Performance Analysis of Machine Learning Algorithms for Classifying Hand Motion-Based EEG Brain Signals

Brain-computer interfaces (BCIs) records brain activity using electroencephalogram (EEG) headsets in the form of EEG signals;these signals can berecorded, processed and classified into different hand movements, which can beused to control other IoT devices. Classification of hand movements will beone step closer to applying these algorithms in real-life situations using EEGheadsets. This paper uses different feature extraction techniques and sophisticatedmachine learning algorithms to classify hand movements from EEG brain signalsto control prosthetic hands for amputated persons. To achieve good classificationaccuracy, denoising and feature extraction of EEG signals is a significant step. Wesaw a considerable increase in all the machine learning models when the movingaverage filter was applied to the raw EEG data. Feature extraction techniques likea fast fourier transform (FFT) and continuous wave transform (CWT) were usedin this study;three types of features were extracted, i.e., FFT Features, CWTCoefficients and CWT scalogram images. We trained and compared differentmachine learning (ML) models like logistic regression, random forest, k-nearestneighbors (KNN), light gradient boosting machine (GBM) and XG boost onFFT and CWT features and deep learning (DL) models like VGG-16, DenseNet201 and ResNet50 trained on CWT scalogram images. XG Boost with FFTfeatures gave the maximum accuracy of 88%.

On Similarities and Differences of Invasive and Non-Invasive Electrical Brain Signals in Brain-Computer Interfacing

We perceive that some Brain-Computer Interface (BCI) researchers believe in totally different origins of invasive and non-invasive electrical BCI signals. Based on available literature we argue, however, that although invasive and non-invasive BCI signals are different, the underlying origin of electrical BCIs signals is the same.

Understanding the link between type 2 diabetes mellitus and Parkinson's disease:role of brain insulin resistance

Type 2 diabetes mellitus and Parkinson's disease are chronic diseases linked to a growing pandemic that affects older adults and causes significant socio-economic burden.Epidemiological data supporting a close relationship between these two aging-related diseases have resulted in the investigation of shared pathophysiological molecular mechanisms.Impaired insulin signaling in the brain has gained increasing attention during the last decade and has been suggested to contribute to the development of Parkinson's disease through the dysregulation of several pathological processes.The contribution of type 2 diabetes mellitus and insulin resistance in neurodegeneration in Parkinson's disease,with emphasis on brain insulin resistance,is extensively discussed in this article and new therapeutic strategies targeting this pathological link are presented and reviewed.

Amino acid sensing in the gut and its mediation in gut-brain signal transduction

Animal gastrointestinal tract is not only a digestive organ, but also a nutrient sensing organ which detects luminal nutrient and thus can regulate food intake. There are many amino acid sensing receptors and transporters in the gut. Amino acids sensing by these receptors and transporters can stimulate the intestinal endocrine cells to release a variety of gut hormones. These hormones trigger a series of physiological effects via the nerve system. This review summarized the recent advance on the amino acid sensing receptors and transporters in the gastrointestinal tract, the gut hormones released from the intestinal endocrine cells and the hormones-induced signal transduction between the gut and brain. A better understanding of these processes may help to gain further insight into the specific role of amino acids in digestion and provide guidelines in developing strategy for the better use of amino acids in the diet.

Icariin ameliorates memory deficits through regulating brain insulin signaling and glucose transporters in 3×Tg-AD mice

Icariin,a major prenylated flavonoid found in Epimedium spp.,is a bioactive constituent of Herba Epimedii and has been shown to exert neuroprotective effects in experimental models of Alzheimer’s disease.In this study,we investigated the neuroprotective mechanism of icariin in an APP/PS1/Tau triple-transgenic mouse model of Alzheimer’s disease.We performed behavioral tests,pathological examination,and western blot assay,and found that memory deficits of the model mice were obviously improved,neuronal and synaptic damage in the cerebral cortex was substantially mitigated,and amyloid-βaccumulation and tau hyperphosphorylation were considerably reduced after 5 months of intragastric administration of icariin at a dose of 60 mg/kg body weight per day.Furthermore,deficits of proteins in the insulin signaling pathway and their phosphorylation levels were significantly reversed,including the insulin receptor,insulin receptor substrate 1,phosphatidylinositol-3-kinase,protein kinase B,and glycogen synthase kinase 3β,and the levels of glucose transporter 1 and 3 were markedly increased.These findings suggest that icariin can improve learning and memory impairments in the mouse model of Alzheimer’s disease by regulating brain insulin signaling and glucose transporters,which lays the foundation for potential clinical application of icariin in the prevention and treatment of Alzheimer’s disease.

