19 research outputs found

    Analysis of Moving Target Defense Against False Data Injection Attacks on Power Grid

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    Recent studies have considered thwarting false data injection (FDI) attacks against state estimation in power grids by proactively perturbing branch susceptances. This approach is known as moving target defense (MTD). However, despite of the deployment of MTD, it is still possible for the attacker to launch stealthy FDI attacks generated with former branch susceptances. In this paper, we prove that, an MTD has the capability to thwart all FDI attacks constructed with former branch susceptances only if (i) the number of branches ll in the power system is not less than twice that of the system states nn (i.e., l≥2nl \geq 2n, where n+1n + 1 is the number of buses); (ii) the susceptances of more than nn branches, which cover all buses, are perturbed. Moreover, we prove that the state variable of a bus that is only connected by a single branch (no matter it is perturbed or not) can always be modified by the attacker. Nevertheless, in order to reduce the attack opportunities of potential attackers, we first exploit the impact of the susceptance perturbation magnitude on the dimension of the \emph{stealthy attack space}, in which the attack vector is constructed with former branch susceptances. Then, we propose that, by perturbing an appropriate set of branches, we can minimize the dimension of the \emph{stealthy attack space} and maximize the number of covered buses. Besides, we consider the increasing operation cost caused by the activation of MTD. Finally, we conduct extensive simulations to illustrate our findings with IEEE standard test power systems

    CLEC7A regulates M2 macrophages to suppress the immune microenvironment and implies poorer prognosis of glioma

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    BackgroundGliomas constitute a category of malignant tumors originating from brain tissue, representing the majority of intracranial malignancies. Previous research has demonstrated the pivotal role of CLEC7A in the progression of various cancers, yet its specific implications within gliomas remain elusive. The primary objective of this study was to investigate the prognostic significance and immune therapeutic potential of CLEC7A in gliomas through the integration of bioinformatics and clinical pathological analyses.MethodsThis investigation involved examining and validating the relationship between CLEC7A and glioma using samples from Hospital, along with data from TCGA, GEO, GTEx, and CGGA datasets. Subsequently, we explored its prognostic value, biological functions, expression location, and impact on immune cells within gliomas. Finally, we investigated its potential impact on the chemotaxis and polarization of macrophages.ResultsThe expression of CLEC7A is upregulated in gliomas, and its levels escalate with the malignancy of tumors, establishing it as an independent prognostic factor. Functional enrichment analysis revealed a significant correlation between CLEC7A and immune function. Subsequent examination of immune cell differential expression demonstrated a robust association between CLEC7A and M2 macrophages. This conclusion was further substantiated through single-cell analysis, immunofluorescence, and correlation studies. Finally, the knockout of CLEC7A in M2 macrophages resulted in a noteworthy reduction in macrophage chemotaxis and polarization factors.ConclusionCLEC7A expression is intricately linked to the pathology and molecular characteristics of gliomas, establishing its role as an independent prognostic factor for gliomas and influencing macrophage function. It could be a promising target for immunotherapy in gliomas

    Semaphorin 3A Contributes to Secondary Blood–Brain Barrier Damage After Traumatic Brain Injury

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    Semaphorin 3A (SEMA3A) is a member of the Semaphorins family, a class of membrane-associated protein that participates in the construction of nerve networks. SEMA3A has been reported to affect vascular permeability previously, but its influence in traumatic brain injury (TBI) is still unknown. To investigate the effects of SEMA3A, we used a mouse TBI model with a controlled cortical impact (CCI) device and a blood–brain barrier (BBB) injury model in vitro with oxygen-glucose deprivation (OGD). We tested post-TBI changes in SEMA3A, and its related receptors (Nrp-1 and plexin-A1) expression and distribution through western blotting and double-immunofluorescence staining, respectively. Neurological outcomes were evaluated by modified neurological severity scores (mNSSs) and beam-walking test. We examined BBB damage through Evans Blue dye extravasation, brain water content, and western blotting for VE-cadherin and p-VE-cadherin in vivo, and we examined the endothelial cell barrier through hopping probe ion conductance microscopy (HPICM), transwell leakage, and western blotting for VE-cadherin and p-VE-cadherin in vitro. Changes in miR-30b-5p were assessed by RT-PCR. Finally, the neuroprotective function of miR-30b-5p is measured by brain water content, mNSSs and beam-walking test. SEMA3A expression varied following TBI and peaked on the third day which expressed approximate fourfold increase compared with sham group, with the protein concentrated at the lesion boundary. SEMA3A contributed to neurological function deficits and secondary BBB damage in vivo. Our results demonstrated that SEMA3A level following OGD injury almost doubled than control group, and the negative effects of OGD injury can be improved by blocking SEMA3A expression. Furthermore, the expression of miR-30b-5p decreased approximate 40% at the third day and 60% at the seventh day post-CCI. OGD injury also exhibited an effect to approximately decrease 50% of miR-30b-5p expression. Additionally, the expression of SEMA3A post-TBI is regulated by miR-30b-5p, and miR-30b-5p could improve neurological outcomes post-TBI efficiently. Our results demonstrate that SEMA3A is a significant factor in secondary BBB damage after TBI and can be abolished by miR-30b-5p, which represents a potential therapeutic target

