Nickel Sulfide/Graphene/Carbon Nanotube Composites as Electrode Material for the Supercapacitor Application in the Sea Flashing Signal System

This work presents NiS/graphene/carbon nanotube （NiS/GNS/CNT） composites as electrode material for the supercapacitor application in sea flashing signal systems. NiS nanosheets were closely anchored on the conductive GNS-CNT networks. As a result, the NiS/GNS/CNT electrode showed a high specific capacitance of 2 377 F.g^-1 at 2 mV.s^-1 and good cycling stability compared with the pure NiS （1 599F.g^-1）. The enhanced electrochemical performances are attributed to the synergetic effect between the conductive carbon and the pseudo-capacitive NiS. The high performance supercapacitor may provide application in the sea flashing signal system.

Longitudinal Performance Assessment of Traffic Signal System Impacted by Long-Term Interstate Construction Diversion Using Connected Vehicle Data

Local arterials can be significantly impacted by diversions from adjacent work zones. These diversions often occur on unofficial detour routes due to guidance received on personal navigation devices. Often, these routes do not have sufficient sensing or communication equipment to obtain infrastructure-based traffic signal performance measures, so other data sources are required to identify locations being significantly affected by diversions. This paper examines the network impact caused by the start of an 18-month closure of the I-65/70 interchange (North Split), which usually serves approximately 214,000 vehicles per day in Indianapolis, IN. In anticipation of some proportion of the public diverting from official detour routes to local streets, a connected vehicle monitoring program was established to provide daily performances measures for over 100 intersections in the area without the need for vehicle sensing equipment. This study reports on 13 of the most impacted signals on an alternative arterial to identify locations and time of day where operations are most degraded, so that decision makers have quantitative information to make informed adjustments to the system. Individual vehicle movements at the studied locations are analyzed to estimate changes in volume, split failures, downstream blockage, arrivals on green, and travel times. Over 130,000 trajectories were analyzed in an 11-week period. Weekly afternoon peak period volumes increased by approximately 455%, split failures increased 3%, downstream blockage increased 10%, arrivals on green decreased 16%, and travel time increase 74%. The analysis performed in this paper will serve as a framework for any agency that wants to assess traffic signal performance at hundreds of locations with little or no existing sensing or communication infrastructure to prioritize tactical retiming and/or longer-term infrastructure investments.

Integrated Performance Measures for Bus Rapid Transit System and Traffic Signal Systems Using Trajectory Data

Bus rapid transit (BRT) systems have been implemented in many cities over the past two decades. Widespread adoption of General Transit Feed Specification (GTFS), the deployment of high-fidelity bus GPS data tracking, and anonymized high-fidelity connected vehicle data from private vehicles have provided new opportunities for performance measures that can be used by both transit agencies and traffic signal system operators. This paper describes the use of trajectory-based data to develop performance measures for a BRT system in Indianapolis, Indiana. Over 3 million data records during the 3-month period between March and May 2022 are analyzed to develop visualizations and performance metrics. A methodology to estimate the average delay and schedule adherence is presented along a route comprised of 74 signals and 28 bus stations. Additionally, this research demonstrates how these performance measures can be used to evaluate dedicated and non-dedicated bus lanes with general traffic. Travel times and reliability of buses are compared with nearly 30 million private vehicle trips. Results show that median travel time for buses on dedicated bi-directional lanes is within one minute of general traffic and during peak periods the buses are often faster. Schedule adherence was observed to be more challenging, with approximately 3% of buses arriving within 1 minute on average during the 5AM hour and 5% of buses arriving 6 - 9 minutes late during the 5PM hour. The framework and performance measures presented in this research provide agencies and transportation professionals with tools to identify opportunities for adjustments and to justify investment decisions.

Initial Experimental Result of Accurately Controlled Routinely Operated Signal System (ACROSS)

The principle of Accurately Controlled Routinely Operated Signal System (ACROSS) is introduced in this paper. A sample machine is made and tested. The experiment shows that the signal stacking technique is effective in improving signal to noise ratio and the sompi cepstrum method is applicable to deconvolute a set of travel times of wave elements from accurate transfer function data in frequency domain.

Digital signal acquisition system for complex nuclear reaction experiments

A digital data-acquisition system based on XIA LLC products was used in a complex nuclear reaction experiment using radioactive ion beams.A flexible trigger system based on a field-programmable gate array(FPGA)parametrization was developed to adapt to different experimental sizes.A user-friendly interface was implemented,which allows converting script language expressions into FPGA internal control parameters.The proposed digital system can be combined with a conventional analog data acquisition system to provide more flexibility.The performance of the combined system was veri-fied using experimental data.

