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.

Inhibitory gamma-aminobutyric acidergic neurons in the anterior cingulate cortex participate in the comorbidity of pain and emotion

Pain is often comorbid with emotional disorders such as anxiety and depression.Hyperexcitability of the anterior cingulate cortex has been implicated in pain and pain-related negative emotions that arise from impairments in inhibitory gamma-aminobutyric acid neurotransmission.This review primarily aims to outline the main circuitry(including the input and output connectivity)of the anterior cingulate cortex and classification and functions of different gamma-aminobutyric acidergic neurons;it also describes the neurotransmitters/neuromodulators affecting these neurons,their intercommunication with other neurons,and their importance in mental comorbidities associated with chronic pain disorders.Improving understanding on their role in pain-related mental comorbidities may facilitate the development of more effective treatments for these conditions.However,the mechanisms that regulate gamma-aminobutyric acidergic systems remain elusive.It is also unclear as to whether the mechanisms are presynaptic or postsynaptic.Further exploration of the complexities of this system may reveal new pathways for research and drug development.

Activation of adult endogenous neurogenesis by a hyaluronic acid collagen gel containing basic fibroblast growth factor promotes remodeling and functional recovery of the injured cerebral cortex

The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury.However,whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions,such as the cortex,remains unknown.In this study,we implanted a hyaluronic acid collagen gel loaded with basic fibroblast growth factor into the motor cortex immediately following traumatic injury.Our findings reveal that this gel effectively stimulated the proliferation and migration of endogenous neural stem/progenitor cells,as well as their differentiation into mature and functionally integrated neurons.Importantly,these new neurons reconstructed the architecture of cortical layers II to VI,integrated into the existing neural circuitry,and ultimately led to improved brain function.These findings offer novel insight into potential clinical treatments for traumatic cerebral cortex injuries.

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.

Comparison and Quality Assessment of Cassia Bark (Cortex Cinnamomi) by Thin Layer Chromatography

Aim To differentiate the genuine cassia bark from its substitutes and adulterants. Methods Six components, phenylpropyl acetate, cinnamyl acetate, cinnamaldehyde, cinnamyl alcohol, coumarin, and cinnamic acid were used as characteristic markers, and an optimized TLC method was developed. Results The TLC profile of cassia bark is similar to its closely related variety Cinnamomum cassia Presl var. macrophyllum Chu but significantly different from other six Cinnamomum species. High content of phenylpropyl acet...

Cortex cinnamomi extract prevents streptozotocin- and cytokine-induced β-cell damage by inhibiting NF-κB

AIM： To clarify the mechanism underlying the antidiabetic activities of cortex cinnamomi extract （CCE）. METHODS： To induce in vivo diabetes, mice were injected with streptozotocin （STZ） via a tail vein （100 mg STZ/kg body weight）. To determine the effects of CCE, mice were administered CCE twice daily for 7 d by oral gavage starting 1 wk before the STZ injection. Blood glucose and plasma insulin concentration were measured as an index of diabetes. Also, to induce cytotoxicity of RINm5F cells, we treated with cytokines （IL-1β （2.0 ng/mL） and IFN-γ （100 U/mL））. Cell viability and nitric oxide production were measured colorimetrically. Inducible nitric oxide synthase （iNOS） mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κβ was assayed by using gel mobility shift assays of nuclear extracts. RESULTS： Treatment of mice with STZ resulted in hyperglycemia and hypoinsulinemia, which was further evidenced by immunohistochemical staining of islets. However, the diabetogenic effects of STZ were completely prevented when mice were pretreated with CCE. The inhibitory effect of CCE on STZ-induced hyperglycemia was mediated through the suppression of iNOS expression. In rat insulinoma RINm5F cells,CCE completely protected against interleukin-1β and interferon-y-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-1β and interferon-y-induced nitric oxide production and in iNOS mRNA and protein expression, and these findings correlated well with in vivo observations. CONCLUSION： The molecular mechanism by which CCE inhibits iNOS gene expression appears to involve the inhibition of NF-κβ activation, These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression,

Wonderful Use of Cinnamomi Cortex to Conduct the Fire Back to the Origin

Cinnamomi Cortex(Rougui)has a lot of functions,including dissipating cold,relieving pain,benefiting joints,tonifying fire and assisting yang,warming blood vessels,dispersing abscesses and nodules and vaporizing fluid and humor.Among all functions,the wonderful use of Cinnamomi Cortex is in conducting the fire back to the origin.It can conduct the fire of triple energizers,which is not possessed by other drugs and is unique to Cinnamomi Cortex.Through observations and practices of some special medical records,it is found that the fire conducting of Cinnamomi Cortex can play a key and decisive role.

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.

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.

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平台的嵌入式系统课程虚拟实验平台设计

针对高校嵌入式系统课程逐渐迁移到全新的Cortex-M平台,设计开发了一套分层次的基于CortexM3的虚拟实验教学平台。实验平台分基础型、综合型和设计型3个层次,采用递进教学方式,由浅入深,循序渐进,以适用不同知识基础的学生。虚拟实验教学平台可在教学时间与教学空间上拓展嵌入式系统课程的学习范围,激发学生的学习兴趣,提高了教学质量。

基于Cortex-M3的S型加减速控制

通过对典型S型加减速控制方法的研究与总结,对时间分段加减速方法做了优化与改进,论证了当约束参数发生变化时S型加减速曲线的实际规划方法。提出了通过指针函数和动态数组进行程序设计的方法,并通过Matlab仿真结果表明该方法能保证S型加减速曲线的柔性,并能准确达到所设定的位移,最后在Cortex-M3开发板上实现了对步进电机的加减速的柔性控制。