Number Of Neurons Research Articles

Discriminating orientation information with phase consistency in alpha and low-gamma frequency bands: an EEG study

Recent studies suggest that noninvasive imaging methods (EEG, MEG) in the human brain scalp can decode the content of visual features information (orientation, color, motion, etc.) in Visual-Working Memory (VWM). Previous work demonstrated that with the sustained low-frequency Event-Related Potential (ERP under 6 Hz) of scalp EEG distributions, it is possible to accurately decode the content of orientation information in VWM during the delay interval. In addition, previous studies showed that the raw data captured by a combination of the occi-parietal electrodes could be used to decode the orientation. However, it is unclear whether the orientation information is available in other frequency bands (higher than 6 Hz) or whether this information is feasible with fewer electrodes. Furthermore, the exploration of orientation information in the phase values of the signal has not been well-addressed. In this study, we propose that orientation information is also accessible through the phase consistency of the occipital region in the alpha band frequency. Our results reveal a significant difference between orientations within 200 ms after stimulus offset in early visual sensory processing, with no apparent effect in power and Event-Related Oscillation (ERO) during this period. Additionally, in later periods (420–500 ms after stimulus offset), a noticeable difference is observed in the phase consistency of low gamma-band activity in the occipital area. Importantly, our findings suggest that phase consistency between trials of the orientation feature in the occipital alpha and low gamma-band can serve as a measure to obtain orientation information in VWM. Furthermore, the study demonstrates that phase consistency in the alpha and low gamma band can reflect the distribution of orientation-selective neuron numbers in the four main orientations in the occipital area.

Orexin Facilitates the Peripheral Chemoreflex via Corticotropin-Releasing Hormone Neurons Projecting to the Nucleus of the Solitary Tract.

We previously showed that orexin neurons are activated by hypoxia and facilitate the peripheral chemoreflex (PCR)-mediated hypoxic ventilatory response (HVR), mostly by promoting the respiratory frequency response. Orexin neurons project to the nucleus of the solitary tract (nTS) and the paraventricular nucleus of the hypothalamus (PVN). The PVN contributes significantly to the PCR and contains nTS-projecting corticotropin-releasing hormone (CRH) neurons. We hypothesized that in male rats, orexin neurons contribute to the PCR by activating nTS-projecting CRH neurons. We used neuronal tract tracing and immunohistochemistry (IHC) to quantify the degree that hypoxia activates PVN-projecting orexin neurons. We coupled this with orexin receptor (OxR) blockade with suvorexant (Suvo, 20 mg/kg, i.p.) to assess the degree that orexin facilitates the hypoxia-induced activation of CRH neurons in the PVN, including those projecting to the nTS. In separate groups of rats, we measured the PCR following systemic orexin 1 receptor (Ox1R) blockade (SB-334867; 1 mg/kg) and specific Ox1R knockdown in PVN. OxR blockade with Suvo reduced the number of nTS and PVN neurons activated by hypoxia, including those CRH neurons projecting to nTS. Hypoxia increased the number of activated PVN-projecting orexin neurons but had no effect on the number of activated nTS-projecting orexin neurons. Global Ox1R blockade and partial Ox1R knockdown in the PVN significantly reduced the PCR. Ox1R knockdown also reduced the number of activated PVN neurons and the number of activated tyrosine hydroxylase neurons in the nTS. Our findings suggest orexin facilitates the PCR via nTS-projecting CRH neurons expressing Ox1R.

The role of elasticity on adhesion and clustering of neurons on soft surfaces

The question of whether material stiffness enhances cell adhesion and clustering is still open to debate. Results from the literature are seemingly contradictory, with some reports illustrating that adhesion increases with surface stiffness and others suggesting that the performance of a system of cells is curbed by high values of elasticity. To address the role of elasticity as a regulator in neuronal cell adhesion and clustering, we investigated the topological characteristics of networks of neurons on polydimethylsiloxane (PDMS) surfaces - with values of elasticity (E) varying in the 0.55–2.65 MPa range. Results illustrate that, as elasticity increases, the number of neurons adhering on the surface decreases. Notably, the small-world coefficient – a topological measure of networks – also decreases. Numerical simulations and functional multi-calcium imaging experiments further indicated that the activity of neuronal cells on soft surfaces improves for decreasing E. Experimental findings are supported by a mathematical model, that explains adhesion and clustering of cells on soft materials as a function of few parameters - including the Young’s modulus and roughness of the material. Overall, results indicate that – in the considered elasticity interval – increasing the compliance of a material improves adhesion, improves clustering, and enhances communication of neurons.