Homeostatic regulation of brain functions by endocannabinoid signaling

Humans have been using Cannabis and its extracts for a few thousand years as a medicinal and recreational drug. How- ever, the chemical component in Cannabis sativa, △9-tet- rahydrocannabinol （△9-THC）, an exogenous cannabinoid, remained unknown until it was isolated and identified as the main psychoactive ingredient （Gaoni and Mechoulam, 1964）.

Susceptibility-weighted imaging is suitable for evaluating signal strength in different brain regions of a rabbit model of acute hemorrhagic anemia

Acute hemorrhagic anemia can decrease blood flow and oxygen supply to brain, and affect its physiological function. While detecting changes in brain function in patients with acute hemorrhagic anemia is helpful for preventing neurological complications and evaluating therapeutic effects, clinical changes in the nervous systems of these patients have not received much attention. In part, this is because current techniques can only indirectly detect changes in brain function following onset of anemia, which leads to lags between real changes in brain function and their detection.

Role of Toll-like receptor 4 and Janus kinase and signal transducer and activator of transcription signal transduction pathway in sepsis-induced brain damage

The Janus kinase and signal transducer and activator of transcription （JAK/STAT） signal transduction pathway is involved in sepsis-induced functional damage to the heart, liver, kidney, and other organs. However, the cellular and molecular mechanisms underlying sepsis-induced brain damage remain elusive. In the present study, we found severe loss of neurons in the hippocampal CA1 region in rats with sepsis-induced brain damage following intraperitoneal injection of endotoxin, The expression of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 was significantly increased in brain tissues following lipopolysaccharide exposure. AG490 （JAK2 antagonist） and rapamycin （STAT3 antagonist） significantly reduced neuronal loss and suppressed the increased expression of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 in the hippocampal CA1 region in sepsis-induced brain damaged rats. Overall, these data suggest that blockade of the JAK/STAT signal transduction pathway is neuroprotective in sepsis-induced brain damage via the inhibition of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 exoression.

Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage

The Wnt/Frizzled signaling pathway participates in many inflammation-linked diseases. However, the inflammatory response mediated by the Wnt/Frizzled signaling pathway in experimental subarachnoid hemorrhage has not been thoroughly investigated. Consequently, in this study, we examined the potential role of the Wnt/Frizzled signaling pathway in early brain injury in rat models of subarachnoid hemorrhage.Simultaneously, possible neuroprotective mechanisms were also investigated. Experimental subarachnoid hemorrhage rat models were induced by injecting autologous blood into the prechiasmatic cistern. Experiment 1 was designed to examine expression of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. In total, 42 adult rats were divided into sham(injection of equivalent volume of saline), 6-, 12-, 24-, 48-, 72-hour, and 1-week subarachnoid hemorrhage groups. Experiment 2 was designed to examine neuroprotective mechanisms of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. Rats were treated with recombinant human Wnt1(rhwnt1), small interfering Wnt1(siwnt1) RNA, and monoclonal antibody of Frizzled1(anti-Frizzled1) at 48 hours after subarachnoid hemorrhage. Expression levels of Wnt1, Frizzled1, β-catenin, peroxisome proliferator-activated receptor-γ, CD36, and active nuclear factor-κB were examined by western blot assay and immunofluorescence staining. Microglia type conversion and inflammatory cytokine levels in brain tissue were examined by immunofluorescence staining and enzyme-linked immunosorbent assay. Our results show that compared with the sham group, expression levels of Wnt1, Frizzled1, and β-catenin were low and reduced to a minimum at 48 hours, gradually returning to baseline at 1 week after subarachnoid hemorrhage. rhwnt1 treatment markedly increased Wnt1 expression and alleviated subarachnoid hemorrhage-induced early brain injury(within 72 hours), including cortical cell apoptosis, brain edema, and neurobehavioral deficits, accompanied by increasing protein levels of β-catenin, CD36, and peroxisome proliferator-activated receptor-γ and decreasing protein levels of nuclear factor-κB. Of note, rhwnt1 promoted M2-type microglia conversion and inhibited release of inflammatory cytokines(interleukin-1β, interleukin-6, and tumor necrosis factor-α). In contrast, siwnt1 RNA and anti-Frizzled1 treatment both resulted in an opposite effect. In conclusion, the Wnt/Frizzled1 signaling pathway may participate in subarachnoid hemorrhage-induced early brain injury via inhibiting the inflammatory response, including regulating microglia type conversion and decreasing inflammatory cytokine release. The study was approved by the Animal Ethics Committee of Anhui Medical University and First Affiliated Hospital of USTC,Division of Life Sciences and Medicine, University of Science and Technology of China(approval No. LLSC-20180202) in May 2017.

