| 2 | Unknown DDoS Attack Detection with Fuzzy C-Means Clustering and Spatial Location Constraint Prototype Loss显示文摘Since its inception,the Internet has been rapidly evolving.With the advancement of science and technology and the explosive growth of the population,the demand for the Internet has been on the rise.Many applications in education,healthcare,entertainment,science,and more are being increasingly deployed based on the internet.Concurrently,malicious threats on the internet are on the rise as well.Distributed Denial of Service(DDoS)attacks are among the most common and dangerous threats on the internet today.The scale and complexity of DDoS attacks are constantly growing.Intrusion Detection Systems(IDS)have been deployed and have demonstrated their effectiveness in defense against those threats.In addition,the research of Machine Learning(ML)and Deep Learning(DL)in IDS has gained effective results and significant attention.However,one of the challenges when applying ML and DL techniques in intrusion detection is the identification of unknown attacks.These attacks,which are not encountered during the system’s training,can lead to misclassification with significant errors.In this research,we focused on addressing the issue of Unknown Attack Detection,combining two methods:Spatial Location Constraint Prototype Loss(SLCPL)and Fuzzy C-Means(FCM).With the proposed method,we achieved promising results compared to traditional methods.The proposed method demonstrates a very high accuracy of up to 99.8%with a low false positive rate for known attacks on the Intrusion Detection Evaluation Dataset(CICIDS2017)dataset.Particularly,the accuracy is also very high,reaching 99.7%,and the precision goes up to 99.9%for unknown DDoS attacks on the DDoS Evaluation Dataset(CICDDoS2019)dataset.The success of the proposed method is due to the combination of SLCPL,an advanced Open-Set Recognition(OSR)technique,and FCM,a traditional yet highly applicable clustering technique.This has yielded a novel method in the field of unknown attack detection.This further expands the trend of applying DL and ML techniques in the development of intrusion detection systems and cybersecurity.Finally,implementing the proposed method in real-world systems can enhance the security capabilities against increasingly complex threats on computer networks. | Thanh-Lam Nguyen HaoKao Thanh-Tuan Nguyen Mong-Fong Horng Chin-Shiuh Shieh | 2024 | Computers, Materials & Continua2024，78，2： | 0 |
| 3 | Natural anti-oxLDL IgM monoclonal antibody in the pathogenesis of atherosclerosis显示文摘Objective To explore the role and the possible molecular mechanisms of natural anti-oxLDL IgM monoclonal antibody played and involved in pathogenesis of atherosclerosis. Methods Natural anti-oxLDL IgM monoclonal antibody 3A6 was generated by using standard hybridoma production techniques. Influence of 3A6 on formation of foam cells was observed by Oil Red O staining and affinity of Na125I-conjugated oxLDL on the naive and LPS-activated macrophages. After LPS stimulation on macrophages, anti-TLR4 neutralizing mAb, p38MAPK specific inhibitor SB203580, NF-kB specific inhibitor PDTC or RNAi targeting Fcα/μ receptor (Fcamr) were applied, respectively. Results Natural anti-oxLDL IgM monoclonal antibody 3 A6 were found specifically inhibit the binding of CuoxLDL to naive macrophages but not the binding of CuoxLDL to LPS-activated macrophages. It also promoted the formation of CuoxLDL-mediated foam macrophages. 3A6 F(ab')2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. LPS up-regulated the expression of Fcamr in macrophages in a dose- and time-dependent manner, which was attenuated by treatment with anti-TLR4. LPS induced the phosphorylation of p38MAPK and translocation of NF-kB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages. Conclusions Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to naive macrophages in vitro. However, LPS, through the Toll-like receptor (TLR)4 receptor, activated the p38MAPK and NF-kB pathways and up-regulated the expression of Fcα/μ receptor in macrophages, which promoted the binding of 3A6/CuoxLDL complex to macrophages through binding with Fc fragments and the formation of foam macrophages. Therefore, our findings provide a new explanation why bacterial infection deteriorates the pathogenesis of atherosclerosis. | Xuyang Feng Ruifen Xu Yan Gao Haokao Gao Zheng He Haichang Wang | 2009 | Journal of Geriatric Cardiology2009，6，1： | 0 |
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