Inhibition of Microglial Activation Ameliorates Inflammation, Reduced Neurogenesis in the hippocampus, and Impaired Brain Function in a Rat Model of Bilirubin Encephalopathy.

Hyperbilirubinemia is one of the most common occurrence in newborns and is toxic to the brain, resulting in neurological sequelae such as auditory impairment, with potential to evolve to chronic bilirubin encephalopathy and long-term cognitive impairment in adults. In the early postnatal period, neurogenesis is rigorous and neuroinflammation is detrimental to the brain. What are the alterations in neurogenesis and the underlying mechanisms of bilirubin encephalopathy during the early postnatal period? This study found that, there were a reduction in the number of neuronal stem/progenitor cells, an increase in microglia in the dentate gyrus (DG) and an inflammatory state in the hippocampus, characterized by increased levels of IL-6, TNF-α, and IL-1β, as well as a decreased level of IL-10 in a rat model of bilirubin encephalopathy (BE). Furthermore, there was a significant decrease in the number of newborn neurons and the expression of neuronal differentiation-associated genes (NeuroD and Ascl1) in the BE group. Additionally, cognitive impairment was observed in this group. The administration of minocycline, an inhibitor of microglial activation, resulted in a reduction of inflammation in the hippocampus, an enhancement of neurogenesis, an increase in the expression of neuron-related genes (NeuroD and Ascl1), and an improvement in cognitive function in the BE group. These results demonstrate that microglia play a critical role in reduced neurogenesis and impaired brain function resulting from bilirubin encephalopathy model, which could inspire the development of novel pharmaceutical and therapeutic strategies.

Low-dose-rate induces more severe cognitive impairment than high-dose-rate in rats exposed to chronic low-dose γ-radiation.

Owing to the long penetration depth of gamma (γ)-rays, individuals working in ionizing radiation environments are chronically exposed to low-dose γ-radiation, resulting in cognitive changes. Dose rate significantly affects radiation-induced biological effects; however, its role in chronic low-dose γ-irradiation-induced cognitive impairment remains unclear. We aimed to investigate whether chronic low-dose γ-irradiation at low-dose-rate (LDR) could induce cognitive impairment and to compare the cognitive alteration caused by chronic low-dose γ-irradiation at LDR and high-dose-rate (HDR). The rats were exposed to γ-irradiation at a LDR of 6 mGy/h and a HDR of 20 mGy/h for 30 days (5 h/day). Functional imaging was performed to assess the brain inflammation and blood-brain barrier (BBB) destruction of rats. Histological and immunofluorescence analyses were used to reveal the neuron damage and the activation of microglia and astrocytes in the hippocampus. RNA sequencing was conducted to investigate changes in gene expression in hippocampus. The rats in the LDR group exhibited more persistent cognitive impairment than those in the HDR group. Furthermore, irradiated rats showed brain inflammation and a compromised BBB. Histologically, the number of hippocampal neurons were comparable in the LDR group but were markedly decreased in the HDR. Additionally, activated M1-like microglia and A1-like astrocytes were observed in the hippocampus of rats in the LDR group; however, only M1-like microglia were activated in the HDR group. Mechanistically, the PI3K-Akt signaling pathway contributed to the different cognitive function change between the LDR group and HDR group. Compared with chronic low-dose γ-irradiation at HDR, LDR induced more severe cognitive impairment which might involve PI3K/Akt signaling pathway.

A cell cycle regulator, E2F2, and glucocorticoid receptor cooperatively transactivate the bovine alphaherpesvirus 1 immediate early transcription unit 1 promoter.

