Neuropathic pain is frequently comorbidity with cognitive deficits.Neuralized1(Neurl1)-mediated ubiquitination of CPEB3 in the hippocampus is critical in learning and memory.However,the role of Neurl1 in the cognitive...Neuropathic pain is frequently comorbidity with cognitive deficits.Neuralized1(Neurl1)-mediated ubiquitination of CPEB3 in the hippocampus is critical in learning and memory.However,the role of Neurl1 in the cognitive impairment in neuropathic pain remains elusive.Herein,we found that lumbar 5 spinal nerve ligation(SNL)in male rat-induced neuropathic pain was followed by learning and memory deficits and LTP impairment in the hippocampus.The Neurl1 expression in the hippocampal CA1 was decreased after SNL.And this decrease paralleled the reduction of ubiquitinated-CPEB3 level and reduced production of GluA1 and GluA2.Overexpression of Neurl1 in the CA1 rescued cognitive deficits and LTP impairment,and reversed the reduction of ubiquitinated-CPEB3 level and the decrease of GluA1 and GluA2 production following SNL.Specific knockdown of Neurl1 or CPEB3 in bilateral hippocampal CA1 in naïve rats resulted in cognitive deficits and impairment of synaptic plasticity.The rescued cognitive function and synaptic plasticity by the treatment of overexpression of Neurl1 before SNL were counteracted by the knockdown of CPEB3 in the CA1.Collectively,the above results suggest that the downregulation of Neurl1 through reducing CPEB3 ubiquitination and,in turn,repressing GluA1 and GluA2 production and mediating synaptic plasticity impairment in hippocampal CA1 leads to the genesis of cognitive deficits in neuropathic pain.展开更多
Chronic migraine(CM)is a prevalent and highly debilitating neurological disorder.Functional magnetic resonance imaging(fMRI)studies have demonstrated associations between abnormal brain region activation and CM,yet th...Chronic migraine(CM)is a prevalent and highly debilitating neurological disorder.Functional magnetic resonance imaging(fMRI)studies have demonstrated associations between abnormal brain region activation and CM,yet the underlying complex neural circuitry mechanisms remain unclear.The spinal trigeminal nucleus caudalis(Sp5C)serves as the primary central hub for orofacial nociceptive input,receiving trigeminal pain signals and projecting to higher-order centers such as the thalamus.Therefore,we sought to investigate whether the Sp5C region and its associated circuits were involved in CM pathogenesis.In this study,we established a CM mouse model through repeated intraperitoneal injections of nitroglycerin(NTG).Using a combination of in vivo fiber photometry and in vitro c-Fos immunohistochemistry,we found a marked periorbital and plantar mechanical allodynia in CM mice,accompanied by increased glutamatergic neuronal activity in Sp5C.Chemogenetic manipulation of Sp5C glutamatergic neurons(Sp5CV^(glut2))bidirectionally modulated migraine-like behaviors and induced pain-related affective states,as evidenced by conditioned place preference/aversion(CPP/CPA)paradigms.Anterograde viral tracing revealed dense projections from Sp5C^(Vglut2)to the subthalamic nucleus(STN),which was activated in CM mice.Optogenetic activation of the Sp5C-STN pathway similarly produced migraine-like behaviors and pain-related aversive memory in mice.Altogether,we revealed a critical role of the Sp5CVglut2-STN circuit in the development and modulation of CM.Our findings provide novel mechanistic insights into the central mechanisms underlying CM,establishing potential theoretical foundations for clinical diagnosis and therapeutic development.展开更多
After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the tim...After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.展开更多
The mechanistic target of rapamycin(m TOR) is a serine/threonine kinase that plays a pivotal role in cellular growth, proliferation, survival, and metabolism. In the central nervous system(CNS), the mTOR pathway regul...The mechanistic target of rapamycin(m TOR) is a serine/threonine kinase that plays a pivotal role in cellular growth, proliferation, survival, and metabolism. In the central nervous system(CNS), the mTOR pathway regulates diverse aspects of neural development and function. Genetic mutations within the m TOR pathway lead to severe neurodevelopmental disorders, collectively known as “mTORopathies”(Crino, 2020). Dysfunctions of m TOR, including both its hyperactivation and hypoactivation, have also been implicated in a wide spectrum of other neurodevelopmental and neurodegenerative conditions, highlighting its importance in CNS health.展开更多
Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted t...Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.展开更多
The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It ha...The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It has been suggested that the size of the brain(brain reserve) and the extent of neural connections acquired through life(neural reserve) set a threshold beyond which noticeable impairments occur.In contrast,cognitive reserve refers to the brain's ability to adapt and reo rganize stru cturally and functionally to resist damage and maintain function,including neural reserve and brain maintenance,resilience,and compensation(Verkhratsky and Zorec,2024).展开更多
The presence or absence of adult neural stem cells in the mammalian forebrain ependyma has been debated for two decades.In this study,we performed single-cell RNA sequencing to investigate the cellular composition of ...The presence or absence of adult neural stem cells in the mammalian forebrain ependyma has been debated for two decades.In this study,we performed single-cell RNA sequencing to investigate the cellular composition of the ependymal surface of the adult mouse forebrain using whole mounts of lateral walls of lateral ventricles.We identified 12 different cell subtypes in the ependymal surface.Immunocytochemical analyses revealed that CD133^(+)multi-ciliated cells comprised 67.6%of ependymal cells,while the remaining 32.4%were CD133^(-).CD133^(+)ependymal cells can be further classified into FOXJ1^(+)/SOX2^(+)/ACTA2^(+)cells,FLT1^(+)/CD31^(+)/CLDN5^(+)endothelial-like cells,and PDGFRB^(+)/VTN^(+)/NG2^(+)pericyte-like cells,as well as endothelial-pericyte-like cells and Foxj1^(+)endothelial-like cells.CD133^(-)ependymal cells can be further divided into endothelial-like cells,Foxj1^(+)ependymal cells,Foxj1^(+)endothelial-like cells,pericyte-like cells,endothelial-pericyte-like cells,VIM^(+)cells,and cells negative for all of these markers.This comprehensive profiling confirms the heterogeneity of the ependymal surface in the adult mouse forebrain.Debate regarding whether adult ependymal cells contain neural stem cells has arisen because different researchers have examined different populations of ependymal cells.Our study provides a new perspective for investigation of clinical endogenous neural stem cells,ultimately paving the way for stem cell therapies in neurological diseases.展开更多
Deep learning has become integral to robotics,particularly in tasks such as robotic grasping,where objects often exhibit diverse shapes,textures,and physical properties.In robotic grasping tasks,due to the diverse cha...Deep learning has become integral to robotics,particularly in tasks such as robotic grasping,where objects often exhibit diverse shapes,textures,and physical properties.In robotic grasping tasks,due to the diverse characteristics of the targets,frequent adjustments to the network architecture and parameters are required to avoid a decrease in model accuracy,which presents a significant challenge for non-experts.Neural Architecture Search(NAS)provides a compelling method through the automated generation of network architectures,enabling the discovery of models that achieve high accuracy through efficient search algorithms.Compared to manually designed networks,NAS methods can significantly reduce design costs,time expenditure,and improve model performance.However,such methods often involve complex topological connections,and these redundant structures can severely reduce computational efficiency.To overcome this challenge,this work puts forward a robotic grasp detection framework founded on NAS.The method automatically designs a lightweight network with high accuracy and low topological complexity,effectively adapting to the target object to generate the optimal grasp pose,thereby significantly improving the success rate of robotic grasping.Additionally,we use Class Activation Mapping(CAM)as an interpretability tool,which captures sensitive information during the perception process through visualized results.The searched model achieved competitive,and in some cases superior,performance on the Cornell and Jacquard public datasets,achieving accuracies of 98.3%and 96.8%,respectively,while sustaining a detection speed of 89 frames per second with only 0.41 million parameters.To further validate its effectiveness beyond benchmark evaluations,we conducted real-world grasping experiments on a UR5 robotic arm,where the model demonstrated reliable performance across diverse objects and high grasp success rates,thereby confirming its practical applicability in robotic manipulation tasks.展开更多
