Vibration-reduced anxiety-like behavior relies on ameliorating abnormalities of the somatosensory cortex and medial prefrontal cortex

Tibetan singing bowls emit low-frequency sounds and produce perceptible harmonic tones and vibrations through manual tapping.The sounds the singing bowls produce have been shown to enhance relaxation and reduce anxiety.However,the underlying mechanism remains unclear.In this study,we used chronic restraint stress or sleep deprivation to establish mouse models of anxiety that exhibit anxiety-like behaviors.We then supplied treatment with singing bowls in a bottomless cage placed on the top of a cushion.We found that unlike in humans,the combination of harmonic tones and vibrations did not improve anxietylike behaviors in mice,while individual vibration components did.Additionally,the vibration of singing bowls increased the level of N-methyl-D-aspartate receptor 1 in the somatosensory cortex and prefrontal cortex of the mice,decreased the level ofγ-aminobutyric acid A(GABA)receptorα1 subtype,reduced the level of CaMKII in the prefrontal cortex,and increased the number of GABAergic interneurons.At the same time,electrophysiological tests showed that the vibration of singing bowls significantly reduced the abnormal low-frequency gamma oscillation peak frequency in the medial prefrontal cortex caused by stress restraint pressure and sleep deprivation.Results from this study indicate that the vibration of singing bowls can alleviate anxiety-like behaviors by reducing abnormal molecular and electrophysiological events in somatosensory and medial prefrontal cortex.

Dopamine in the prefrontal cortex plays multiple roles in the executive function of patients with Parkinson's disease

Parkinson’s disease can affect not only motor functions but also cognitive abilities,leading to cognitive impairment.One common issue in Parkinson’s disease with cognitive dysfunction is the difficulty in executive functioning.Executive functions help us plan,organize,and control our actions based on our goals.The brain area responsible for executive functions is called the prefrontal co rtex.It acts as the command center for the brain,especially when it comes to regulating executive functions.The role of the prefrontal cortex in cognitive processes is influenced by a chemical messenger called dopamine.However,little is known about how dopamine affects the cognitive functions of patients with Parkinson’s disease.In this article,the authors review the latest research on this topic.They start by looking at how the dopaminergic syste m,is alte red in Parkinson’s disease with executive dysfunction.Then,they explore how these changes in dopamine impact the synaptic structure,electrical activity,and connection components of the prefrontal cortex.The authors also summarize the relationship between Parkinson’s disease and dopamine-related cognitive issues.This information may offer valuable insights and directions for further research and improvement in the clinical treatment of cognitive impairment in Parkinson’s disease.

Morphological disruption and visual tuning alterations in the primary visual cortex in glaucoma(DBA/2J)mice

Glaucoma is a leading cause of irreve rsible blindness wo rldwide,and previous studies have shown that,in addition to affecting the eyes,it also causes abnormalities in the brain.However,it is not yet clear how the primary visual cortex(V1)is altered in glaucoma.This study used DBA/2J mice as a model for spontaneous secondary glaucoma.The aim of the study was to compare the electrophysiological and histomorphological chara cteristics of neurons in the V1between 9-month-old DBA/2J mice and age-matched C57BL/6J mice.We conducted single-unit recordings in the V1 of light-anesthetized mice to measure the visually induced responses,including single-unit spiking and gamma band oscillations.The morphology of layerⅡ/Ⅲneurons was determined by neuronal nuclear antigen staining and Nissl staining of brain tissue sections.Eighty-seven neurons from eight DBA/2J mice and eighty-one neurons from eight C57BL/6J mice were examined.Compared with the C57BL/6J group,V1 neurons in the DBA/2J group exhibited weaker visual tuning and impaired spatial summation.Moreove r,fewer neuro ns were observed in the V1 of DBA/2J mice compared with C57BL/6J mice.These findings suggest that DBA/2J mice have fewer neurons in the VI compared with C57BL/6J mice,and that these neurons have impaired visual tuning.Our findings provide a better understanding of the pathological changes that occur in V1 neuron function and morphology in the DBA/2J mouse model.This study might offer some innovative perspectives regarding the treatment of glaucoma.