Bovine alpha-herpesvirus 1 (BoHV-1) acute infection in cattle leads to establishment of latency in sensory neurons in the trigeminal ganglia (TG). A synthetic corticosteroid dexamethasone consistently initiates BoHV-1 reactivation in latently infected calves. The BoHV-1 immediate early transcription unit 1 (IEtu1) promoter regulates expression of infected cell protein 0 (bICP0) and bICP4, two viral transcriptional regulators. Hence, the IEtu1 promoter must be activated for the reactivation to occur. The number of TG neurons expressing E2F2, a transcription factor and cell cycle regulator, increased during early stages of reactivation from latency. The glucocorticoid receptor (GR) and E2F2, but not E2F1, E2F3a, or E2F3b, cooperatively transactivated a 436-bp cis-regulatory module (CRM) in the IEtu1 promoter that contains two GR responsive elements. Chromatin immunoprecipitation studies revealed that E2F2 occupies IEtu1 promoter sequences in cultured cells. GR and E2F2 mediate cooperative transactivation of IEtu1 promoter activity, which is predicted to stimulate viral replication following stressful stimuli.

Jiaotaiwan improves brain glucose metabolism in a mouse model of Alzheimer's disease by activating the PI3K/AKT signaling pathway

To investigate the effect of Jiaotaiwan on brain insulin-PI3K/AKT pathway in a mouse model of Alzheimer's disease (AD). Fifty 3-month-old male APP/PS1 double transgenic mice were randomized into AD model group, low-, medium- and high-dose Jiaotaiwan treatment groups, and donepezil treatment group. Cognitive functions of the mice were assessed using water maze and open field tests, and neuronal pathologies were observed with HE staining and Nissl staining; immunohistochemistry was used to detect amyloid Aβ deposition in the brain. Fasting serum insulin levels of the mice were measured, and the expressions of Aβ42, insulin-PI3K/AKT pathway components and downstream glucose transporters in the brain tissue were detected with RT-qPCR and Western blotting. The AD mouse models exhibited obvious impairment of learning and memory abilities, significantly reduced hippocampal neurons, and obvious Aβ amyloid plaques in the brain tissue with increased Aβ42 protein expression (P < 0.05) and insulin resistance index, decreased hippocampal PI3K expressions, lowered expressions of AKT and InR, reduced expressions of GLUT1, GLUT3, and GLUT4, and increased expression of GSK3β in both the hippocampus and cortex. Treatment with Jiaotaiwan and donepezil both effectively improved memory ability of the mouse models, increased the number of hippocampal neurons, reduced Aβ amyloid plaques and increased the expressions of PI3K, AKT, InR, GLUT1, GLUT3 and GLUT4 in the hippocampus and cortex. Jiaotaiwan improves learning and memory abilities of APP/PS1 double transgenic mice and delay the development of AD by activating the PI3K/AKT pathway and regulating the expression levels of its downstream GLUTs in the brain.

Repeated mild traumatic brain injury in the parietal cortex inhibits expressions of NLG-1 and PSD-95 in the medulla oblongata of mice

To assess the effects of repeated mild traumatic brain injury (rmTBI) in the parietal cortex on neuronal morphology and synaptic plasticity in the medulla oblongata of mice. Thirty-two male ICR mice were randomly divided into sham operation group (n=8) and rmTBI group (n=24). The mice in the latter group were subjected to repeated mild impact injury of the parietal cortex by a free-falling object. The mice surviving the injuries were evaluated for neurological deficits using neurological severity scores (NSS), righting reflex test and forced swimming test, and pathological changes of the neuronal cells in the medulla oblongata were observed with HE and Nissl staining. Western blotting and immunofluorescence staining were used to detect the expressions of neuroligin 1(NLG-1) and postsynaptic density protein 95(PSD-95) in the medulla oblongata of the mice that either survived rmTBI or not. None of the mice in the sham-operated group died, while the mortality rate was 41.67% in rmTBI group. The mice surviving rmTBI showed significantly reduced NSS, delayed recovery of righting reflex, increased immobility time in forced swimming test (P < 0.05), and loss of Nissl bodies; swelling and necrosis were observed in a large number of neurons in the medulla oblongata, where the expression levels of NLG-1 and PSD-95 were significantly downregulated (P < 0.05). The mice that did not survive rmTBI showed distorted and swelling nerve fibers and decreased density of neurons in the medulla oblongina with lowered expression levels of NLG-1 and PSD-95 compared with the mice surviving the injuries (P < 0.01). The structural and functional anomalies of the synapses in the medulla oblongata may contribute to death and neurological impairment following rmTBI in mice.

