Signal Conducting System with Effective Optimization Using Deep Learning for Schizophrenia Classification

Signal processing based research was adopted with Electroencephalogram(EEG)for predicting the abnormality and cerebral activities.The proposed research work is intended to provide an automatic diagnostic system to determine the EEG signal in order to classify the brain function which shows whether a person is affected with schizophrenia or not.Early detection and intervention are vital for better prognosis.However,the diagnosis of schizophrenia still depends on clinical observation to date.Without reliable biomarkers,schizophrenia is difficult to detect in its early phase and hence we have proposed this idea.In this work,the EEG signal series are divided into non-linear feature mining,classification and validation,and t-test integrated feature selection process.For this work,19-channel EEG signals are utilized from schizophrenia class and normal pattern.Here,the datasets initially execute the splitting process based on raw 19-channel EEG into 6250 sample point’s sequences.With this process,1142 features of normal and schizophrenia class patterns can be obtained.In other hand,157 features from each EEG patterns are utilized based on Non-linear feature extraction process where 14 principal features can be identified in terms of considering the essential features.At last,the Deep Learning(DL)technique incorporated with an effective optimization technique is adopted for classification process called a Deep Convolutional Neural Network(DCNN)with mayfly optimization algorithm.The proposed technique is implemented into the platform of MATLAB in order to obtain better results and is analyzed based on the performance analysis framework such as accuracy,Signal to Noise Ratio(SNR),Mean Square Error,Normalized Mean Square Error(NMSE)and Loss.Through comparison,the proposed technique is proved to a better technique than other existing techniques.

Calcium bridges built by mitochondria-associated endoplasmic reticulum membranes:potential targets for neural repair in neurological diseases

The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions and metabolic levels.Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels between the endoplasmic reticulum membrane and the mitochondrial outer membrane,formed by various proteins and protein complexes.This microstructural domain mediates several specialized functions,including calcium(Ca^(2+))signaling,autophagy,mitochondrial morphology,oxidative stress response,and apoptosis.Notably,the dysregulation of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes is a critical factor in the pathogenesis of neurological diseases.Certain proteins or protein complexes within these membranes directly or indirectly regulate the distance between the endoplasmic reticulum and mitochondria,as well as the transduction of Ca^(2+)signaling.Conversely,Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes influences other mitochondria-associated endoplasmic reticulum membraneassociated functions.These functions can vary significantly across different neurological diseases—such as ischemic stroke,traumatic brain injury,Alzheimer's disease,Parkinson's disease,amyotrophic lateral sclerosis,and Huntington's disease—and their respective stages of progression.Targeted modulation of these disease-related pathways and functional proteins can enhance neurological function and promote the regeneration and repair of damaged neurons.Therefore,mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling plays a pivotal role in the pathological progression of neurological diseases and represents a significant potential therapeutic target.This review focuses on the effects of protein complexes in mitochondria-associated endoplasmic reticulum membranes and the distinct roles of mitochondria-associated endoplasmic reticulum membranes-mediated Ca^(2+)signaling in neurological diseases,specifically highlighting the early protective effects and neuronal damage that can result from prolonged mitochondrial Ca^(2+)overload or deficiency.This article provides a comprehensive analysis of the various mechanisms of Ca^(2+)signaling mediated by mitochondria-associated endoplasmic reticulum membranes in neurological diseases,contributing to the exploration of potential therapeutic targets for promoting neuroprotection and nerve repair.

Effect of Serum from Overfatigue Rats on JNK/c-Jun/HO-1 Pathway in Human Umbilical Vein Endothelial Cells and the Intervening Effect of Tongxinluo(通心络)Superfine Powder

Objective:To cultivate human umbilical vein endothelial cells (HUVECs) in the serum of overfatigue rats with the intervention of Tongxinluo (通心络) superfine powder (TXLSP).By examining the variation of the activity of JNK/c-Jun/HO-1 pathway,the possible mechanisms of vascular endothelial dysfunction under overfatigue conditions and the intervening effect of TXLSP were explored.Methods:The HUVECs were randomly divided into the normal control group,the model group,the SP600125 (a specific antagonist of JNK)gro...

A new viewpoint and model of neural signal generation and transmission: Signal transmission on unmyelinated neurons

We establish a preliminary model of neural signal generation and transmission based on our previous research,and use this model to study signal transmission on unmyelinated nerves.In our model,the characteristics of neural signals are studied both on a long-time and a short time scale.On the long-time scale,the model is consistent with the circuit model.On the short time scale,the neural system exhibits a THz and infrared electromagnetic oscillation but the energy envelope curve of the rapidly oscillating signal varies slowly.In addition,the numerical method is used to solve the equations of neural signal generation and transmission,and the effects of the temperature on signal transmission are studied.It is found that overly high and overly low temperatures are not conducive to the transmission of neural signals.