Iterative Signal Detection Based Soft Interference Cancellation for Satellite-Terrestrial Downlink NOMA Systems

To improve the bit error rate(BER)performance of multi-user signal detection in satelliteterrestrial downlink non-orthogonal multiple access(NOMA)systems,an iterative signal detection algorithm based on soft interference cancellation with optimal power allocation is proposed.Given that power allocation has a significant impact on BER performance,the optimal power allocation is obtained by minimizing the average BER of NOMA users.According to the allocated powers,successive interference cancellation(SIC)between NOMA users is performed in descending power order.For each user,an iterative soft interference cancellation is performed,and soft symbol probabilities are calculated for soft decision.To improve detection accuracy and without increasing the complexity,the aforementioned algorithm is optimized by adding minimum mean square error(MMSE)signal estimation before detection,and in each iteration soft symbol probabilities are utilized for soft-decision of the current user and also for the update of soft interference of the previous user.Simulation results illustrate that the optimized algorithm i.e.MMSE-IDBSIC significantly outperforms joint multi-user detection and SIC detection by 7.57dB and 8.03dB in terms of BER performance.

Low-complexity signal detection for massive MIMO systems via trace iterative method

Linear minimum mean square error(MMSE)detection has been shown to achieve near-optimal performance for massive multiple-input multiple-output(MIMO)systems but inevitably involves complicated matrix inversion,which entails high complexity.To avoid the exact matrix inversion,a considerable number of implicit and explicit approximate matrix inversion based detection methods is proposed.By combining the advantages of both the explicit and the implicit matrix inversion,this paper introduces a new low-complexity signal detection algorithm.Firstly,the relationship between implicit and explicit techniques is analyzed.Then,an enhanced Newton iteration method is introduced to realize an approximate MMSE detection for massive MIMO uplink systems.The proposed improved Newton iteration significantly reduces the complexity of conventional Newton iteration.However,its complexity is still high for higher iterations.Thus,it is applied only for first two iterations.For subsequent iterations,we propose a novel trace iterative method(TIM)based low-complexity algorithm,which has significantly lower complexity than higher Newton iterations.Convergence guarantees of the proposed detector are also provided.Numerical simulations verify that the proposed detector exhibits significant performance enhancement over recently reported iterative detectors and achieves close-to-MMSE performance while retaining the low-complexity advantage for systems with hundreds of antennas.

Using Pearson’s System of Curves to Approximate the Distributions of the Difference between Two Correlated Estimates of Signal-to-Noise Ratios: The Cases of Bivariate Normal and Bivariate Lognormal Distributions

Background: The signal-to-noise ratio (SNR) is recognized as an index of measurements reproducibility. We derive the maximum likelihood estimators of SNR and discuss confidence interval construction on the difference between two correlated SNRs when the readings are from bivariate normal and bivariate lognormal distribution. We use the Pearsons system of curves to approximate the difference between the two estimates and use the bootstrap methods to validate the approximate distributions of the statistic of interest. Methods: The paper uses the delta method to find the first four central moments, and hence the skewness and kurtosis which are important in the determination of the parameters of the Pearsons distribution. Results: The approach is illustrated in two examples;one from veterinary microbiology and food safety data and the other on data from clinical medicine. We derived the four central moments of the target statistics, together with the bootstrap method to evaluate the parameters of Pearsons distribution. The fitted Pearsons curves of Types I and II were recommended based on the available data. The R-codes are also provided to be readily used by the readers.

Deep Learning Based Signal Detector for OFDM Systems

In this paper,we propose a novel deep learning(DL)-based receiver design for orthogonal frequency division multiplexing(OFDM)systems.The entire process of channel estimation,equalization,and signal detection is replaced by a neural network(NN),and hence,the detector is called a NN detector(N^(2)D).First,an OFDM signal model is established.We analyze both temporal and spectral characteristics of OFDM signals,which are the motivation for DL.Then,the generated data based on the simulation of channel statistics is used for offline training of bi-directional long short-term memory(Bi-LSTM)NN.Especially,a discriminator(F)is added to the input of Bi-LSTM NN to look for subcarrier transmission data with optimal channel gain(OCG),which can greatly improve the performance of the detector.Finally,the trained N^(2)D is used for online recovery of OFDM symbols.The performance of the proposed N^(2)D is analyzed theoretically in terms of bit error rate(BER)by Monte Carlo simulation under different parameter scenarios.The simulation results demonstrate that the BER of N^(2)D is obviously lower than other algorithms,especially at high signal-to-noise ratios(SNRs).Meanwhile,the proposed N^(2)D is robust to the fluctuation of parameter values.