    SoccerNet 2023 Challenges Results

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    peer reviewedThe SoccerNet 2023 challenges were the third annual video understanding challenges organized by the SoccerNet team. For this third edition, the challenges were composed of seven vision-based tasks split into three main themes. The first theme, broadcast video understanding, is composed of three high-level tasks related to describing events occurring in the video broadcasts: (1) action spotting, focusing on retrieving all timestamps related to global actions in soccer, (2) ball action spotting, focusing on retrieving all timestamps related to the soccer ball change of state, and (3) dense video captioning, focusing on describing the broadcast with natural language and anchored timestamps. The second theme, field understanding, relates to the single task of (4) camera calibration, focusing on retrieving the intrinsic and extrinsic camera parameters from images. The third and last theme, player understanding, is composed of three low-level tasks related to extracting information about the players: (5) re-identification, focusing on retrieving the same players across multiple views, (6) multiple object tracking, focusing on tracking players and the ball through unedited video streams, and (7) jersey number recognition, focusing on recognizing the jersey number of players from tracklets. Compared to the previous editions of the SoccerNet challenges, tasks (2-3-7) are novel, including new annotations and data, task (4) was enhanced with more data and annotations, and task (6) now focuses on end-to-end approaches. More information on the tasks, challenges, and leaderboards are available on https://www.soccer-net.org. Baselines and development kits can be found on https://github.com/SoccerNet

    TDJEE: A Document-Level Joint Model for Financial Event Extraction

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    Extracting financial events from numerous financial announcements is very important for investors to make right decisions. However, it is still challenging that event arguments always scatter in multiple sentences in a financial announcement, while most existing event extraction models only work in sentence-level scenarios. To address this problem, this paper proposes a relation-aware Transformer-based Document-level Joint Event Extraction model (TDJEE), which encodes relations between words into the context and leverages modified Transformer to capture document-level information to fill event arguments. Meanwhile, the absence of labeled data in financial domain could lead models be unstable in extraction results, which is known as the cold start problem. Furthermore, a Fonduer-based knowledge base combined with the distant supervision method is proposed to simplify the event labeling and provide high quality labeled training corpus for model training and evaluating. Experimental results on real-world Chinese financial announcement show that, compared with other models, TDJEE achieves competitive results and can effectively extract event arguments across multiple sentences

    Oil and gas pipeline locating method based on improved Unscented Kalman Filter

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    [Objective] Part of oil and gas pipelines in China, which have been in operation for a long time, are facing problems such as the lack of specific geographic information and deviation of the pipeline from the designed laying location. However, traditional pipeline localization methods possess limitations of significant cumulative errors and low accuracy. [Methods] To enhance the precision of oil and gas pipeline localization, a new method was proposed based on improved Unscented Kalman Filter(UKF) algorithm. The primary equipment,which is an inertial measurement unit consisting of a gyroscope and an accelerometer, supplemented by a wheel odometer and ground markers as auxiliary locator devices was utilized in this method. The attitude, velocity, and position errors of the pipeline detector were taken as state variables, and the speed of the wheel odometer and attitude information obtained from the solution of accelerometer data were taken as observables, to establish a nonlinear error propagation model of strap-down inertial navigation system. An improved UKF algorithm was employed to estimate the error transfer model for reducing the impact of noise on localization accuracy. The angular velocity and acceleration information were corrected by combining forward-backward smoothing filter method and straight and curved pipe identification method,to further reduce cumulative errors in the system solution process. [Results] Numerical simulations and physical experiments revealed that the proposed oil and gas pipeline localization system has significantly reduced cumulative errors in locating long-distance pipelines. The maximum error in determining the specific location of oil and gas pipelines was found to be 0.56%. The UKF algorithm, which was proposed in this paper, showed a locating accuracy level of approximately 34.2% higher compared to the traditional Kalman Filter(KF) algorithm and 30.2% higher compared to the UKF algorithm under constant testing conditions. [Conclusion] The proposed oil and gas pipeline locating method based on an improved UKF presents high practical value for long-distance pipeline localization as it has lower cumulative errors in the system solution process and higher accuracy in pipeline localization

    Recombinant Human Annexin A5 Alleviated Traumatic-Brain-Injury Induced Intestinal Injury by Regulating the Nrf2/HO-1/HMGB1 Pathway