Three important components in the regeneration of the cavernous nerve： brain-derived neurotrophic factor, vascular endothelial growth factor and the JAK/STAT signaling pathway

Retroperitoneal operations, such as radical prostatectomy, often damage the cavernous nerve, resulting in a high incidence of erectile dysfunction. Although improved nerve-sparing techniques have reduced the incidence of nerve injury, and the administration of phosphodiesterase type 5 inhibitors has revolutionized the treatment of erectile dysfunction, this problem remains a considerable challenge. In recent years, scientists have focused on brain-derived neurotrophic factor and vascular endothelial growth factor in the treatment of cavernous nerve injury in rat models. Results showed that both compounds were capable of enhancing the regeneration of the cavernous nerve and that activation of the Janus kinase （JAK）/signal transducer and activator of transcription （STAT） pathway played a major role in the process.

Acupuncture activates signal transduction pathways related to brain-tissue restoration after ischemic injury

A middle cerebral artery occlusion-model was established in rats using the improved thread embolism method.Rats were treated with acupuncture at either Dazhui（DU14）,Renzhong（DU26）, Baihui（DU20）,or a non-meridian point.Detection with protein-chip technology showed that the level of protein phosphorylation in both groups was upregulated or downregulated depending on the signaling pathway compared with the model group that did not receive acupuncture.Analysis of proteins showing downregulated phosphorylation revealed that five signaling pathways were activated in the acupuncture-treatment group,while only two were activated in the acupuncture-control group.In contrast,analysis of proteins showing upregulated phosphorylation revealed only one pathway was activated in the acupuncture-treatment group,whereas four pathways were activated in the acupuncture-control group.Furthermore,the number of activated proteins in the acupuncture-treatment group was not only higher than the acupuncture-control group,but unlike the acupuncture-control group,the majority of activated proteins were key proteins in the signaling pathways.Our findings indicate that acupuncture at specific points can activate multiple signaling pathways to promote the restoration of brain tissue following ischemic injury,and that this is based on a combination of effects resulting from multiple pathways,targets,and means.

