非参数方法检验绿色技术创新对碳排放的非线性影响,分析能源消费结构及产业结构的中介作用,同时探讨环境规制、科创支持、市场化程度和公众关注的调节作用。研究发现:①基准回归结果表明,绿色技术创新与碳排放呈显著倒“U”型关系;②异质性检验结果表明,倒“U”型关系仅在非资源型城市、低碳试点城市和高质量绿色技术创新体现明显;③中介效应检验结果表明,绿色技术创新既能通过优化能源消费结构降低碳排放,又会通过阻碍产业结构升级增加碳排放;④调节效应分析结果表明,公众关注、科创支持和市场化程度对绿色技术创新与碳排放倒“U”型关系起正向调节作用,使倒“U”型曲线更陡峭,而环境规制对绿色技术创新与碳排放倒“U”型关系起负向调节作用,使倒“U”型曲线更平缓。据此,提出提升绿色技术创新能力、推动清洁能源发展、加强政策配套支持、完善市场机制、构建政府公众共治体系等建议。

数字乡村建设赋能农业经济韧性的影响机制及效应

数字经济为我国农业高质量发展带来新的机遇与挑战,探寻数字乡村建设对农业经济韧性的影响,可为我国推动农业农村现代化发展和建设农业强国提供理论与实证支撑。文章基于2011—2021年中国30个省份的面板数据,采用双向固定效应模型与面板门槛模型实证分析数字乡村建设对农业经济韧性的影响机制。研究发现:数字乡村建设通过促进产业结构升级显著提升了农业经济韧性;数字乡村建设赋能农业经济韧性的效果具有区域异质性,在西部地区的正向效应更显著;数字乡村建设赋能农业经济韧性的效果具有门槛效应,并且其赋能效果呈递减趋势。

数字经济赋能共同富裕的作用机制与门槛效应——来自浙江的经验证据

数字经济赋能共同富裕是实现中国式现代化的强劲动能。文章在构建共同富裕和数字经济综合评价指标体系基础上,使用固定效应、中介效应和门槛回归等计量方法,多维度实证检验了数字经济赋能共同富裕的影响效应,得到以下研究结论:数字经济可以显著促进共同富裕水平提升;产业结构升级、空间联动、政府支持在数字经济赋能共同富裕进程中发挥中介效应;数字经济赋能共同富裕存在以产业结构升级、空间联动、政府支持为门槛变量的门槛效应,且产业结构升级、空间联动和政府支持均为双重门槛,且在不同门槛区间,数字经济对共同富裕的影响效应不同。最后基于研究结论,提出了相应的对策建议。

机构投资者调研与公司审计意见购买行为:刺激效应还是抑制效应?

公司管理层实施审计意见购买行为及其监管治理是审计学界与监管部门长期关注的重要问题。机构投资者调研作为投资者发掘公司内部信息并缓解信息不对称的一种非正式制度安排,会抑制还是刺激公司实施审计意见购买行为?本文基于我国上市公司的机构投资者调研数据,通过实证研究发现:机构投资者调研会刺激公司实施审计意见购买行为,参与调研机构数量越多、调研频数越高,被调研公司的审计意见购买动机越强,审计意见激进度也越高。进一步分析发现,在机构投资者调研的刺激效应下,公司主要通过选聘“中小”事务所实施审计意见购买,其目的是掩盖公司盈余管理及经营风险的“不利信号”。在缓解内生问题、排除替代性解释、考虑审计轮换制度影响等一系列稳健测试之后,上述结论依然成立。因此,建议会计师事务所应重视由机构投资者调研衍生的客户公司审计风险,市场监管部门应加强公司审计师选聘行为监管,提高机构投资者调研的外部治理效应。

上市公司ESG表现与分析师盈余预测偏差——基于“信息效应”与“治理效应”的双重视角

本文以2010—2021年沪深A股上市公司数据作为研究样本,探究上市公司ESG表现对分析师盈余预测偏差产生的影响。实证结果表明,上市公司ESG表现越好,分析师盈余预测越准确;该种关系在审计质量较差、机构投资者持股比例较低以及非国有企业中更显著。通过机制检验表明上市公司ESG表现能够通过发挥“信息效应”与“治理效应”来影响分析师盈余预测偏差。

数字基础设施的家庭收入效应——基于中国家庭金融调查(CHFS)的实证研究

数字基础设施建设践行与彰显共同富裕的本质要求。基于2011—2019年五轮中国家庭金融调查(CHFS)数据,借助“宽带中国”战略准自然实验,研究了数字基础设施建设与家庭收入之间的关系。研究发现,数字基础设施建设显著提高了家庭收入,而且还有效抑制了收入差距。从作用机制来看,数字基础设施建设通过增加创业机会、就业机会,提高家庭收入,具有显著的“创业效应”和“就业效应”。数字基础设施建设的家庭收入效应在城市、城镇化率高的地区,年龄中等、受教育程度高的群体中更为显著,表现出明显的地区差异和人力资本差异。

数字经济对生态效率的非线性影响--基于门槛效应的检验

数字经济与生态环境是关乎中国式现代化发展的重要议题。本文从数字产业化与产业数字化两个维度,运用熵权法对中国30个省(区、市)2011—2021年数字经济发展水平进行测度,并利用双向固定效应、门槛效应等方法实证分析了数字经济对生态效率的影响。研究发现:数字经济显著促进了生态效率的提升,且这一结论通过了工具变量法、调整样本期和改变模型设定等稳健性检验;数字经济对生态效率的促进效应具有非线性关系,存在以数字经济、环境规制强度为门槛变量的单一门槛效应;进一步的异质性分析表明,数字经济对生态效率的促进效应、单一门槛效应以及“边际效应”递增的非线性特征在南方地区和不同数字经济维度下显著。最后,根据研究结论就如何发展数字经济提升生态效率的路径提出政策建议。