Gut microbiota dysbiosis contributes toα-synuclein-related pathology associated with C/EBPβ/AEP signaling activation in a mouse model of Parkinson’s disease

Parkinson’s disease is a neurodegenerative disease characterized by motor and gastrointestinal dysfunction.Gastrointestinal dysfunction can precede the onset of motor symptoms by several years.Gut microbiota dysbiosis is involved in the pathogenesis of Parkinson’s disease,whether it plays a causal role in motor dysfunction,and the mechanism underlying this potential effect,remain unknown.CCAAT/enhancer binding proteinβ/asparagine endopeptidase(C/EBPβ/AEP)signaling,activated by bacterial endotoxin,can promoteα-synuclein transcription,thereby contributing to Parkinson’s disease pathology.In this study,we aimed to investigate the role of the gut microbiota in C/EBPβ/AEP signaling,α-synuclein-related pathology,and motor symptoms using a rotenone-induced mouse model of Parkinson’s disease combined with antibiotic-induced microbiome depletion and fecal microbiota transplantation.We found that rotenone administration resulted in gut microbiota dysbiosis and perturbation of the intestinal barrier,as well as activation of the C/EBP/AEP pathway,α-synuclein aggregation,and tyrosine hydroxylase-positive neuron loss in the substantia nigra in mice with motor deficits.However,treatment with rotenone did not have any of these adverse effects in mice whose gut microbiota was depleted by pretreatment with antibiotics.Importantly,we found that transplanting gut microbiota derived from mice treated with rotenone induced motor deficits,intestinal inflammation,and endotoxemia.Transplantation of fecal microbiota from healthy control mice alleviated rotenone-induced motor deficits,intestinal inflammation,endotoxemia,and intestinal barrier impairment.These results highlight the vital role that gut microbiota dysbiosis plays in inducing motor deficits,C/EBPβ/AEP signaling activation,andα-synuclein-related pathology in a rotenone-induced mouse model of Parkinson’s disease.Additionally,our findings suggest that supplementing with healthy microbiota may be a safe and effective treatment that could help ameliorate the progression of motor deficits in patients with Parkinson’s disease.

Melatonin improves synapse development by PI3K/Akt signaling in a mouse model of autism spectrum disorder

Autism spectrum disorders are a group of neurodevelopmental disorders involving more than 1100 genes,including Ctnnd2 as a candidate gene.Ctnnd2knockout mice,serving as an animal model of autis m,have been demonstrated to exhibit decreased density of dendritic spines.The role of melatonin,as a neuro hormone capable of effectively alleviating social interaction deficits and regulating the development of dendritic spines,in Ctnnd2 deletion-induced nerve injury remains unclea r.In the present study,we discove red that the deletion of exon 2 of the Ctnnd2 gene was linked to social interaction deficits,spine loss,impaired inhibitory neurons,and suppressed phosphatidylinositol-3-kinase(PI3K)/protein kinase B(Akt) signal pathway in the prefrontal cortex.Our findings demonstrated that the long-term oral administration of melatonin for 28 days effectively alleviated the aforementioned abnormalities in Ctnnd2 gene-knockout mice.Furthermore,the administration of melatonin in the prefro ntal cortex was found to improve synaptic function and activate the PI3K/Akt signal pathway in this region.The pharmacological blockade of the PI3K/Akt signal pathway with a PI3K/Akt inhibitor,wo rtmannin,and melatonin receptor antagonists,luzindole and 4-phenyl-2-propionamidotetralin,prevented the melatonin-induced enhancement of GABAergic synaptic function.These findings suggest that melatonin treatment can ameliorate GABAe rgic synaptic function by activating the PI3K/Akt signal pathway,which may contribute to the improvement of dendritic spine abnormalities in autism spectrum disorders.

Na^(+)/K^(+)-ATPase:ion pump,signal transducer,or cytoprotective protein,and novel biological functions

Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.