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    Aims: Annexin A5 (ANXA5) exhibited potent antithrombotic, antiapoptotic, and anti-inflammatory properties in a previous study. The role of ANXA5 in traumatic brain injury (TBI)-induced intestinal injury is not fully known. Main methods: Recombinant human ANXA5 (50 µg/kg) or vehicle (PBS) was administered to mice via the tail vein 30 min after TBI. Mouse intestine tissue was gathered for hematoxylin and eosin staining 0.5 d, 1 d, 2 d, and 7 d after modeling. Intestinal Western blotting, immunofluorescence, TdT-mediated dUTP nick-end labeling staining, and enzyme-linked immunosorbent assays were performed 2 days after TBI. A series of kits were used to assess lipid peroxide indicators such as malonaldehyde, superoxide dismutase activity, and catalase activity. Key findings: ANXA5 treatment improved the TBI-induced intestinal mucosa injury at different timepoints and significantly increased the body weight. It significantly reduced apoptosis and matrix metalloproteinase-9 and inhibited the degradation of tight-junction-associated protein in the small intestine. ANXA5 treatment improved intestinal inflammation by regulating inflammation-associated factors. It also mitigated the lipid peroxidation products 4-HNE, 8-OHDG, and malonaldehyde, and enhanced the activity of the antioxidant enzymes, superoxide dismutase and catalase. Lastly, ANXA5 significantly enhanced nuclear factor E2-related factor 2 (Nrf2) and hemeoxygenase-1, and decreased high mobility group box 1 (HMGB1). Significance: Collectively, the results suggest that ANXA5 inhibits TBI-induced intestinal injury by restraining oxidative stress and inflammatory responses. The mechanisms involved sparking the Nrf2/hemeoxygenase-1-induced antioxidant system and suppressing the HMGB1 pathway. ANXA5 may be an attractive therapeutic candidate for protecting against TBI-induced intestinal injury

    Gene delivery using dendrimer-entrapped gold nanoparticles as nonviral vectors

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    Development of highly efficient nonviral gene delivery vectors still remains a great challenge. In this study, we report a new gene delivery vector based on dendrimer-entrapped gold nanoparticles (Au DENPs) with significantly higher gene transfection efficiency than that of dendrimers without AuNPs entrapped. Amine-terminated generation 5 poly(amidoamine) (PAMAM) dendrimers (G5.NH(2)) were utilized as templates to synthesize AuNPs with different Au atom/dendrimer molar ratios (25:1, 50:1, 75:1, and 100:1, respectively). The formed Au DENPs were used to complex two different pDNAs encoding luciferase (Luc) and enhanced green fluorescent protein (EGFP), respectively for gene transfection studies. The Au DENPs/pDNA polyplexes with different N/P ratios and compositions of Au DENPs were characterized by gel retardation assay, light scattering, zeta potential measurements, and atomic force microscopic imaging. We show that the Au DENPs can effectively compact the pDNA, allowing for highly efficient gene transfection into the selected cell lines as demonstrated by both Luc assay and fluorescence microscopic imaging of the EGFP expression. The transfection efficiency of Au DENPs with Au atom/dendrimer molar ratio of 25:1 was at least 100 times higher than that of G5.NH(2) dendrimers without AuNPs entrapped at the N/P ratio of 2.5:1. The higher gene transfection efficiency of Au DENPs is primarily due to the fact that the entrapment of AuNPs helps preserve the 3-dimensional spherical morphology of dendrimers, allowing for more efficient interaction between dendrimers and DNA. With the less cytotoxicity than that of G5.NH(2) dendrimers demonstrated by thiazoyl blue tetrazolium bromide assay and higher gene transfection efficiency, it is expected that Au DENPs may be used as a new gene delivery vector for highly efficient transfection of different genes for various biomedical applications.info:eu-repo/semantics/publishedVersio

    Circulating extracellular vesicles from patients with traumatic brain injury induce cerebrovascular endothelial dysfunction

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    Endothelial dysfunction is a key proponent of pathophysiological process of traumatic brain injury (TBI). We previously demonstrated that extracellular vesicles (EVs) released from injured brains led to endothelial barrier disruption and vascular leakage. However, the molecular mechanisms of this EV-induced endothelial dysfunction (endotheliopathy) remain unclear. Here, we enriched plasma EVs from TBI patients (TEVs), and detected high mobility group box 1 (HMGB1) exposure to 50.33 ± 10.17% of TEVs and the number of HMGB1+TEVs correlated with injury severity. We then investigated for the first time the impact of TEVs on endothelial function using adoptive transfer models. We found that TEVs induced dysfunction of cultured human umbilical vein endothelial cells and mediated endothelial dysfunction in both normal and TBI mice, which were propagated through the HMGB1-activated receptor for advanced glycation end products (RAGE)/Cathepsin B signaling, and the resultant NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and canonical caspase-1/gasdermin D (GSDMD)-dependent pyroptosis. Finally, von Willebrand factor (VWF) was detected on the surface of 77.01 ± 7.51% of HMGB1+TEVs. The TEV-mediated endotheliopathy was reversed by a polyclonal VWF antibody, indicating that VWF might serve a coupling factor that tethered TEVs to ECs, thus facilitating HMGB1-induced endotheliopathy. These results suggest that circulating EVs isolated from patients with TBI alone are sufficient to induce endothelial dysfunction and contribute to secondary brain injury that are dependent on immunologically active HMGB1 exposed on their surface. This finding provided new insight for the development of potential therapeutic targets and diagnostic biomarkers for TBI
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