The chronic cerebral hypoperfusion model induces proinflammatory cascades in Alzheimer's disease

Cerebral neuroinflammation has emerged as a significant pathway contributing to the progression of Alzheimer's disease (AD) pathology. Research implicates the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome complex, initiating caspase 1-mediated maturation of interleukin-1 β (IL-1β) and interleukin-18 (IL-18). This study investigates whether chronic cerebral hypoperfusion (CCH), induced via permanent bilateral occlusion of the common carotid arteries (PBOCCA), leads to cognitive dysfunction and NLRP3 inflammasome activation. Twenty male Sprague Dawley (SD) rats underwent PBOCCA to induce CCH. Two weeks post-surgery, locomotor and Morris water maze (MWM) tests were conducted to examine motor functions, spatial learning, and memory, respectively. The gene expression levels of cathepsin B, NLRP3, an apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1 were analysed using real-time PCR, while the expression levels of the inflammatory cytokines were estimated using the ELISA method. Structural damage to the hippocampus was assessed using hematoxylin and eosin (HE) staining. Escape latencies and time spent in specific quadrants in PBOCCA significantly increased compared to sham-operated animals. There was no notable difference in locomotor activity between the PBOCCA and sham-operated groups. The number of pyknotic neurons with cytoplasmic shrinkage increased in the hippocampus. Gene expression of cathepsin B, NLRP3, ASC, and caspase-1 was upregulated in the PBOCCA group. The expression levels of IL-1β, IL-18, interleukin-6 (IL-6), and amyloid-β 1-42 (Aβ 1-42) were elevated in the PBOCCA group relative to sham. The findings confirm NLRP3 inflammasome induction, cognitive dysfunction, and inflammatory cytokines associated with AD and cerebral ischemia. The PBOCCA model provides a valuable tool for studying neurodegenerative including AD.

Exploring the parity paradox: Differential effects on neuroplasticity and inflammation by APOEe4 genotype at middle age

Female sex and Apolipoprotein E (APOE) ε4 genotype are top non-modifiable risk factors for Alzheimer’s disease (AD). Although female-unique experiences like parity (pregnancy and motherhood) have positive effects on neuroplasticity at middle age, previous pregnancy may also contribute to AD risk. To explore these seemingly paradoxical long-term effects of parity, we investigated the impact of parity with APOEε4 genotype by examining behavioural and neural biomarkers of brain health in middle-aged female rats. Our findings show that primiparous (parous one time) hAPOEε4 rats display increased use of a non-spatial cognitive strategy and exhibit decreased number and recruitment of new-born neurons in the ventral dentate gyrus of the hippocampus in response to spatial working memory retrieval. Furthermore, primiparity and hAPOEε4 genotype synergistically modulate inflammatory markers in the ventral hippocampus. Collectively, these findings demonstrate that previous parity in hAPOEε4 rats confers an added risk to present with reduced activity and engagement of the hippocampus as well as elevated pro-inflammatory signaling, and underscore the importance of considering female-specific factors and genotype in health research.