Glial response in the midcingulate cortex in Huntington’s disease

Huntington’s disease(HD)is a genetic disease characterized by the progressive degeneration of the striatum and cortex.Patients can present with a variety of symptoms that can broadly be classified into motor symptoms,inclusive of choreatic movements and rigidity,mood and psychiatric symptoms,such as depression and apathy,and cognitive symptoms,such as cognitive decline.The causal mutation underlying HD results from an expansion of a CAG repeat sequence on the IT15 gene,resulting in the formation and accumulation of a mutant huntingtin protein.

The dorsolateral pre-frontal cortex bi-polar error-related potential in a locked-in patient implanted with a daily use brain–computer interface

While brain computer interfaces(BCIs)ofer the potential of allowing those sufering from loss of muscle control to once again fully engage with their environment by bypassing the afected motor system and decoding user intentions directly from brain activity,they are prone to errors.One possible avenue for BCI performance improvement is to detect when the BCI user perceives the BCI to have made an unintended action and thus take corrective actions.Error-related potentials(ErrPs)are neural correlates of error awareness and as such can provide an indication of when a BCI system is not performing according to the user’s intentions.Here,we investigate the brain signals of an implanted BCI user sufering from locked-in syndrome(LIS)due to late-stage ALS that prevents her from being able to speak or move but not from using her BCI at home on a daily basis to communicate,for the presence of error-related signals.We frst establish the presence of an ErrP originating from the dorsolateral pre-frontal cortex(dLPFC)in response to errors made during a discrete feedback task that mimics the click-based spelling software she uses to communicate.Then,we show that this ErrP can also be elicited by cursor movement errors in a continuous BCI cursor control task.This work represents a frst step toward detecting ErrPs during the daily home use of a communications BCI.

Neuropsychological Profile of a Patient with Acquired Brain Damage Following Vascular Lesion of the Left Anterior Cingulate Cortex

Stroke is a physiological alteration associated with changes in blood flow that can result in sudden-onset cognitive impairment. It has a heterogenous clinical presentation with varying degrees of severity correlated with specific central nervous system zones or areas, and its prognosis is uncertain. This case study describes a 62-year-old male patient with acquired brain damage of the anterior cingulate cortex as a result of an ischemic event in the territory of the left anterior cerebral artery. Cognitive function was assessed using the neuropsychological executive function and frontal lobe test battery (BANFE-2) as well as other neuropsychological tests. The results show a profile of higher mental functions characterized by the presence of dysexecutive syndrome with marked behavioral alteration and diencephalic amnesia. .

Regulation of specific abnormal calcium signals in the hippocampal CA1 and primary cortex M1 alleviates the progression of temporal lobe epilepsy

Temporal lobe epilepsy is a multifactorial neurological dysfunction syndrome that is refractory,resistant to antiepileptic drugs,and has a high recurrence rate.The pathogenesis of temporal lobe epilepsy is complex and is not fully understood.Intracellular calcium dynamics have been implicated in temporal lobe epilepsy.However,the effect of fluctuating calcium activity in CA1 pyramidal neurons on temporal lobe epilepsy is unknown,and no longitudinal studies have investigated calcium activity in pyramidal neurons in the hippocampal CA1 and primary motor cortex M1 of freely moving mice.In this study,we used a multichannel fiber photometry system to continuously record calcium signals in CA1 and M1 during the temporal lobe epilepsy process.We found that calcium signals varied according to the grade of temporal lobe epilepsy episodes.In particular,cortical spreading depression,which has recently been frequently used to represent the continuously and substantially increased calcium signals,was found to correspond to complex and severe behavioral characteristics of temporal lobe epilepsy ranging from gradeⅡto gradeⅤ.However,vigorous calcium oscillations and highly synchronized calcium signals in CA1 and M1 were strongly related to convulsive motor seizures.Chemogenetic inhibition of pyramidal neurons in CA1 significantly attenuated the amplitudes of the calcium signals corresponding to gradeⅠepisodes.In addition,the latency of cortical spreading depression was prolonged,and the above-mentioned abnormal calcium signals in CA1 and M1 were also significantly reduced.Intriguingly,it was possible to rescue the altered intracellular calcium dynamics.Via simultaneous analysis of calcium signals and epileptic behaviors,we found that the progression of temporal lobe epilepsy was alleviated when specific calcium signals were reduced,and that the end-point behaviors of temporal lobe epilepsy were improved.Our results indicate that the calcium dynamic between CA1 and M1 may reflect specific epileptic behaviors corresponding to different grades.Furthermore,the selective regulation of abnormal calcium signals in CA1 pyramidal neurons appears to effectively alleviate temporal lobe epilepsy,thereby providing a potential molecular mechanism for a new temporal lobe epilepsy diagnosis and treatment strategy.