Adult neurogenesis is a highly dynamic process that leads to the production of new neurons from a population of quiescent neural stem cells(NSCs).In response to specific endogenous and/or external stimuli,NSCs enter a...Adult neurogenesis is a highly dynamic process that leads to the production of new neurons from a population of quiescent neural stem cells(NSCs).In response to specific endogenous and/or external stimuli,NSCs enter a state of mitotic activation,initiating proliferation and differentiation pathways.Throughout this process,NSCs give rise to neural progenitors,which undergo multiple replicative and differentiative steps,each governed by precise molecular pathways that coordinate cellular changes and signals from the surrounding neurogenic niche.展开更多
Photonic neural networks(PNNs)of sufficiently large physical dimensions and high operation accuracies are envisaged as ideal candidates for breaking the major bottlenecks in the current artificial intelligence archite...Photonic neural networks(PNNs)of sufficiently large physical dimensions and high operation accuracies are envisaged as ideal candidates for breaking the major bottlenecks in the current artificial intelligence architectures in terms of latency,energy efficiency,and computational power.To achieve this vision,it is of vital importance to scale up the PNNs while simultaneously reducing the high demand on the dimensions required by them.The underlying cause of this strategy is the enormous gap between the scales of photonic and electronic integrated circuits.Here,we demonstrate monolithically integrated optical convolutional processors on thin film lithium niobate(TFLN)that harness inherent parallelism in photonics to enable large-scale programmable convolution kernels and,in turn,greatly reduce the dimensions required by subsequent fully connected layers.Experimental validation achieves high classification accuracies of 96%(86%)on the MNIST(Fashion-MNIST)dataset and 84.6%on the AG News dataset while dramatically reducing the required subsequent fully connected layer dimensions to 196×10(from 784×10)and 175×4(from 800×4),respectively.Furthermore,our devices can be driven by commercial field-programmable gate array systems;a unique advantage in addition to their scalable channel number and kernel size.Our architecture provides a solution to build practical machine learning photonic devices.展开更多
In the era of big data and artificial intelligence,optical neural networks(ONNs)have emerged as a promising alternative to conventional electronic approaches,offering superior parallelism,ultrafast processing speeds,a...In the era of big data and artificial intelligence,optical neural networks(ONNs)have emerged as a promising alternative to conventional electronic approaches,offering superior parallelism,ultrafast processing speeds,and high energy efficiency[1-3].However,a major bottleneck in the practical implementation of ONNs is the absence of effective nonlinear activation functions.Self-driven photodetectors have emerged as versatile optical to electrical converters,opening innovative avenues for energy-effective and flexibly integrated activation functions in ONNs through their reconfigurable optoelectronic nonlinearity.展开更多
Embedded printing is a highly promising approach for creating complex structures within a yield-stress support bath.However,the accurate prediction and control of printability remain fundamental challenges due to the ...Embedded printing is a highly promising approach for creating complex structures within a yield-stress support bath.However,the accurate prediction and control of printability remain fundamental challenges due to the complex interactions between inks and support baths.Here,we present an artificial intelligence(AI)-driven framework that interprets and predicts embedded printability using rheological data.Using a standardized workflow,we extracted 21 rheological descriptors and established 12 indicators to evaluate structural continuity and geometric fidelity.Interpretable machine learning models revealed that direction-dependent defects are governed by the synergistic interplay among ink yield stress,support bath zero shear viscosity,flow behavior index,and time constant.To enable the prediction of printability in a generalizable manner,we further developed a cascaded neural network,which achieved mean relative prediction errors below 15%across all indicators.Experimental validation using three-dimensional(3 D)-printed constructs and micro-computed tomography(μCT)reconstructions confirmed a strong correlation between predicted and actual fidelity.This work establishes a physics-informed,data-driven paradigm for decoding and optimizing embedded printing,offering broad applicability and providing a robust tool for the rapid pairing of suitable printable ink-support bath combinations.展开更多