Hypoglycemic mechanism of Tegillarca granosa polysaccharides on type 2 diabetic mice by altering gut microbiota and regulating the PI3K-akt signaling pathwaye

Type 2 diabetes mellitus(T2DM)is a complex metabolic disease threatening human health.We investigated the effects of Tegillarca granosa polysaccharide(TGP)and determined its potential mechanisms in a mouse model of T2DM established through a high-fat diet and streptozotocin.TGP(5.1×10^(3) Da)was composed of mannose,glucosamine,rhamnose,glucuronic acid,galactosamine,glucose,galactose,xylose,and fucose.It could significantly alleviate weight loss,reduce fasting blood glucose levels,reverse dyslipidemia,reduce liver damage from oxidative stress,and improve insulin sensitivity.RT-PCR and Western blotting indicated that TGP could activate the phosphatidylinositol-3-kinase/protein kinase B signaling pathway to regulate disorders in glucolipid metabolism and improve insulin resistance.TGP increased the abundance of Allobaculum,Akkermansia,and Bifidobacterium,restored the microbiota abundance in the intestinal tracts of mice with T2DM,and promoted short-chain fatty acid production.This study provides new insights into the antidiabetic effects of TGP and highlights its potential as a natural hypoglycemic nutraceutical.

Fanlian Huazhuo Formula alleviates high-fat diet-induced nonalcoholic fatty liver disease by modulating autophagy and lipid synthesis signaling pathway

BACKGROUND Fanlian Huazhuo Formula(FLHZF)has the functions of invigorating spleen and resolving phlegm,clearing heat and purging turbidity.It has been identified to have therapeutic effects on type 2 diabetes mellitus(T2DM)in clinical application.Non-alcoholic fatty liver disease(NAFLD)is frequently diagnosed in patients with T2DM.However,the therapeutic potential of FLHZF on NAFLD and the underlying mechanisms need further investigation.AIM To elucidate the effects of FLHZF on NAFLD and explore the underlying hepatoprotective mechanisms in vivo and in vitro.METHODS HepG2 cells were treated with free fatty acid for 24 hours to induce lipid accumulation cell model.Subsequently,experiments were conducted with the different concentrations of freeze-dried powder of FLHZF for 24 hours.C57BL/6 mice were fed a high-fat diet for 8-week to establish a mouse model of NAFLD,and then treated with the different concentrations of FLHZF for 10 weeks.RESULTS FLHZF had therapeutic potential against lipid accumulation and abnormal changes in biochemical indicators in vivo and in vitro.Further experiments verified that FLHZF alleviated abnormal lipid metabolism might by reducing oxidative stress,regulating the AMPKα/SREBP-1C signaling pathway,activating autophagy,and inhibiting hepatocyte apoptosis.CONCLUSION FLHZF alleviates abnormal lipid metabolism in NAFLD models by regulating reactive oxygen species,autophagy,apoptosis,and lipid synthesis signaling pathways,indicating its potential for clinical application in NAFLD.

Timosaponin AⅢ induces drug-metabolizing enzymes by activating constitutive androstane receptor (CAR) via dephosphorylation of the EGFR signaling pathway

The current study aimed to assess the effect of timosaponin AⅢ(T-AⅢ)on drug-metabolizing enzymes during anticancer therapy.The in vivo experiments were conducted on nude and ICR mice.Following a 24-day administration of T-AⅢ,the nude mice exhibited an induction of CYP2B10,MDR1,and CYP3A11 expression in the liver tissues.In the ICR mice,the expression levels of CYP2B10 and MDR1 increased after a three-day T-AⅢ administration.The in vitro assessments with HepG2 cells revealed that T-AⅢ induced the expression of CYP2B6,MDR1,and CYP3A4,along with constitutive androstane receptor(CAR)activation.Treatment with CAR siRNA reversed the T-AⅢ-induced increases in CYP2B6 and CYP3A4 expression.Furthermore,other CAR target genes also showed a significant increase in the expression.The up-regulation of murine CAR was observed in the liver tissues of both nude and ICR mice.Subsequent findings demonstrated that T-AⅢ activated CAR by inhibiting ERK1/2 phosphorylation,with this effect being partially reversed by the ERK activator t-BHQ.Inhibition of the ERK1/2 signaling pathway was also observed in vivo.Additionally,T-AⅢ inhibited the phosphorylation of EGFR at Tyr1173 and Tyr845,and suppressed EGF-induced phosphorylation of EGFR,ERK,and CAR.In the nude mice,T-AⅢ also inhibited EGFR phosphorylation.These results collectively indicate that T-AⅢ is a novel CAR activator through inhibition of the EGFR pathway.