基于KeystoneⅡ构架的Cortex A15内核系统设计与异常处理策略

阐述以高性能SOC TMS320C66AK2H的Cortex A15内核为例,利用Cortex A15内核中断控制器(GIC 400)和SOC中断处理控制器(CIC2)实现一个系统异常处理机制,能够准确快速的定位系统运行出错的地方。以Cortex A15内核使用EDMA3模块非法访问共享内存MSMC为例,验证系统异常处理机制的可行性,经测试该方法准确有效。

Massively parallel characterization of regulatory elements in the developing human cortex

Nucleotide changes in gene regulatory elements are important determinants of neuronal development and diseases.Using massively parallel reporter assays in primary human cells from mid-gestation cortex and cerebral organoids,we interrogated the cis-regulatory activity of 102,767 open chromatin regions,including thousands of sequences with cell type-specific accessibility and variants associated with brain gene regulation.In primary cells,we identified 46,802 active enhancer sequences and 164 variants that alter enhancer activity.Activity was comparable in organoids and primary cells,suggesting that organoids provide an adequate model for the developing cortex.Using deep learning we decoded the sequence basis and upstream regulators of enhancer activity.This work establishes a comprehensive catalog of functional gene regulatory elements and variants in human neuronal development.

Enhancing m^(6)A modification in the motor cortex facilitates corticospinal tract remodeling after spinal cord injury

Spinal cord injury typically causes corticospinal tract disruption. Although the disrupted corticospinal tract can self-regenerate to a certain degree, the underlying mechanism of this process is still unclear. N6-methyladenosine(m^(6)A) modifications are the most common form of epigenetic regulation at the RNA level and play an essential role in biological processes. However, whether m^(6)A modifications participate in corticospinal tract regeneration after spinal cord injury remains unknown. We found that expression of methyltransferase 14 protein(METTL14) in the locomotor cortex was high after spinal cord injury and accompanied by elevated m^(6)A levels. Knockdown of Mettl14 in the locomotor cortex was not favorable for corticospinal tract regeneration and neurological recovery after spinal cord injury. Through bioinformatics analysis and methylated RNA immunoprecipitation-quantitative polymerase chain reaction, we found that METTL14 regulated Trib2 expression in an m^(6)A-regulated manner, thereby activating the mitogen-activated protein kinase pathway and promoting corticospinal tract regeneration. Finally, we administered syringin, a stabilizer of METTL14, using molecular docking. Results confirmed that syringin can promote corticospinal tract regeneration and facilitate neurological recovery by stabilizing METTL14. Findings from this study reveal that m^(6)A modification is involved in the regulation of corticospinal tract regeneration after spinal cord injury.

基于Cortex-M3的串口与CAN转换模块的设计与实现

针对采用控制器局域网络(CAN:Controller Area Network)总线的自动操舵系统和采用串口通讯的航海导航设备之间通讯的不匹配问题,设计了一种基于Cortex-M3嵌入式平台的通信转换模块,实现了串口与CAN总线数据的双向转换功能。同时对传统CAN收发器CTM1050存在的信号稳定性不足、波特率精准度低等问题,提出并实现了一种硬件电路的替代方案,提高了数据通讯的时效性和稳定性。基于CAN2.0B扩展帧,设计了自动操舵系统内部CAN总线协议。该协议可根据报文信息优先级分配标识帧,保证了总线数据的有序传输。实验结果表明,该通讯模块功能使用正常且通讯效果良好,具有一定通用性,可在多种需要转换的设备系统上推广使用。