In the early stages of traumatic spinal cord injury,extensive accumulation of autophagosomes creates a neurotoxic microenvironment,exacerbating neuronal cell death and worsening tissue damage,ultimately hindering neur...In the early stages of traumatic spinal cord injury,extensive accumulation of autophagosomes creates a neurotoxic microenvironment,exacerbating neuronal cell death and worsening tissue damage,ultimately hindering neurofunctional recovery.Activin A is a critical growth factor necessary for the development of the embryonic nervous system and for maintaining neuronal function in the adult cerebral cortex.It can inhibit excessive autophagy in ischemic stroke to reduce neuronal damage.However,the specific mechanism through which Activin A functions in the spinal cord remains poorly understood.In this study,we administered different concentrations of Activin A to neural stem cells from the spinal cord and found that Activin A stimulated the proliferation and neuronal differentiation of neural stem cells.Then,we established an in vitro oxidative stress model by using hydrogen peroxide to stimulate the neural stem cells-induced neurons.We found that Activin A could reduce apoptosis caused by oxidative stress.Subsequently,we treated a mouse model of spinal cord contusion with intrathecal injection of Activin A.Behavioral and electrophysiological results showed that Activin A promoted recovery of motor function and reconstruction of neural circuits in the model mice.Finally,RNA sequencing indicated that Activin A inhibited autophagy by activating the PI3K/AKT/mTOR pathway and upregulating the expression of synaptogenesis-related factor Sema3A in the spinal cord.These results suggest that Activin A may mediate the excessive autophagic response after spinal cord injury,promote the reconstruction of damaged neural circuits,and restore neurological function in the injured spinal cord.展开更多
The hippocampus is part of the brain limbic system and plays an important role in learning and memory.Moreover,its ability to form,consolidate,and retrieve different types of memories makes it a central component in t...The hippocampus is part of the brain limbic system and plays an important role in learning and memory.Moreover,its ability to form,consolidate,and retrieve different types of memories makes it a central component in the cognitive functions necessary for everyday life.Understanding the role of the hippocampus helps comprehend how memories are created,stored,and recalled and sheds light on the impact of hippocampal damage in conditions such as Alzheimer’s disease and other forms of dementia.展开更多
基金supported by the National Natural Science Foundation of China(82171237,82471246,and 82401462)the Natural Science Foundation of Henan Province,China(242300420381).
文摘Neuropathic pain is frequently comorbidity with cognitive deficits.Neuralized1(Neurl1)-mediated ubiquitination of CPEB3 in the hippocampus is critical in learning and memory.However,the role of Neurl1 in the cognitive impairment in neuropathic pain remains elusive.Herein,we found that lumbar 5 spinal nerve ligation(SNL)in male rat-induced neuropathic pain was followed by learning and memory deficits and LTP impairment in the hippocampus.The Neurl1 expression in the hippocampal CA1 was decreased after SNL.And this decrease paralleled the reduction of ubiquitinated-CPEB3 level and reduced production of GluA1 and GluA2.Overexpression of Neurl1 in the CA1 rescued cognitive deficits and LTP impairment,and reversed the reduction of ubiquitinated-CPEB3 level and the decrease of GluA1 and GluA2 production following SNL.Specific knockdown of Neurl1 or CPEB3 in bilateral hippocampal CA1 in naïve rats resulted in cognitive deficits and impairment of synaptic plasticity.The rescued cognitive function and synaptic plasticity by the treatment of overexpression of Neurl1 before SNL were counteracted by the knockdown of CPEB3 in the CA1.Collectively,the above results suggest that the downregulation of Neurl1 through reducing CPEB3 ubiquitination and,in turn,repressing GluA1 and GluA2 production and mediating synaptic plasticity impairment in hippocampal CA1 leads to the genesis of cognitive deficits in neuropathic pain.