缺血性脑损伤中铁死亡及中药干预调控的作用与机制

背景:铁死亡是一种铁依赖性脂质过氧化调控的程序性细胞死亡方式,与缺血性脑损伤的发生、发展及转归密切相关。近年来,随着对铁死亡研究的不断深入,发现中药复方、中药单体可通过减轻铁超载、减少活性氧产生、调控脂质合成等方式调节铁死亡,减轻脑缺血损伤,促进神经功能恢复。目的:探讨铁死亡与缺血性脑损伤的关系及中药调控铁死亡治疗缺血性脑损伤的作用机制。方法:以“铁死亡,缺血性中风,脑损伤,活性氧,脂质代谢,中药复方,萜类,黄酮,酚类,生物碱,苯酞类等”为中文检索词,以“Iron death,ischemic stroke,brain injury,reactive oxygen species,lipid metabolism,traditional Chinese medicine formulas,terpenes,flavonoids,phenols,alkaloids,phthalides,etc”为英文检索词,检索2018年1月至2024年5月中国知网和PubMed数据库中有关铁死亡与缺血性脑损伤及中药调控机制的文献,排除与文章相关性不高及重复、过时的文献。共检索出1526篇相关文献,最终纳入87篇文献进行综述。结果与结论:大量实验研究证实,铁死亡在缺血性脑损伤中具有重要作用,中医方药可通过多种方式调节铁死亡,如三七总皂苷可调节铁代谢,抑制脂质过氧化;香芹酚通过增加谷胱甘肽过氧化物酶4表达,抑制神经元铁死亡;中药复方和单体有效成分可调控铁死亡相关通路——谷胱甘肽/谷胱甘肽过氧化物酶4(GPX4)、核因子E2相关因子2(Nrf2)/血红素加氧酶1(HO-1)、铁死亡抑制蛋白1(FSP1)/CoQ10及鸟苷三磷酸环水解酶1(GCH1)/四氢生物喋呤(BH4)等,减少神经元损伤和死亡,发挥脑保护作用。

Enhanced Adaptive Brain-Computer Interface Approach for Intelligent Assistance to Disabled Peoples

Assistive devices for disabled people with the help of Brain-Computer Interaction(BCI)technology are becoming vital bio-medical engineering.People with physical disabilities need some assistive devices to perform their daily tasks.In these devices,higher latency factors need to be addressed appropriately.Therefore,the main goal of this research is to implement a real-time BCI architecture with minimum latency for command actuation.The proposed architecture is capable to communicate between different modules of the system by adopting an automotive,intelligent data processing and classification approach.Neuro-sky mind wave device has been used to transfer the data to our implemented server for command propulsion.Think-Net Convolutional Neural Network(TN-CNN)architecture has been proposed to recognize the brain signals and classify them into six primary mental states for data classification.Data collection and processing are the responsibility of the central integrated server for system load minimization.Testing of implemented architecture and deep learning model shows excellent results.The proposed system integrity level was the minimum data loss and the accurate commands processing mechanism.The training and testing results are 99%and 93%for custom model implementation based on TN-CNN.The proposed real-time architecture is capable of intelligent data processing unit with fewer errors,and it will benefit assistive devices working on the local server and cloud server.

Electromagnetic Fields and Calcium Signaling by the Voltage Dependent Anion Channel

Electromagnetic fields (EMFs) can interact with biological tissues exerting positive as well as negative effects on cell viability, but the underlying sensing and signaling mechanisms are largely unknown. So far in excitable cells EMF exposure was postulated to cause Ca2+ influx through voltage-dependent Ca channels (VDCC) leading to cell activation and an antioxidant response. Upon further activation oxidative stress causing DNA damage or cell death may follow. Here we report collected evidence from literature that voltage dependent anion channels (VDAC) located not only in the outer microsomal membrane but also in the cytoplasmic membrane convert to Ca2+ conducting channels of varying capacities upon subtle changes of the applied EMF even in non-excitable cells like erythrocytes. Thus, VDAC can be targeted by external EMF in both types of membranes to release Ca2+ into the cytosol. The role of frequency, pulse modulation or polarization remains to be investigated in suitable cellular models. VDACs are associated with several other proteins, among which the 18 kDa translocator (TSPO) is of specific interest since it was characterized as the central benzodiazepine receptor in neurons. Exhibiting structural similarities with magnetoreceptors we propose that TSPO could sense the magnetic component of the EMF and thus together with VDAC could trigger physiological as well as pathological cellular responses. Pulsed EMFs in the frequency range of the brain-wave communication network may explain psychic disturbances of electromagnetic hypersensitive persons. An important support is provided from human psychology that states deficits like insomnia, anxiety or depression can be treated with diazepines that indicates apparent connections between the TSPO/VDAC complex and organismic responses to EMF.