基于Cortex-M4的CNTR/CTRU密钥封装高效实现

量子计算技术的迅猛发展对现有的公钥密码体制造成了极大的威胁,为了抵抗量子计算的攻击,后量子密码成为当前密码学界的研究热点.目前,物联网的安全问题备受关注,ARM Cortex-M4作为低功耗嵌入式处理器,被广泛应用于物联网设备中,在其上部署后量子密码算法将为物联网设备的安全提供更加可靠的保障.CNTR和CTRU是我国学者提出的NTRU格基密钥封装方案,相比于基于LWE技术路线的格基密钥封装方案在安全性和其他性能上具有综合优势,并在我国密标委得到立项.本文工作首次在ARM Cortex-M4平台上高效紧凑地实现了CNTR和CTRU方案,充分利用单指令多数据(Single Instruction Multiple Data,SIMD)指令,调整运算结构和指令安排,优化核心的多项式运算,从而在算法实现速度和堆栈空间上进行全面优化升级.本文主要工作如下:本文首次在ARM Cortex-M4上实现耗时模块多项式中心二项分布采样,采样速度提升32.49%;使用混合基数论变换(Number Theoretic Transform,NTT)加速非NTT友好多项式乘法运算,充分利用浮点单元(Floating-Point Unit,FPU)寄存器,在NTT实现中采用层融合技术,最大化减少加载和存储等耗时指令使用,使得正向NTT和逆向NTT的速度分别提升84.24%、81.15%;通过NTT过程系数范围分析进行延迟约减,进而减少约减次数,并使用改进的Barrett约减和Montgomery约减技术实现降低约减汇编指令条数;使用循环展开技术实现多项式求逆,优化多项式求逆这一耗时过程,速度优化率为68.85%;针对解密过程中的非NTT友好素数模数多项式环乘法,采用多模数NTT和中国剩余定理(Chinese Remainder Theorem,CRT)结合的方法进行加速,完成解密过程96.26%的速度提升;使用空间复用的方法优化堆栈空间,CNTR和CTRU的堆栈空间分别减少了29.86%、28.17%.实验结果表明:提出的优化技术大幅提升了算法实现效率,与C参考实现相比,CNTR和CTRU的整体速度优化率分别为85.54%、85.56%.与其他格基密钥封装方案最新ARM Cortex-M4实现相比,本文的优化实现在速度、空间和安全性上具有综合性的优势.

基于Cortex-M3的组合罗经显控软件的设计与实现

为解决传统光纤陀螺罗经系统价格昂贵的问题,利用低成本的光纤陀螺罗经和双天线卫星定位定向系统组成组合罗经的主罗经单元成为重要措施。组合罗经显控单元的主控芯片采用基于Cortex-M3的LPC1768,为了减少大量代码的编写、缩短软件开发周期,屏幕选用迪文串口屏,通过串口接收主罗经发来的报文,将船舶航向以罗盘图片的方式在屏幕上实时显示出来。同时,为了方便不同的用户使用,设计了3种显示模式:罗经模式、航向模式以及导航模式。经实船测试,该显控软件的设计可行且能够满足航行要求。

基于Arm Cortex-M0的视频处理系统

设计一种基于Arm Cortex-M0的视频处理系统,旨在满足视频处理在各个应用领域的需求。系统基于EG4S20现场可编程逻辑门阵列(Field Programmable Gate Array,FPGA)开发板进行开发,搭建基于Arm Cortex-M0的系统级芯片(System on Chip,SoC)架构,实现了多种图像信号处理(Image Signal Processing,ISP)算法。系统通过安全数字(Secure Digital,SD)存储卡读取原始视频数据,经过ISP硬件加速处理,通过高清多媒体接口(High Definition Multimedia Interface,HDMI)实时显示处理后的图像。系统集成了键盘、数码管和蜂鸣器模块,实现了智能化的视频处理和控制,极大地提高了处理效率和效果。

基于ARM Cortex-M3内核的嵌入式运动控制箱的设计与实现

通过研究现有运动控制方案,发现常见的运动控制解决方案都要用到运动控制卡,成本较高,体积较大,不适合控制精度要求不太高、成本要求较高的运动控制场景。从ARM Cortex-M3为内核的32位微控制器、光电隔离接口电路、PWM信号调制、供电电源、软件设计5个方面进行设计,调试并实现一套具有更高性价比的嵌入式运动控制箱。该嵌入式微控制器经光电隔离接口电路读取外部数字化输入信号,经过嵌入式微控制器CPU处理,输出数字化信号和调制PWM信号,经光电隔离接口电路隔离转换,以控制伺服电机和外部其他设备。该运动控制箱成本低、功能强大、体积小,适用于对成本要求较高、对运动精度和难度要求不太高的场合。实际应用表明,该运动控制箱可实现4通道PWM输出、20通道的数字输入和16通道的数字输出,性能良好,性价比高,效果良好。