基金supported by the National Natural Science Foundation of China(No.32571336 and 32271048)Research Funds of Centre for Leading Medicine and Advanced Technologies of IHM(No.2025IHM01100)。
文摘Chronic migraine(CM)is a prevalent and highly debilitating neurological disorder.Functional magnetic resonance imaging(fMRI)studies have demonstrated associations between abnormal brain region activation and CM,yet the underlying complex neural circuitry mechanisms remain unclear.The spinal trigeminal nucleus caudalis(Sp5C)serves as the primary central hub for orofacial nociceptive input,receiving trigeminal pain signals and projecting to higher-order centers such as the thalamus.Therefore,we sought to investigate whether the Sp5C region and its associated circuits were involved in CM pathogenesis.In this study,we established a CM mouse model through repeated intraperitoneal injections of nitroglycerin(NTG).Using a combination of in vivo fiber photometry and in vitro c-Fos immunohistochemistry,we found a marked periorbital and plantar mechanical allodynia in CM mice,accompanied by increased glutamatergic neuronal activity in Sp5C.Chemogenetic manipulation of Sp5C glutamatergic neurons(Sp5CV^(glut2))bidirectionally modulated migraine-like behaviors and induced pain-related affective states,as evidenced by conditioned place preference/aversion(CPP/CPA)paradigms.Anterograde viral tracing revealed dense projections from Sp5C^(Vglut2)to the subthalamic nucleus(STN),which was activated in CM mice.Optogenetic activation of the Sp5C-STN pathway similarly produced migraine-like behaviors and pain-related aversive memory in mice.Altogether,we revealed a critical role of the Sp5CVglut2-STN circuit in the development and modulation of CM.Our findings provide novel mechanistic insights into the central mechanisms underlying CM,establishing potential theoretical foundations for clinical diagnosis and therapeutic development.
基金supported by the National Key Research and Development Program of China,No.2023YFC3603705(to DX)the National Natural Science Foundation of China,No.82302866(to YZ).
文摘After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.
基金supported by grants from Simons Foundation (SFARI 479754),CIHR (PJT-180565)the Scottish Rite Charitable Foundation of Canada (to YL)funding from the Canada Research Chairs program。
文摘The mechanistic target of rapamycin(m TOR) is a serine/threonine kinase that plays a pivotal role in cellular growth, proliferation, survival, and metabolism. In the central nervous system(CNS), the mTOR pathway regulates diverse aspects of neural development and function. Genetic mutations within the m TOR pathway lead to severe neurodevelopmental disorders, collectively known as “mTORopathies”(Crino, 2020). Dysfunctions of m TOR, including both its hyperactivation and hypoactivation, have also been implicated in a wide spectrum of other neurodevelopmental and neurodegenerative conditions, highlighting its importance in CNS health.
基金supported by the National Natural Science Foundation of China,Nos.32271389,31900987(both to PY)the Natural Science Foundation of Jiangsu Province,No.BK20230608(to JJ)。
文摘Regulatory T cells,a subset of CD4^(+)T cells,play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties.Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair,emphasizing their multifaceted roles in immune regulation.This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration.Beyond their classical immune-regulatory functions,emerging evidence points to non-immune mechanisms of regulatory T cells,particularly their interactions with stem cells and other non-immune cells.These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration,positioning non-immune pathways as a promising direction for future research.By modulating immune and non-immune cells,including neurons and glia within neural tissues,Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems.Preclinical studies have revealed that Treg cells interact with neurons,glial cells,and other neural components to mitigate inflammatory damage and support functional recovery.Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment.However,research on the mechanistic roles of regulatory T cells in other diseases remains limited,highlighting substantial gaps and opportunities for exploration in this field.Laboratory and clinical studies have further advanced the application of regulatory T cells.Technical advances have enabled efficient isolation,ex vivo expansion and functionalization,and adoptive transfer of regulatory T cells,with efficacy validated in animal models.Innovative strategies,including gene editing,cell-free technologies,biomaterial-based recruitment,and in situ delivery have expanded the therapeutic potential of regulatory T cells.Gene editing enables precise functional optimization,while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites.These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair.By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair,regulatory T cells–based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.
