Search Results (102)

In realistic hyperspectral image (HSI) cross-scene classification tasks, it is ideal to obtain target domain samples during the training phase. Therefore, a model needs to be trained on one or more source domains (SD) and achieve robust domain generalization (DG) performance on an unknown target domain (TD). Popular DG strategies constrain the model’s predictive behavior in synthetic space through deep, nonlinear source expansion, and an HSI generation model is usually adopted to enrich the diversity of training samples. However, recent studies have shown that the activation functions of neurons in a network exhibit asymmetry for different categories, which results in the learning of task-irrelevant features while attempting to learn task-related features (called “feature contamination”). For example, even if some intrinsic features of HSIs (lighting conditions, atmospheric environment, etc.) are irrelevant to the label, the neural network still tends to learn them, resulting in features that make the classification related to these spurious components. To alleviate this problem, this study replaces the common nonlinear generative network with a specific linear projection transformation, to reduce the number of neurons activated nonlinearly during training and alleviate the learning of contaminated features. Specifically, this study proposes a dimensionally decoupled spatial spectral linear extrapolation (SSLE) strategy to achieve sample augmentation. Inspired by the weakening effect of water vapor absorption and Rayleigh scattering on band reflectivity, we simulate a common spectral drift based on Markov random fields to achieve linear spectral augmentation. Further considering the common co-occurrence phenomenon of patch images in space, we design spatial weights combined with label determinism of the center pixel to construct linear spatial enhancement. Finally, to ensure the cognitive unity of the high-level features of the discriminator in the sample space, we use inter-class contrastive learning to align the back-end feature representation. Extensive experiments were conducted on four datasets, an ablation study showed the effectiveness of the proposed modules, and a comparative analysis with advanced DG algorithms showed the superiority of our model in the face of various spectral and category shifts. In particular, on the Houston18/Shanghai datasets, its overall accuracy was 0.51%/0.83% higher than the best results of the other methods, and its Kappa coefficient was 0.78%/2.07% higher, respectively. Full article

We examined the neuroanatomical substrates and signaling mechanisms underlying the suppressive effect of GLP1 on homeostatic and hedonic feeding. Electrophysiological and behavioral studies were conducted in agouti-related peptide (AgRP)-cre and tyrosine hydroxylase (TH)-cre mice, and AgRP-cre/pituitary adenylyl cyclase-activating polypeptide (PACAP) type I receptor (PAC1R)^fl/fl animals. GLP1 (30 pmol) delivered directly into the arcuate nucleus (ARC) decreased homeostatic feeding and diminished the rate of consumption. This anorexigenic effect was associated with an inhibitory outward current in orexigenic neuropeptide Y (NPY)/AgRP neurons. GLP1 injected into the ventral tegmental area reduced binge feeding, coupled with decrements in the rate of consumption and the percent daily caloric consumption during the binge interval. These reductions were associated with a GLP1-induced outward current in mesolimbic (A₁₀) dopamine neurons. GLP1 administered into the ventromedial nucleus (VMN) reduced homeostatic feeding that again was associated with a diminished rate of consumption and abrogated by the GLP1 receptor antagonist exendin 9–39 and in AgRP-cre/PAC1R^fl/fl mice. This suppressive effect was linked with a GLP-induced inward current in VMN PACAP neurons, and further supported by the fact that GLP1 neurons in the nucleus tractus solitarius project to the VMN. Conversely, intra-VMN GLP1 had modest effects on binge feeding behavior. Finally, apoptotic ablation of VMN PACAP neurons obliterated the anorexigenic effect of intra-VMN GLP1 on homeostatic feeding in PACAP-cre mice but not their wildtype counterparts. Collectively, these data demonstrate that GLP1 acts within the homeostatic and hedonic circuits to curb appetitive behavior by exciting PACAP neurons, and inhibiting NPY/AgRP and A₁₀ dopamine neurons. Full article