Design of Software Reliability Prediction using Radial Basis Function Networks with Nonlinear Analysis and Topological Considerations

This study presents a thorough methodology for predicting software reliability by employing Radial Basis Function Networks (RBFNs). By using machine learning methodologies such as Radial Basis Function Networks (RBFNs), software development teams are enabled to make well-informed decisions, optimize resource allocation, and proactively mitigate potential dependability concerns. Consequently, this results in improved software quality and heightened customer happiness. This methodology involves multiple stages, starting with data collection and preprocessing. We assemble a comprehensive dataset comprising historical software performance metrics, defect reports, and relevant development process information. After data cleansing and feature engineering, we split the dataset into training, validation, and testing subsets. The core of this approach lies in the construction and training of RBFNs. These neural networks consist of an input layer, a hidden layer with radial basis functions, and an output layer. The architecture parameters, particularly the number of hidden neurons and the spread parameter of the radial basis functions, are optimized through a systematic hyperparameter tuning process using the validation dataset. Upon achieving an optimal model configuration, we rigorously evaluate the RBFN predictive capabilities using the testing dataset.

Discovering physics-informed neural networks model for solving partial differential equations through evolutionary computation

In recent years, the researches about solving partial differential equations (PDEs) based on artificial neural network have attracted considerable attention. In these researches, the neural network models are usually designed depend on human experience or trial and error. Despite the emergence of several model searching methods, these methods primarily concentrate on optimizing the hyperparameters of fully connected neural network model based on the framework of physics-informed neural networks (PINNs), and the corresponding search spaces are relatively restricted, thereby limiting the exploration of superior models. This article proposes an evolutionary computation method aimed at discovering the PINNs model with higher approximation accuracy and faster convergence rate. In addition to searching the numbers of layers and neurons per hidden layer, this method concurrently explores the optimal shortcut connections between the layers and the novel parametric activation functions expressed by the binary trees. In evolution, the strategy about dynamic population size and training epochs (DPSTE) is adopted, which significantly increases the number of models to be explored and facilitates the discovery of models with fast convergence rate. In experiments, the performance of different models that are searched through Bayesian optimization, random search and evolution is compared in solving Klein–Gordon, Burgers, and Lamé equations. The experimental results affirm that the models discovered by the proposed evolutionary computation method generally exhibit superior approximation accuracy and convergence rate, and these models also show commendable generalization performance with respect to the source term, initial and boundary conditions, equation coefficient and computational domain. The corresponding code is available at https://github.com/MathBon/Discover-PINNs-Model.

Hypothalamic vasopressin sex differentiation is observed by embryonic day 15 in mice and is disrupted by the xenoestrogen bisphenol A

Arginine vasopressin (AVP) neurons of the hypothalamic paraventricular region (AVPPVN) mediate sex-biased social behaviors across most species, including mammals. In mice, neural sex differences are thought to be established during a critical window around birth ( embryonic (E) day 18 to postnatal (P) day 2) whereby circulating testosterone from the fetal testis is converted to estrogen in sex-dimorphic brain regions. Here, we found that AVPPVN neurons are sexually dimorphic by E15.5, prior to this critical window, and that gestational bisphenol A (BPA) exposure permanently masculinized female AVPPVN neuronal numbers, projections, and electrophysiological properties, causing them to display male-like phenotypes into adulthood. Moreover, we showed that nearly twice as many neurons that became AVP+ by P0 were born at E11 in males and BPA-exposed females compared to control females, suggesting that AVPPVN neuronal masculinization occurs between E11 and P0. We further narrowed this sensitive period to around the timing of neurogenesis by demonstrating that exogenous estrogen exposure from E14.5 to E15.5 masculinized female AVPPVN neuronal numbers, whereas a pan-estrogen receptor antagonist exposed from E13.5 to E15.5 blocked masculinization of males. Finally, we showed that restricting BPA exposure to E7.5-E15.5 caused adult females to display increased social dominance over control females, consistent with an acquisition of male-like behaviors. Our study reveals an E11.5 to E15.5 window of estrogen sensitivity impacting AVPPVN sex differentiation, which is impacted by prenatal BPA exposure.