文摘针对果实分拣中存在识别精度低、耗时长等问题,设计实现了一种基于深度学习的智能水果分拣系统.首先,该系统采用残差网络(Residual network,ResNet)模型,通过引入动态残差门控机制优化梯度传播有效解决了深层网络训练中的梯度消失和爆炸问题,使得网络能够通过跳跃连接学习到更有效的特征表示;其次,对ResNet-18模型进行了轻量化设计,利用交叉熵损失函数(CrossEntropy loss,CELoss)和Adam优化器(Adaptive moment estimation,Adam)来进行模型的训练;最后,对数据集peach-split进行实验分析,结果表明构建的智能分拣系统对提高水果分拣精度研究具有一定的实用价值.
文摘The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It has been suggested that the size of the brain(brain reserve) and the extent of neural connections acquired through life(neural reserve) set a threshold beyond which noticeable impairments occur.In contrast,cognitive reserve refers to the brain's ability to adapt and reo rganize stru cturally and functionally to resist damage and maintain function,including neural reserve and brain maintenance,resilience,and compensation(Verkhratsky and Zorec,2024).
基金supported by the State Key Program of the National Natural Science Foundation of China,No.82030035(to YES)Peak Disciplines(Type IV)of Institutions of Higher Learning in Shanghai(to LZ).
文摘The presence or absence of adult neural stem cells in the mammalian forebrain ependyma has been debated for two decades.In this study,we performed single-cell RNA sequencing to investigate the cellular composition of the ependymal surface of the adult mouse forebrain using whole mounts of lateral walls of lateral ventricles.We identified 12 different cell subtypes in the ependymal surface.Immunocytochemical analyses revealed that CD133^(+)multi-ciliated cells comprised 67.6%of ependymal cells,while the remaining 32.4%were CD133^(-).CD133^(+)ependymal cells can be further classified into FOXJ1^(+)/SOX2^(+)/ACTA2^(+)cells,FLT1^(+)/CD31^(+)/CLDN5^(+)endothelial-like cells,and PDGFRB^(+)/VTN^(+)/NG2^(+)pericyte-like cells,as well as endothelial-pericyte-like cells and Foxj1^(+)endothelial-like cells.CD133^(-)ependymal cells can be further divided into endothelial-like cells,Foxj1^(+)ependymal cells,Foxj1^(+)endothelial-like cells,pericyte-like cells,endothelial-pericyte-like cells,VIM^(+)cells,and cells negative for all of these markers.This comprehensive profiling confirms the heterogeneity of the ependymal surface in the adult mouse forebrain.Debate regarding whether adult ependymal cells contain neural stem cells has arisen because different researchers have examined different populations of ependymal cells.Our study provides a new perspective for investigation of clinical endogenous neural stem cells,ultimately paving the way for stem cell therapies in neurological diseases.
基金funded by Guangdong Basic and Applied Basic Research Foundation(2023B1515120064)National Natural Science Foundation of China(62273097).