Traumatic brain injury (TBI) pathology is significantly mediated by an inflammatory response involving inflammasome activation, resulting in the release of interleukin (IL)-1β and pyroptotic cell death through gasdermin-D (GSDMD) cleavage. Inflammasome components are transported through extracellular vesicles (EVs) to mediate systemic inflammation in peripheral organs, including the gut. The purpose of this study was to determine the protective effect of GSDMD knockout (KO) on TBI-induced inflammasome activation, EV signaling, and gut function. GSDMD-KO and C57BL6 (WT) mice were subjected to the controlled cortical impact model of TBI. Cytokine expression was assessed with electrochemiluminescent immunoassay and immunoblotting of the cerebral cortex and gut. EVs were examined for pathology-associated markers using flow cytometry, and gut permeability was determined. GSDMD-KO attenuated IL-1β and IL-6 expression in the cerebral cortex and reduced IL-1β and IL-18 in the gut 3 days post-injury. GSDMD-KO mice had decreased neuronal- and gut-derived EVs compared to WT mice post-TBI. GSDMD-KO EVs also had decreased IL-1β and different surface marker expression post-TBI. GSDMD-KO mice had decreased gut permeability after TBI. These data demonstrate that GSDMD ablation improves post-TBI inflammation and gut pathology, suggesting that GSDMD may serve as a potential therapeutic target for the improvement of TBI-associated pathologies. Full article

Background: Deoxynivalenol (DON) poses a threat to animal and human health, particularly causing damage to the nervous system. Intestinal flora can regulate the nervous system through the gut–brain axis; however, there is currently a lack of evidence on the effect of changing the intestinal flora on the damage to the nervous system caused by DON. Therefore, this study aims to investigate the effect of gut microbiota ablation on neurotoxicity induced by exposure to deoxynivalenol. Methods: One hundred-twenty (120) specific pathogen-free (SPF) male C57BL/6j mice were randomly divided into four groups (control group, microbiota-uncleaned group + 5 mg/kg/BW DON, microbiota-cleared group, and microbiota-cleared group + 5 mg/kg/BW DON). The open field and Morris behavior tests were used to evaluate behavior changes after DON exposure. After 14 days of treatment, the mice were euthanized and brain tissues were collected for further analysis. Results: The tests showed that DON exposure led to anxiety and decreased learning ability in mice with no gut microbiota ablation. We also observed pathological changes including neuronal shrinkage, degeneration, and cortical edema in the mice with no microbiota ablation after DON exposure. In addition, the protein and mRNA levels of tight junction proteins and anti-inflammatory factors were decreased in the mice with no microbiota ablation after DON exposure compared with mice with ablated microbiota. Conclusions: We concluded that the presence of microbiota plays a key role in the neurotoxicity induced by DON; thus, ablation of the intestinal microbiota can effectively improve brain damage caused by DON. Full article

(1) Background: At present, the bio-inspired visual neural models have made significant achievements in detecting the motion direction of the translating object. Variable contrast in the figure-ground and environmental noise interference, however, have a strong influence on the existing model. The responses of the lobula plate tangential cell (LPTC) neurons of Drosophila are robust and stable in the face of variable contrast in the figure-ground and environmental noise interference, which provides an excellent paradigm for addressing these challenges. (2) Methods: To resolve these challenges, we propose a bio-inspired visual neural model, which consists of four stages. Firstly, the photoreceptors (R1–R6) are utilized to perceive the change in luminance. Secondly, the change in luminance is divided into parallel ON and OFF pathways based on the lamina monopolar cell (LMC), and the spatial denoising and the spatio-temporal lateral inhibition (LI) mechanisms can suppress environmental noise and improve motion boundaries, respectively. Thirdly, the non-linear instantaneous feedback mechanism in divisive contrast normalization is adopted to reduce local contrast sensitivity; further, the parallel ON and OFF contrast pathways are activated. Finally, the parallel motion and contrast pathways converge on the LPTC in the lobula complex. (3) Results: By comparing numerous experimental simulations with state-of-the-art (SotA) bio-inspired models, we can draw four conclusions. Firstly, the effectiveness of the contrast neural computation and the spatial denoising mechanism is verified by the ablation study. Secondly, this model can robustly detect the motion direction of the translating object against variable contrast in the figure-ground and environmental noise interference. Specifically, the average detection success rate of the proposed bio-inspired model under the pure and real-world complex noise datasets was increased by 5.38% and 5.30%. Thirdly, this model can effectively reduce the fluctuation in this model response against variable contrast in the figure-ground and environmental noise interference, which shows the stability of this model; specifically, the average inter-quartile range of the coefficient of variation in the proposed bio-inspired model under the pure and real-world complex noise datasets was reduced by 38.77% and 47.84%, respectively. The average decline ratio of the sum of the coefficient of variation in the proposed bio-inspired model under the pure and real-world complex noise datasets was 57.03% and 67.47%, respectively. Finally, the robustness and stability of this model are further verified by comparing other early visual pre-processing mechanisms and engineering denoising methods. (4) Conclusions: This model can robustly and steadily detect the motion direction of the translating object under variable contrast in the figure-ground and environmental noise interference. Full article