Dexmedetomidine, an alpha-2 adrenoceptors agonist, provides a neuroprotective effect for dopaminergic neurons in the substantia nigra and attenuates glucose imbalance in the 6-hydroxydopamine animal model of Parkinson’s disease

ABSTRACT Introduction Studies have shown that dexmedetomidine (DEX, an a2-adrenoceptors agonist) provides a neuroprotective effect and influences blood glucose levels. Here, we evaluated the effect of prolonged treatment with low doses of DEX on the survival rate of dopaminergic (DAergic) neurons in the substantia nigra and also serum glucose levels in 6-hydroxydopamine (6-OHDA) – induced Parkinson’s disease (PD) in the rat. Material and Methods The neurotoxin of 6-OHDA was injected into the medial forebrain bundle by stereotaxic surgery. DEX (25 and 50 µg/kg, i.p) and yohimbine, an a2-adrenoceptor antagonist (1 mg/kg, i.p) were administered before the surgery to the 13 weeks afterward. Apomorphine-induced rotational tests and blood sampling were carried out before the surgery and multiple weeks after that. Thirteen weeks after the surgery, the rats’ brain was transcardially perfused to assess the survival rate of DAergic neurons using the tyrosine hydroxylase (TH) immunohistochemistry. Results DEX remarkably attenuated the severity of rotational behavior and reversed the progress of the PD. It also increased the number of TH-labeled neurons by up to 60%. The serum glucose levels in 6-OHDA-received rats did not change in the third and seventh weeks after the surgery but decreased significantly in the thirteenth week. Treatment with DEX prevented this decrement in glucose levels. On the other hand, Treatment with yohimbine did not affect PD symptoms and glucose levels. Conclusion Our data indicate that DEX through neuroprotective activity attenuates the severity of 6-OHDA-induced PD in rats. DEX might also prevent hypoglycemia during the progress of the PD.

SVM-assisted ANN model with principal component analysis based dimensionality reduction for enhancing state-of-charge estimation in LiFePO4 batteries

Accurate estimation of state-of-charge (SoC) is significant for monitoring the operation of LiFePO4 batteries. This paper addresses the challenges posed by the nonlinear characteristics of LiFePO4 batteries, which adversely affect the accuracy of SoC estimation. The proposed novel methodology for SoC estimation in LiFePO4 batteries involves a Support Vector Machine (SVM) assisted Artificial Neural Network (ANN) model incorporating principal component analysis (PCA) to efficiently interpret the input data. To improve the prediction accuracy, the non-linear characteristics of LiFePO4 are divided into three parts and each of these parts is used to train a separate ANN model. Further, an optimal number of hidden layers and neurons are selected for each ANN model to minimize the prediction errors. The usage of dedicated smaller datasets for each ANN model simplifies the structure. SVM classifies the battery operating regions and selects the most suitable ANN model for SoC estimation. PCA is applied to process the obtained experimental data resulting in three principal components serving as inputs for the SVM-assisted ANN model. Further, with PCA the input dimensions are reduced from four to three, thereby leading to computational simplicity. The input data comprises of current, voltage, open-circuit voltage and temperature of the battery. An experimental prototype, comprising a customized battery pack and sensing mechanisms, is developed for data collection for training SVM and ANN models. With the proposed SVM-assisted ANN involving PCA, the loss function is minimized and an average Root Mean Square Error (RMSE) of 0.3133 is achieved. This demonstrates the feasibility, accuracy and applicability of SoC estimation with the developed SVM-assisted ANN model for LiFePO4 batteries.

Adenosine mediates the amelioration of social novelty deficits during rhythmic light treatment of 16p11.2 deletion female mice.

Non-invasive brain stimulation therapy for autism spectrum disorder (ASD) has shown beneficial effects. Recently, we and others demonstrated that visual sensory stimulation using rhythmic 40 Hz light flicker effectively improved cognitive deficits in mouse models of Alzheimer's disease and stroke. However, whether rhythmic visual 40 Hz light flicker stimulation can ameliorate behavioral deficits in ASD remains unknown. Here, we show that 16p11.2 deletion female mice exhibit a strong social novelty deficit, which was ameliorated by treatment with a long-term 40 Hz light stimulation. The elevated power of local-field potential (LFP) in the prefrontal cortex (PFC) of 16p11.2 deletion female mice was also effectively reduced by 40 Hz light treatment. Importantly, the 40 Hz light flicker reversed the excessive excitatory neurotransmission of PFC pyramidal neurons without altering the firing rate and the number of resident PFC neurons. Mechanistically, 40 Hz light flicker evoked adenosine release in the PFC to modulate excessive excitatory neurotransmission of 16p11.2 deletion female mice. Elevated adenosine functioned through its cognate A1 receptor (A1R) to suppress excessive excitatory neurotransmission and to alleviate social novelty deficits. Indeed, either blocking the A1R using a specific antagonist DPCPX or knocking down the A1R in the PFC using a shRNA completely ablated the beneficial effects of 40 Hz light flicker. Thus, this study identified adenosine as a novel neurochemical mediator for ameliorating social novelty deficit by reducing excitatory neurotransmission during 40 Hz light flicker treatment. The 40 Hz light stimulation warrants further development as a non-invasive ASD therapeutics.