文摘Deep learning has become integral to robotics,particularly in tasks such as robotic grasping,where objects often exhibit diverse shapes,textures,and physical properties.In robotic grasping tasks,due to the diverse characteristics of the targets,frequent adjustments to the network architecture and parameters are required to avoid a decrease in model accuracy,which presents a significant challenge for non-experts.Neural Architecture Search(NAS)provides a compelling method through the automated generation of network architectures,enabling the discovery of models that achieve high accuracy through efficient search algorithms.Compared to manually designed networks,NAS methods can significantly reduce design costs,time expenditure,and improve model performance.However,such methods often involve complex topological connections,and these redundant structures can severely reduce computational efficiency.To overcome this challenge,this work puts forward a robotic grasp detection framework founded on NAS.The method automatically designs a lightweight network with high accuracy and low topological complexity,effectively adapting to the target object to generate the optimal grasp pose,thereby significantly improving the success rate of robotic grasping.Additionally,we use Class Activation Mapping(CAM)as an interpretability tool,which captures sensitive information during the perception process through visualized results.The searched model achieved competitive,and in some cases superior,performance on the Cornell and Jacquard public datasets,achieving accuracies of 98.3%and 96.8%,respectively,while sustaining a detection speed of 89 frames per second with only 0.41 million parameters.To further validate its effectiveness beyond benchmark evaluations,we conducted real-world grasping experiments on a UR5 robotic arm,where the model demonstrated reliable performance across diverse objects and high grasp success rates,thereby confirming its practical applicability in robotic manipulation tasks.
文摘Adult neurogenesis is a highly dynamic process that leads to the production of new neurons from a population of quiescent neural stem cells(NSCs).In response to specific endogenous and/or external stimuli,NSCs enter a state of mitotic activation,initiating proliferation and differentiation pathways.Throughout this process,NSCs give rise to neural progenitors,which undergo multiple replicative and differentiative steps,each governed by precise molecular pathways that coordinate cellular changes and signals from the surrounding neurogenic niche.
基金supported by the National Natural Science Foundation of China (Grant Nos.12192251,12334014,62335019,12134001,1230441812474378)+1 种基金the Quantum Science and Technology National Science and Technology Major Project(Grant No.2021ZD0301403)the Shanghai Municipal Science and Technology Major Project (Grant No.2019SHZDZX01)。
文摘Photonic neural networks(PNNs)of sufficiently large physical dimensions and high operation accuracies are envisaged as ideal candidates for breaking the major bottlenecks in the current artificial intelligence architectures in terms of latency,energy efficiency,and computational power.To achieve this vision,it is of vital importance to scale up the PNNs while simultaneously reducing the high demand on the dimensions required by them.The underlying cause of this strategy is the enormous gap between the scales of photonic and electronic integrated circuits.Here,we demonstrate monolithically integrated optical convolutional processors on thin film lithium niobate(TFLN)that harness inherent parallelism in photonics to enable large-scale programmable convolution kernels and,in turn,greatly reduce the dimensions required by subsequent fully connected layers.Experimental validation achieves high classification accuracies of 96%(86%)on the MNIST(Fashion-MNIST)dataset and 84.6%on the AG News dataset while dramatically reducing the required subsequent fully connected layer dimensions to 196×10(from 784×10)and 175×4(from 800×4),respectively.Furthermore,our devices can be driven by commercial field-programmable gate array systems;a unique advantage in addition to their scalable channel number and kernel size.Our architecture provides a solution to build practical machine learning photonic devices.
基金supported by the National Natural Science Foundation of China(52422107,T2394471,and 62571319)Beijing Nova Program(20240484531)+1 种基金China Postdoctoral Science Foundation(2022M710074)and Open Research Fund Program of Beijing National Research Center for Information Science and Technology(04410304023).
文摘In the era of big data and artificial intelligence,optical neural networks(ONNs)have emerged as a promising alternative to conventional electronic approaches,offering superior parallelism,ultrafast processing speeds,and high energy efficiency[1-3].However,a major bottleneck in the practical implementation of ONNs is the absence of effective nonlinear activation functions.Self-driven photodetectors have emerged as versatile optical to electrical converters,opening innovative avenues for energy-effective and flexibly integrated activation functions in ONNs through their reconfigurable optoelectronic nonlinearity.