电针联合低频经颅超声刺激对创伤性脑损伤大鼠脑电信号的影响

背景:创伤性脑损伤是由头部受到撞击、打击而导致大脑正常功能被破坏的疾病,目前需要寻找有效治疗方式和客观指标,帮助医生判别损伤状况及恢复患者脑功能。目的:探究电针联合低频经颅超声刺激对创伤性脑损伤大鼠脑电信号的影响。方法:将40只6周龄SPF级雄性SD大鼠随机分为假手术组、模型组、电针组、低频经颅超声刺激组和联合组(n=8),后4组采用Feeney自由落体法造模,假手术组只开骨窗而不打击。各干预组均于造模后1 d开始实施干预,电针组进行电针干预,低频经颅超声刺激组进行低频经颅超声刺激干预,联合组进行两者联合干预,共干预7 d。造模后8 h,用改良神经功能缺损评分评定大鼠神经功能缺损情况;干预7 d后观察大鼠Y迷宫自发轮流行为百分比,而后采集脑电信号,利用快速傅里叶变换分解出α、β、θ和δ波段,计算各频段振荡幅值、能量占比百分比以及Lempel-Ziv复杂度、样本熵。结果与结论:①造模后8 h,模型组、电针组、低频经颅超声刺激组和联合组的改良神经功能缺损评分显著高于假手术组(P<0.05);②造模后第7天,模型组的α波、δ波频带振荡幅值、δ波能量占比百分比显著高于假手术组(P<0.05),自发轮流行为百分比、α波、β波能量占比百分比、Lempel-Ziv复杂度、样本熵显著低于假手术组(P<0.05);③与模型组比较,联合组的α波、δ波频带振荡幅值显著下降(P<0.05),电针组、低频经颅超声刺激组、联合组的α波、β波频带能量占比百分比显著升高(P<0.05),δ波能量占比百分比显著下降(P<0.05);④与电针组和低频经颅超声刺激组相比,联合组的δ波能量占比百分比显著降低(P<0.05),自发轮流行为百分比、α波、β波能量占比百分比、Lempel-Zi复杂度、样本熵显著升高(P<0.05);⑤结果显示,创伤性脑损伤大鼠出现脑电信号异常,而电针联合低频经颅超声刺激干预后可以改善大鼠脑电信号的异常情况,提示脑电频域特征和非线性特征可用来评估创伤性脑损伤情况。

Longitudinal follow-up of patients with mild traumatic brain injury by magnetic resonance spectroscopic technique

Objective:To explore the changes in the concentrations of neural markers immediately or several months after mild traumatic brain injury(mTBI).Methods:The metabolic markers of neurons in white matter tissues above the lateral ventricle were semi-quantitatively determined by employing 1H magnetic resonance spectroscopic technique(1-H-MRS) in 30 clinically diagnosed cases of mTBI.At the same time,the neurological functions of the subjects,including ability to pay attention,memory,working memory and operational capacity etc were also assessed. Results:The patients were followed up for,on average,13 days after mTB1 and the results showed that Cre,PCre and Glx in the white matter tissues were significantly elevated in mTBI patients.17 patients(57%) recovered from the injury during the follow-up(median was defined as the 40th post-trauma day).Comparison in terms of intelligence among groups revealed that the levels of neural markers of intelligence development was positively related with intelligence scores).Conclusions:Change in Clx concentrations is most sensitive during trauma or in ensuing repairing processes,and might be different from normal status in the following months and Clx level tends to be accompanied with change in Cre,another energy-related marker.