Artificial neural network, machine learning modelling of compressive strength of recycled coarse aggregate based self-compacting concrete.

This research study aims to understand the application of Artificial Neural Networks (ANNs) to forecast the Self-Compacting Recycled Coarse Aggregate Concrete (SCRCAC) compressive strength. From different literature, 602 available data sets from SCRCAC mix designs are collected, and the data are rearranged, reconstructed, trained and tested for the ANN model development. The models were established using seven input variables: the mass of cementitious content, water, natural coarse aggregate content, natural fine aggregate content, recycled coarse aggregate content, chemical admixture and mineral admixture used in the SCRCAC mix designs. Two normalization techniques are used for data normalization to visualize the data distribution. For each normalization technique, three transfer functions are used for modelling. In total, six different types of models were run in MATLAB and used to estimate the 28th day SCRCAC compressive strength. Normalization technique 2 performs better than 1 and TANSING is the best transfer function. The best k-fold cross-validation fold is k = 7. The coefficient of determination for predicted and actual compressive strength is 0.78 for training and 0.86 for testing. The impact of the number of neurons and layers on the model was performed. Inputs from standards are used to forecast the 28th day compressive strength. Apart from ANN, Machine Learning (ML) techniques like random forest, extra trees, extreme boosting and light gradient boosting techniques are adopted to predict the 28th day compressive strength of SCRCAC. Compared to ML, ANN prediction shows better results in terms of sensitive analysis. The study also extended to determine 28th day compressive strength from experimental work and compared it with 28th day compressive strength from ANN best model. Standard and ANN mix designs have similar fresh and hardened properties. The average compressive strength from ANN model and experimental results are 39.067 and 38.36 MPa, respectively with correlation coefficient is 1. It appears that ANN can validly predict the compressive strength of concrete.

Lipid nanoparticle-encapsulated lncRNA DLX6-AS1 knockdown ameliorates cerebral ischemic injury via the Nrf2/HO-1/NLRP3 axis

ABSTRACT Objective Cerebral ischemia is a neurological disorder that leads to permanent disability. This research focuses on exploring the ameliorative effects of lipid nanoparticle (LNP)-encapsulated lncRNA DLX6-AS1 knockdown in cerebral ischemic injury via the Nrf2/HO-1/NLRP3 axis. Methods LNP-encapsulated lncRNA DLX6-AS1 was prepared. Cerebral ischemic injury mouse models were established utilizing middle cerebral artery occlusion (MCAO). The mice were treated by intravenous injection of LNP-encapsulated lncRNA DLX6-AS1. The neurological deficits, Inflammatory factor levels, pathological characteristics were observed. In vitro N2a cell oxygen and glucose deprivation (OGD) models were established, and the cells were treated with LNP-encapsulated lncRNA DLX6-AS1 or Nrf2 inhibitor (ML385). Cell viability and apoptosis were tested. DLX6-AS1, Nrf2, HO-1, and NLRP3 expression levels were assessed. Results LncRNA DLX6-AS1 levels were elevated in the brain tissues of mice with cerebral ischemic injury and OGD-induced N2a cells. LNP-encapsulated DLX6-AS1 siRNA (si-DLX6-AS1) improved neurological deficit scores, reduced the levels of inflammatory factors, improved brain tissue pathological damage, and raised the number of survival neurons in CA1. LNP-encapsulated si-DLX6-AS1 ameliorated the OGD-induced N2a cell viability decrease and apoptosis rate increase, and ML385 (Nrf2 inhibitor) reversed the ameliorative effects of LNP-encapsulated si-DLX6-AS1. In cerebral ischemic injury mice and OGD-induced N2a cells, Nrf2 and HO-1 levels were reduced and NLRP3 levels were increased. LNP-encapsulated si-DLX6-AS1 raised Nrf2 and HO-1 levels and reduced NLRP3 levels. Nrf2 inhibitor ML385 treatment reversed the ameliorative effects of LNP-encapsulated si-DLX6-AS1 on OGD-induced N2a cell viability and apoptosis. Conclusion Lipid nanoparticle-encapsulated si-DLX6-AS1 ameliorates cerebral ischemic injury via the Nrf2/HO-1/NLRP3 axis.