基于Cortex主控芯片的MCU测试验证方法研究

随着国家在芯片技术方面投入的加大,越来越多的国产化芯片实现量产,测试验证成为确保芯片设计与工艺质量可靠性的关键环节,可以提前判定器件功能和参数的可靠性。基于Cortex-M3内核的微处理器(MCU)芯片和V93000自动测试设备研究了一种MCU测试验证方法及流程。通过测试母版原理设计和测试向量生成,测试分析了芯片功能和关键直流参数,形成了一套芯片测试验证流程及方法,对于MCU芯片国产化测试验证具有一定的借鉴意义。

Transient neurogenesis in ischemic cortex from Sox2^(+)astrocytes

The adult cortex has long been regarded as non-neurogenic.Whether injury can induce neurogenesis in the adult cortex is still controversial.Here,we report that focal ischemia stimulates a transient wave of local neurogenesis.Using 5′-bromo-2′-deoxyuridine labeling,we demonstrated a rapid generation of doublecortin-positive neuroblasts that died quickly in mouse cerebral cortex following ischemia.Nestin-Cre^(ER)-based cell ablation and fate mapping showed a small contribution of neuroblasts by subventricular zone neural stem cells.Using a mini-photothrombotic ischemia mouse model and retrovirus expressing green fluorescent protein labeling,we observed maturation of locally generated new neurons.Furthermore,fate tracing analyses using PDGFRα-,GFAP-,and Sox2-Cre^(ER) mice showed a transient wave of neuroblast generation in mild ischemic cortex and identified that Sox2-positive astrocytes were the major neurogenic cells in adult cortex.In addition,a similar upregulation of Sox2 and appearance of neuroblasts were observed in the focal ischemic cortex of Macaca mulatta.Our findings demonstrated a transient neurogenic response of Sox2-positive astrocytes in ischemic cortex,which suggests the possibility of inducing neuronal regeneration by amplifying this intrinsic response in the future.

Cortex A57的轻量级人脸检测算法研究

针对高性能人脸检测模型参数量大、计算复杂度高,难以在嵌入式设备进行边缘部署的问题,对RetinaFace模型进行轻量化改进,提出一种轻量级人脸检测算法。采用MobileNetV2_0.5×作为特征提取骨干,应用轻量的PANLite对多尺度特征进行双向融合,增强特征表征能力。采用RFBLite实现特征增强,在增大特征感受野的同时合并上下文信息。使用滤波器剪枝算法对训练后的模型进行剪枝处理,再次训练微调网络参数后部署到嵌入式端Nvidia Jetson Nano进行模型推理。实验结果表明,该轻量级模型能够以较少的参数量和较低的计算复杂度实现较高的人脸检测性能,且能在嵌入式平台上进行实时推理。

Plasticity of callosal neurons in the contralesional cortex following traumatic brain injury

Traumatic brain injury(TBI) represents a significant cause of disability worldwide.It creates a vast array of damaging macro-and microscopic changes in the affected brain area(s),ranging from neuronal cell death,changes in structural spine integrity and dynamics to axonal injury and ove rall neuronal circuit disruption,ultimately leading to functional and cognitive deficits in both humans and animal models(N udo,2013).

Effect of Transcranial Direct Current Stimulation of Motor Cortex versus Insula Cortex on Chronic Post-Mastectomy Pain: Randomized Sham-Controlled Trial

Background: Transcranial direct current stimulation (tDCS) across cortical brain areas appears to improve various forms of pain, yet evidence of tDCS efficiency and ideal stimulation target is lacking. This study aimed to compare the add-on analgesic efficacy of concentric electrode transcranial direct current stimulation (CE-tDCS) stimulation over the primary motor cortex versus the insular cortex on the management of chronic postmastectomy pain. Method: Prospective randomized double-blind sham-controlled study enrolled eighty patients with chronic postmastectomy pain that were randomly assigned to four groups: active motor (AM), sham motor (SM), active insula (AI) and sham insula (SI) group, each received 5 sessions for 20-minute duration with 2 mA tDCS over the targeted area of the contralateral side of pain. Our primary outcome was VAS score, the secondary outcomes were VDS score, LANSS score and depression symptoms by HAM-D scores, assessment was done at 4 time points (prestimulation, after 5th session, 15th day and one month after the last session). Results: Both active tDCS groups (motor and insula) showed reduction of VAS (P Conclusion: Active tDCS stimulation either targeting the primary motor cortex or the insula cortex has add-on analgesic effect for controlling neuropathic chronic post mastectomy pain and the maximum effect was at 15 days after the last session.