基于双子空间PCA降维的脑力负荷分类

人类社会至今的飞速发展使得大量体力劳动被机械工程替代,工作者的任务重心也从体力劳动逐渐转变为脑力劳动,对操作者脑力负荷进行实时评估以增强工作效率在当下有着重大意义。目前人类对于脑力负荷评估共有3种方式,有研究表明,采用生物电信号进行脑力负荷分类效果较其余两种方法更客观。但脑电信号经过特征提取后维数极高,所需数据量和运算量巨大,需要对其进行降维。目前降维方面最广泛运用的两种算法为主成分分析(principal component analysis,PCA)和线性判别分析(linear discriminate analysis,LDA)。针对PCA的非监督性和LDA的特征冗余敏感性,提出一种二分类下基于双子空间主成分分析的降维算法,分别对不同类别的训练集数据进行主成分分析,并将所有训练集数据映射到生成的空间中,再次进行PCA-LDA降维,以此提高降维后数据的可分性。实验结果表明,双子空间PCA-LDA降维算法在二分类任务下测试集精度整体高于单子空间PCA-LDA算法,以此为脑力负荷分类领域和高维数据降维领域提供了新思路。

Mitogen-Activated Protein Kinase Pathways Following Traumatic Brain Injury

The mechanisms underlying the secondary or delayed cell death in the hippocampus and cerebral hemisphere after traumatic brain injury (TBI) have been poorly understood. Recent data suggesting that TBI may have relationship with both an inflammatory and a neurodegenerative factors are also presented. Mitogen-activated protein kinases (MAPK), which play a crucial role in signal transduction, are activated by phosphorylation in response to a variety of mitogenic signals. In this article, we review the clinical and experimental evidence for brain damage after TBI. In addition, the MAPK pathways, closely involved in signal transduction after TBI, which could therefore be a new and potentially effective therapeutic target in TBI. Further investigations are therefore necessary to better understand cerebral traumatic damage and delineate the best practice strategies needed to improve the patient outcomes after TBI.

Constraint-induced movement therapy promotes motor function recovery and downregulates phosphorylated extracellular regulated protein kinase expression in ischemic brain tissue of rats

Motor function impairment is a common outcome of stroke.Constraint-induced movement therapy（CIMT）involving intensive use of the impaired limb while restraining the unaffected limb is widely used to overcome the effects of＇learned non-use＇and improve limb function after stroke.However,the underlying mechanism of CIMT remains unclear.In the present study,rats were randomly divided into a middle cerebral artery occlusion（model）group,a CIMT＋model（CIMT）group,or a sham group.Restriction of the affected limb by plaster cast was performed in the CIMT and sham groups.Compared with the model group,CIMT significantly improved the forelimb functional performance in rats.By western blot assay,the expression of phosphorylated extracellular regulated protein kinase in the bilateral cortex and hippocampi of cerebral ischemic rats in the CIMT group was significantly lower than that in the model group,and was similar to sham group levels.These data suggest that functional recovery after CIMT may be related to decreased expression of phosphorylated extracellular regulated protein kinase in the bilateral cortex and hippocampi.

Effect of Buyanghuanwu Decoction on PI3K/AKT Signaling Pathway and Aquaporin AQP4 in Cerebral Hemorrhage Rats

[Objectives] To explore the effect of Buyanghuanwu decoction on PI3K/AKT signaling pathway and aquaporin AQP4 in cerebral hemorrhage rats and clarify the mechanism to provide clear direction and target for cerebral hemorrhage treatment caused by cerebral edema.[Methods]SD rats were randomly divided into six groups: model group,sham operation group,Buyanghuanwu decoction low,medium and high dose groups,and Ginkgo biloba group. Model group,Buyanghuanwu decoction group,G. biloba group were prepared to be intracerebral hemorrhage rat models by referring to Rosenberg law. While the expression of " polarity" of aquaporin AQP4 was detected by immunofluorescence labeling method,the Evans blue( Evans Blue,EB) content of brain tissue was determined by Spectrophotometry. In addition,the water content of brain tissue was detected by wet and dry weight method. [Results] When compared to the model group,the Buyang Huanwu decoction group,G. biloba group of PI3K and AKT proteins expression increased significantly( P < 0. 05) and AQP4 in Astrocyte end feet membrane concentrated expression significantly increased( P < 0. 05),EB content and water content of brain tissue significantly reduced( P <0. 05).[Conclusions]The protective mechanisms of Buyanghuanwu decoction on cerebral hemorrhage can work might because it can activate PI3K/AKT signaling pathway,regulate AQP4 " polar" expression,and reduce the permeability of the blood brain barrier and cerebral edema.