Astrocytes play critical roles in supporting structural and metabolic homeostasis in the central nervous system (CNS). CNS injury leads to the development of a range of reactive phenotypes in astrocytes whose molecular determinants are poorly understood. Finding ways to modulate astrocytic injury responses and leverage a pro-recovery phenotype holds promise in treating CNS injury. Recently, it has been demonstrated that ablation of astrocytic transglutaminase 2 (TG2) shifts reactive astrocytes towards a phenotype that improves neuronal injury outcomes both in vitro and in vivo. Additionally, in an in vivo mouse model, pharmacological inhibition of TG2 with the irreversible inhibitor VA4 phenocopied the neurosupportive effects of TG2 deletion in astrocytes. In this study, we extended our comparisons of VA4 treatment and TG2 deletion to provide insights into the mechanisms by which TG2 attenuates neurosupportive astrocytic function after injury. Using a neuron–astrocyte co-culture model, we found that VA4 treatment improves the ability of astrocytes to support neurite outgrowth on an injury-relevant matrix, as we previously showed for astrocytic TG2 deletion. We hypothesize that TG2 mediates its influence on astrocytic phenotype through transcriptional regulation, and our previous RNA sequencing suggests that TG2 is primarily transcriptionally repressive in astrocytes, although it can facilitate both up- and downregulation of gene expression. Therefore, we asked whether VA4 inhibition could alter TG2’s interaction with Zbtb7a, a transcription factor that we previously identified as a functionally relevant TG2 nuclear interactor. We found that VA4 significantly decreased the interaction of TG2 and Zbtb7a. Additionally, we assessed the effect of TG2 deletion and VA4 treatment on transcriptionally permissive histone acetylation and found significantly greater acetylation in both experimental groups. Consistent with these findings, our present proteomic analysis further supports the predominant transcriptionally repressive role of TG2 in astrocytes. Our proteomic data additionally unveiled pronounced changes in lipid and antioxidant metabolism in astrocytes with TG2 deletion or inhibition, which likely contribute to the enhanced neurosupportive function of these astrocytes. Full article

As a crop with significant medicinal value and nutritional components, the market demand for bitter melon continues to grow. The diversity of bitter melon shapes has a direct impact on its market acceptance and consumer preferences, making precise identification of bitter melon germplasm resources crucial for breeding work. To address the limitations of time-consuming and less accurate traditional manual identification methods, there is a need to enhance the automation and intelligence of bitter melon phenotype detection. This study developed a bitter melon phenotype detection model named CSW-YOLO. By incorporating the ConvNeXt V2 module to replace the backbone network of YOLOv8, the model’s focus on critical target features is enhanced. Additionally, the SimAM attention mechanism was introduced to compute attention weights for neurons without increasing the parameter count, further enhancing the model’s recognition accuracy. Finally, WIoUv3 was introduced as the bounding box loss function to improve the model’s convergence speed and positioning capabilities. The model was trained and tested on a bitter melon image dataset, achieving a precision of 94.6%, a recall of 80.6%, a mAP50 of 96.7%, and an F1 score of 87.04%. These results represent improvements of 8.5%, 0.4%, 11.1%, and 4% in precision, recall, mAP50, and F1 score, respectively, over the original YOLOv8 model. Furthermore, the effectiveness of the improvements was validated through heatmap analysis and ablation experiments, demonstrating that the CSW-YOLO model can more accurately focus on target features, reduce false detection rates, and enhance generalization capabilities. Comparative tests with various mainstream deep learning models also proved the superior performance of CSW-YOLO in bitter melon phenotype detection tasks. This research provides an accurate and reliable method for bitter melon phenotype identification and also offers technical support for the visual detection technologies of other agricultural products. Full article