Expression of ChAT, Iba-1, and nNOS in the Central Nervous System following Facial Nerve Injury.

Facial nerve injury can cause significant functional impairment, impacting both the peripheral and central nervous systems. The present study evaluated changes in facial motor function, numbers of cholinergic neurons and microglia, and nNOS levels in the facial nucleus of the central nervous system (CNS) following peripheral facial nerve injury. Facial nerve function, as determined by eyeblink and whisker-movement reflexes, was evaluated at baseline and 1, 2, 3, 4, 8, and 12 weeks after inducing facial nerve injury through compression or axotomy. The expression of choline acetyltransferase (ChAT), ionized calcium-binding adaptor molecule 1 (Iba-1), and neuronal nitric oxide synthase (nNOS) in the facial nucleus of the CNS was analyzed 2, 4, and 12 weeks after peripheral facial nerve injury. Compression-induced facial nerve injury was found to lead to temporary facial motor impairment, whereas axotomy resulted in persistent impairment. Moreover, both compression and axotomy reduced ChAT expression and increased Iba-1 and nNOS expression in the facial nucleus, indicating upregulation of an inflammatory response and neurodegeneration. These results indicate that, compared with compression-induced injury, axotomy-induced facial nerve injury results in greater facial motor dysfunction and more persistent microglial and nitric oxide activation in the facial nucleus of the CNS.

Antennal chemoreceptors in the European ectoparasitoid Sclerodermus cereicollis (Hymenoptera: Bethylidae).

Sclerodermus cereicollis is a European flat wasp ectoparasitoid of some longhorn beetle species. This species is important as a suitable biological control agent against xylophagous pests. To better understand its chemical ecology, the ultrastructure of the antennal sensilla of the adult was studied using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The sensilla are located mainly in the ventro-medial side of the antennae. We report a clearly sexual dimorphism with respect to antennae length, and to types, number, and distribution of chemosensilla. The antennae in males are significantly longer than those of females. We describe in detail the external and internal structure of different chemoreceptors represented by sensilla placodea, long sensilla basiconica, multiporous sensilla chaetica, grooved sensilla ampullacea, uniporous grooved sensilla chaetica. The potential involvement of the different kinds of chemoreceptors in inter- (mainly sexual recognition and social behavior-kin recognition) or intra-specific communication (mainly host selection) is discussed on the basis of behavioral and electrophysiological investigations performed on other parasitoid species belonging to the same family. Other sensilla with morphology that is not consistent with that of chemoreceptors are represented by grooved pegs, coeloconic pegs, trichoid sensilla. Such detailed ultrastructural investigation of the flagellar chemoreceptors of S. cereicollis, clarifying the number of chemosensory neurons innervating the different sensilla, is crucial for further electrophysiological investigations on this important species. RESEARCH HIGHLIGHTS: Evident sexual dimorphism concerning antennae length, type, number, and distribution of chemosensilla. Long sensilla basiconica (LSB) present only in females could play a role in host location and/or maternal care. Multiporous sensilla chaetica (MSC), significantly longer and mostly represented in males, could play a role in the perception of sexual pheromones. Detailed ultrastructural study is crucial for electrophysiological investigations on this important species.