PHD17 acts as a target of miR1320 to negatively control cold tolerance via JA-activated signaling in rice

Plant Homeo Domain(PHD)proteins are involved in diverse biological processes during plant growth.However,the regulation of PHD genes on rice cold stress response remains largely unknown.Here,we reported that PHD17 negatively regulated cold tolerance in rice seedlings as a cleavage target of miR1320.PHD17 expression was greatly induced by cold stress,and was down-regulated by miR1320 overexpression and up-regulated by miR1320 knockdown.Through 5'RACE and dual luciferase assays,we found that miR1320 targeted and cleaved the 3'UTR region of PHD17.PHD17 was a nuclearlocalized protein and acted as a transcriptional activator in yeast.PHD17 overexpression reduced cold tolerance of rice seedlings,while knockout of PHD17 increased cold tolerance,partially via the CBF cold signaling.By combining transcriptomic and physiological analyses,we demonstrated that PHD17 modulated ROS homeostasis and flavonoid accumulation under cold stress.K-means clustering analysis revealed that differentially expressed genes in PHD17 transgenic lines were significantly enriched in the jasmonic acid(JA)biosynthesis pathway,and expression of JA biosynthesis and signaling genes was verified to be affected by PHD17.Cold stress tests applied with MeJA or IBU(JA synthesis inhibitor)further suggested the involvement of PHD17 in JA-mediated cold signaling.Taken together,our results suggest that PHD17 acts downstream of miR1320 and negatively regulates cold tolerance of rice seedlings through JA-mediated signaling pathway.

Argatroban promotes recovery of spinal cord injury by inhibiting the PAR1/JAK2/STAT3 signaling pathway

Argatroban is a synthetic thrombin inhibitor approved by U.S.Food and Drug Administration for the treatment of thrombosis.However,whether it plays a role in the repair of spinal cord injury is unknown.In this study,we established a rat model of T10 moderate spinal cord injury using an NYU Impactor ModerⅢand performed intraperitoneal injection of argatroban for 3 consecutive days.Our results showed that argatroban effectively promoted neurological function recovery after spinal cord injury and decreased thrombin expression and activity in the local injured spinal cord.RNA sequencing transcriptomic analysis revealed that the differentially expressed genes in the argatroban-treated group were enriched in the JAK2/STAT3 pathway,which is involved in astrogliosis and glial scar formation.Western blotting and immunofluorescence results showed that argatroban downregulated the expression of the thrombin receptor PAR1 in the injured spinal cord and the JAK2/STAT3 signal pathway.Argatroban also inhibited the activation and proliferation of astrocytes and reduced glial scar formation in the spinal cord.Taken together,these findings suggest that argatroban may inhibit astrogliosis by inhibiting the thrombin-mediated PAR1/JAK2/STAT3 signal pathway,thereby promoting the recovery of neurological function after spinal cord injury.

Calmodulins and calmodulin-like proteins-mediated plant organellar calcium signaling networks under abiotic stress

Plant calmodulins(CaMs)and calmodulin-like proteins(CMLs)mediate Ca~(2+)signaling in response to abiotic stresses.Manipulation of this signaling in crops could increase stress tolerance.We review methods for detecting Ca~(2+)signals,regulatory roles of Ca Ms and CMLs,binding targets,and Ca~(2+)networks under abiotic stress in organelles.

Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage

Preclinical and clinical studies have shown that microglia and macrophages participate in a multiphasic brain damage repair process following intracerebral hemorrhage.The E26 transformation-specific sequence-related transcription factor Spi1 regulates microglial/macrophage commitment and maturation.However,the effect of Spi1 on intracerebral hemorrhage remains unclear.In this study,we found that Spi1 may regulate recovery from the neuroinflammation and neurofunctional damage caused by intracerebral hemorrhage by modulating the microglial/macrophage transcriptome.We showed that high Spi1expression in microglia/macrophages after intracerebral hemorrhage is associated with the activation of many pathways that promote phagocytosis,glycolysis,and autophagy,as well as debris clearance and sustained remyelination.Notably,microglia with higher levels of Soil expression were chara cterized by activation of pathways associated with a variety of hemorrhage-related cellular processes,such as complement activation,angiogenesis,and coagulation.In conclusion,our results suggest that Spi1 plays a vital role in the microglial/macrophage inflammatory response following intracerebral hemorrhage.This new insight into the regulation of Spi1 and its target genes may advance our understanding of neuroinflammation in intracerebral hemorrhage and provide therapeutic targets for patients with intracerebral hemorrhage.