Toxoplasma gondii forms tissue cysts in neurons and astrocytes in the brain to establish chronic infection, and astrocytes express the CXCL10 chemokine in chronically infected mice. Since chemokines mediate the migration of T cells to attack their targets, and since CXCL10 plays key roles in T cell-mediated control of the proliferation of tachyzoites (the acute stage form) of T. gondii during the acute stage of infection, we examined whether CXCL10 is involved in recruiting anti-cyst CD8⁺ cytotoxic T cells to eliminate the cysts in their brains. We employed adoptive transfer of CD8⁺ immune T cells to infected, T cell-deficient SCID and RAG1^−/− mice in combination with blocking CXCL10 activity by neutralizing antibody or a deletion of this chemokine gene. The treatment of chronically infected (infected and treated with sulfadiazine) SCID mice with the anti-CXCL10 antibody did not inhibit the recruitment of the transferred CD8⁺ T cells into their brains and the removal of cerebral T. gondii cysts by the T cells. In addition, the neutralization of CXCL10 did not reduce the cerebral expression of mRNA for the mediators (perforin and granzyme B [GzmB]) of the cytotoxic activity of CD8⁺ T cells in the SCID mice. Consistently, the adoptive transfer of CD8⁺ immune T cells to chronically infected RAG1^−/−CXCL10^−/− mice did not show any defects in recruiting the CD8⁺ T cells into their brains and eliminating the cysts when compared to infected RAG1^−/− mice. The former rather displayed enhanced cyst removal with increased cerebral expression of GzmB mRNA. These results indicate that the absence of CXCL10 activity does not ablate the capability of CD8⁺ cytotoxic T cells to migrate into the brain and eliminate T. gondii cysts from the brains of chronically infected mice. These results also suggest that the immune system utilizes distinct chemokines to control T. gondii depending on the two different life cycle stages, tachyzoite and cyst, of this protozoan parasite. Full article

Self-Supervised Representation Learning (SSRL) has become a potent strategy for addressing the growing threat of Global Positioning System (GPS) spoofing to small Unmanned Aerial Vehicles (UAVs) by capturing more abstract and high-level contributing features. This study focuses on enhancing attack detection capabilities by incorporating SSRL techniques. An innovative hybrid architecture integrates Long Short-Term Memory (LSTM) and Gated Recurrent Unit (GRU) models to detect attacks on small UAVs alongside two additional architectures, LSTM-Recurrent Neural Network (RNN) and Deep Neural Network (DNN), for detecting GPS spoofing attacks. The proposed model leverages SSRL, autonomously extracting meaningful features without the need for many labelled instances. Key configurations include LSTM-GRU, with 64 neurons in the input and concatenate layers and 32 neurons in the second layer. Ablation analysis explores various parameter settings, with the model achieving an impressive 99.9% accuracy after 10 epoch iterations, effectively countering GPS spoofing attacks. To further enhance this approach, transfer learning techniques are also incorporated, which help to improve the adaptability and generalisation of the SSRL model. By saving and applying pre-trained weights to a new dataset, we leverage prior knowledge to improve performance. This integration of SSRL and transfer learning yields a validation accuracy of 79.0%, demonstrating enhanced generalisation to new data and reduced training time. The combined approach underscores the robustness and efficiency of GPS spoofing detection in UAVs. Full article