基金supported by the National Natural Science Foundation of China(Nos.52305314 and U21A20394)the Beijing Natural Science Foundation(Nos.7252285 and L246001)the National Key Research and Development Program of China(No.2023YFB4605800)。
文摘Embedded printing is a highly promising approach for creating complex structures within a yield-stress support bath.However,the accurate prediction and control of printability remain fundamental challenges due to the complex interactions between inks and support baths.Here,we present an artificial intelligence(AI)-driven framework that interprets and predicts embedded printability using rheological data.Using a standardized workflow,we extracted 21 rheological descriptors and established 12 indicators to evaluate structural continuity and geometric fidelity.Interpretable machine learning models revealed that direction-dependent defects are governed by the synergistic interplay among ink yield stress,support bath zero shear viscosity,flow behavior index,and time constant.To enable the prediction of printability in a generalizable manner,we further developed a cascaded neural network,which achieved mean relative prediction errors below 15%across all indicators.Experimental validation using three-dimensional(3 D)-printed constructs and micro-computed tomography(μCT)reconstructions confirmed a strong correlation between predicted and actual fidelity.This work establishes a physics-informed,data-driven paradigm for decoding and optimizing embedded printing,offering broad applicability and providing a robust tool for the rapid pairing of suitable printable ink-support bath combinations.
基金supported by the National Natural Science Foundation of China,Nos.82271419,81901902(to YZ),82202702(to ZW),82202351(to XH),82301550(to LYang),82271418(to XX)the Shanghai Rising-Star Program,No.22QA1408200(to YZ)the Fundamental Research Fundsfor the Central Universities,No.22120220555(to YZ).
文摘In the early stages of traumatic spinal cord injury,extensive accumulation of autophagosomes creates a neurotoxic microenvironment,exacerbating neuronal cell death and worsening tissue damage,ultimately hindering neurofunctional recovery.Activin A is a critical growth factor necessary for the development of the embryonic nervous system and for maintaining neuronal function in the adult cerebral cortex.It can inhibit excessive autophagy in ischemic stroke to reduce neuronal damage.However,the specific mechanism through which Activin A functions in the spinal cord remains poorly understood.In this study,we administered different concentrations of Activin A to neural stem cells from the spinal cord and found that Activin A stimulated the proliferation and neuronal differentiation of neural stem cells.Then,we established an in vitro oxidative stress model by using hydrogen peroxide to stimulate the neural stem cells-induced neurons.We found that Activin A could reduce apoptosis caused by oxidative stress.Subsequently,we treated a mouse model of spinal cord contusion with intrathecal injection of Activin A.Behavioral and electrophysiological results showed that Activin A promoted recovery of motor function and reconstruction of neural circuits in the model mice.Finally,RNA sequencing indicated that Activin A inhibited autophagy by activating the PI3K/AKT/mTOR pathway and upregulating the expression of synaptogenesis-related factor Sema3A in the spinal cord.These results suggest that Activin A may mediate the excessive autophagic response after spinal cord injury,promote the reconstruction of damaged neural circuits,and restore neurological function in the injured spinal cord.
基金supported by a National Research Foundation of Korea (NRF) grant funded by the Korean government (2020M3E5D9079764, RS-2024-00408736)(to KS)supported by Korea Drug Development Fund funded by Ministry of Science and ICT,Ministry of Trade,Industry,and Energy,and Ministry of Health and Welfare (RS-2024-00335752)(to KS)。
文摘The hippocampus is part of the brain limbic system and plays an important role in learning and memory.Moreover,its ability to form,consolidate,and retrieve different types of memories makes it a central component in the cognitive functions necessary for everyday life.Understanding the role of the hippocampus helps comprehend how memories are created,stored,and recalled and sheds light on the impact of hippocampal damage in conditions such as Alzheimer’s disease and other forms of dementia.