Amyotrophic lateral sclerosis (ALS) is a fatal disease that causes degeneration of motor neurons (MNs) and paralysis. ALS can be caused by mutations in the gene that encodes copper/zinc superoxide dismutase (SOD1). SOD1 is known mostly as a cytosolic antioxidant protein, but SOD1 is also in the nucleus of non-transgenic (tg) and human SOD1 (hSOD1) tg mouse MNs. SOD1’s nuclear presence in different cell types and subnuclear compartmentations are unknown, as are the nuclear functions of SOD1. We examined hSOD1 nuclear localization and DNA damage in tg mice expressing mutated and wildtype variants of hSOD1 (hSOD1-G93A and hSOD1-wildtype). We also studied ALS patient-derived induced pluripotent stem (iPS) cells to determine the nuclear presence of SOD1 in undifferentiated and differentiated MNs. In hSOD1-G93A and hSOD1-wildtype tg mice, choline acetyltransferase (ChAT)-positive MNs had nuclear hSOD1, but while hSOD1-wildtype mouse MNs also had nuclear ChAT, hSOD1-G93A mouse MNs showed symptom-related loss of nuclear ChAT. The interneurons had preserved parvalbumin nuclear positivity in hSOD1-G93A mice. hSOD1-G93A was seen less commonly in spinal cord astrocytes and, notably, oligodendrocytes, but as the disease emerged, the oligodendrocytes had increased mutant hSOD1 nuclear presence. Brain and spinal cord subcellular fractionation identified mutant hSOD1 in soluble nuclear extracts of the brain and spinal cord, but mutant hSOD1 was concentrated in the chromatin nuclear extract only in the spinal cord. Nuclear extracts from mutant hSOD1 tg mouse spinal cords had altered protein nitration, footprinting peroxynitrite presence, and the intact nuclear extracts had strongly increased superoxide production as well as the active NADPH oxidase marker, p47phox. The comet assay showed that MNs from hSOD1-G93A mice progressively (6–14 weeks of age) accumulated DNA single-strand breaks. Ablation of the NCF1 gene, encoding p47phox, and pharmacological inhibition of NADPH oxidase with systemic treatment of apocynin (10 mg/kg, ip) extended the mean lifespan of hSOD1-G93A mice by about 25% and mitigated genomic DNA damage progression. In human postmortem CNS, SOD1 was found in the nucleus of neurons and glia; nuclear SOD1 was increased in degenerating neurons in ALS cases and formed inclusions. Human iPS cells had nuclear SOD1 during directed differentiation to MNs, but mutant SOD1-expressing cells failed to establish wildtype MN nuclear SOD1 levels. We conclude that SOD1 has a prominent nuclear presence in the central nervous system, perhaps adopting aberrant contexts to participate in ALS pathobiology. Full article

Research has been conducted investigating the neuronal pathways responsible for the generation of chronic neuropathic pain, including the components of it in conditions such as chronic post-surgical pain, phantom limb pain, and cluster headaches. Forming part of the management of such conditions, capsaicin as a molecule has proven effective. This review has investigated the central nervous system modifications exhibited in such conditions and the pharmacological mechanisms of capsaicin relevant to this. The current paradigm for explaining topical capsaicin-induced analgesia is that TRPV1-mediated calcium ion influx induces calpain, in turn causing axonal ablation and functional defunctionalisation in the PNS (Peripheral Nervous System). Demonstrated through the analysis of existing data, this review demonstrates the changes seen in the CNS (Central Nervous System) in chronic neuropathic pain, as well as some of the evidence for capsaicin modulation on the CNS. Further supporting this, the specific molecular mechanisms of capsaicin-induced analgesia will also be explored, including the action of TRPV1, as well as discussing the further need for clinical research into this area of uncertainty due to the limited specific data with suitable parameters. Further research this review identified as potentially useful in this field included fMRI (functional Magnetic Resonance Imaging) studies, though more specific observational studies of patients who have already been administered capsaicin as a current treatment may prove helpful in studying the modification of the CNS in the long term. Full article

Canonical transient receptor potential channel 3 (TRPC3) is the most abundant TRPC channel in the brain and is highly expressed in all subfields of the hippocampus. Previous studies have suggested that TRPC3 channels may be involved in the hyperexcitability of hippocampal pyramidal neurons and seizures. Genetic ablation of TRPC3 channel expression reduced the intensity of pilocarpine-induced status epilepticus (SE). However, the underlying cellular mechanisms remain unexplored and the contribution of TRPC3 channels to SE-induced neurodegeneration is not determined. In this study, we investigated the contribution of TRPC3 channels to the electrophysiological properties of hippocampal pyramidal neurons and hippocampal synaptic plasticity, and the contribution of TRPC3 channels to seizure-induced neuronal cell death. We found that genetic ablation of TRPC3 expression did not alter basic electrophysiological properties of hippocampal pyramidal neurons and had a complex impact on epileptiform bursting in CA3. However, TRPC3 channels contribute significantly to long-term potentiation in CA1 and SE-induced neurodegeneration. Our results provided further support for therapeutic potential of TRPC3 inhibitors and raised new questions that need to be answered by future studies. Full article

Background: Alcohol use disorder (AUD) is related to mental and somatic disorders that result in alcohol withdrawal syndrome (AWS), with 30% of AWS cases leading to life-threatening delirium tremens (DTs). Currently, studies do not support using any one biomarker in DTs. Neurotrophins affect neuromodulation, playing a role in the pathogenesis of AUD, AWS, and DTs. Methods: This review aims to summarize experimental and clinical data related to neurotrophins and S100B in neuroplasticity, as well as neurodegeneration in the context of AUD, AWS, and DTs. This work used publications that were selected based on the protocol consistent with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. Results: The BDNF level could be a good candidate biomarker for relapse susceptibility, as it is significantly reduced during consumption and gradually increases during abstinence. GDNF influences AUD through its integral role in the function of dopaminergic neurons and ablates the return to alcohol-drinking behavior. NGF protects neurons from ethanol-induced cytotoxic damage and affects recovery from cognitive deficits after brain damage. The NT-3 level is decreased after alcohol exposure and is involved in compensatory mechanisms for cognitive decline in AUD. NT-4 affects oxidative stress, which is associated with chronic alcohol consumption. S100B is used as a biomarker of brain damage, with elevated levels in serum in AUD, and can protect 5-HT neurons from the damage caused by alcohol. Conclusions: BDNF, GDNF, NT-3, NT-4, NGF, and S100B may be valuable markers for withdrawal syndrome. In particular, the most relevant is their association with the development of delirium complications. However, there are few data concerning some neurotrophins in AWS and DTs, suggesting the need for further research. Full article

It has been known for a long time that epileptic seizures provoke brain neuroinflammation involving the activation of microglial cells. However, the role of these cells in this disease context and the consequences of their inflammatory activation on subsequent neuron network activity remain poorly understood so far. To fill this gap of knowledge and gain a better understanding of the role of microglia in the pathophysiology of epilepsy, we used an established zebrafish Dravet syndrome epilepsy model based on Scn1Lab sodium channel loss-of-function, combined with live microglia and neuronal Ca²⁺ imaging, local field potential (LFP) recording, and genetic microglia ablation. Data showed that microglial cells in scn1Lab-deficient larvae experiencing epileptiform seizures displayed morphological and biochemical changes characteristic of M1-like pro-inflammatory activation; i.e., reduced branching, amoeboid-like morphology, and marked increase in the number of microglia expressing pro-inflammatory cytokine Il1β. More importantly, LFP recording, Ca²⁺ imaging, and swimming behavior analysis showed that microglia-depleted scn1Lab-KD larvae displayed an increase in epileptiform seizure-like neuron activation when compared to that seen in scn1Lab-KD individuals with microglia. These findings strongly suggest that despite microglia activation and the synthesis of pro-inflammatory cytokines, these cells provide neuroprotective activities to epileptic neuronal networks, making these cells a promising therapeutic target in epilepsy. Full article

Phosphatase and tensin homolog (Pten) is a key regulator of cell proliferation and a potential target to stimulate postnatal enteric neuro- and/or gliogenesis. To investigate this, we generated two tamoxifen-inducible Cre recombinase murine models in which Pten was conditionally ablated, (1) in glia (Plp1-expressing cells) and (2) in neurons (Calb2-expressing cells). Tamoxifen-treated adult (7–12 weeks of age; n = 4–15) mice were given DSS to induce colitis, EdU to monitor cell proliferation, and were evaluated at two timepoints: (1) early (3–4 days post-DSS) and (2) late (3–4 weeks post-DSS). We investigated gut motility and evaluated the enteric nervous system. Pten inhibition in Plp1-expressing cells elicited gliogenesis at baseline and post-DSS (early and late) in the colon, and neurogenesis post-DSS late in the proximal colon. They also exhibited an increased frequency of colonic migrating motor complexes (CMMC) and slower whole gut transit times. Pten inhibition in Calb2-expressing cells did not induce enteric neuro- or gliogenesis, and no alterations were detected in CMMC or whole gut transit times when compared to the control at baseline or post-DSS (early and late). Our results merit further research into Pten modulation where increased glia and/or slower intestinal transit times are desired (e.g., short-bowel syndrome and rapid-transit disorders). Full article