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The rise of Distributed Denial of Service (DDoS) attacks on the internet has necessitated the development of robust and efficient detection mechanisms. DDoS attacks continue to present a significant threat, making it imperative to find efficient ways to detect and prevent these attacks promptly. Traditional machine learning approaches raise privacy concerns when handling sensitive data. In response, federated learning has emerged as a promising paradigm, allowing model training across decentralized devices without centralizing data. However, challenges such as the non-IID (Non-Independent and Identically Distributed) problem persist due to data distribution imbalances among devices. In this research, we propose personalized federated learning (PFL) as a solution for detecting DDoS attacks. PFL preserves data privacy by keeping sensitive information localized on individual devices during model training, thus addressing privacy concerns that are inherent in traditional approaches. In this paper, we propose federated learning with DBSCAN clustering (FedDB). By combining personalized training with model aggregation, our approach effectively mitigates the common challenge of non-IID data in federated learning setups. The integration of DBSCAN clustering further enhances our method by effectively handling data distribution imbalances and improving the overall detection accuracy. Results indicate that our proposed model improves performance, achieving relatively consistent accuracy across all clients, demonstrating that our method effectively overcomes the non-IID problem. Evaluation of our approach utilizes the CICDDOS2019 dataset. Through comprehensive experimentation, we demonstrate the efficacy of personalized federated learning in enhancing detection accuracy while safeguarding data privacy and mitigating non-IID concerns. [ABSTRACT FROM AUTHOR]

Flow-based particle separation usually requires a sheath flow for particle manipulation. Sheath fluid is a specialized buffer solution that directs the alignment of particles or cells into the center of the stream. By utilizing sheath flow, the particles or cells can be focused on the middle line of the microchannel, where they can be individually analyzed. However, the method requires an additional design for creating a suitable sheath flow. Purity and separation efficiency may also be influenced by the sheath flow. In this study, we present a sheathless device for particle focusing and separation using standing surface acoustic waves (SSAWs). The device comprises two regions: the focusing and separation regions. In the focusing region, particles in a continuous flow are aligned in the middle of the microchannel by SSAWs; in the separation region, tilted-angle SSAW-based particle separation is used to control particle migration. Varying particle sizes were focused in the focusing region and then separated in the separation region in the sheathless device. Experiments and simulations were also utilized to optimize a sheathless device. 10 and 20 μm particle focusing and separation were conducted in a sheathless device for the first time. We demonstrate that the separation of particles with a diameter of 10 and 20 μm has 90.8 ± 1.75% and 99.5 ± 0.8% separation efficiency, and 98 ± 3.4 and 97.9 ± 0.9% purity. Compared with other focusing and separation technologies, our device can also provide high purity, high separation efficiency, and high device density. [ABSTRACT FROM AUTHOR]

Lung cancer is the leading cause of cancer‐related deaths worldwide. Patients with lung cancer usually exhibit poor prognoses and low 5‐year survival rates. Idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) are both chronic lung dysfunctions resulting in lung fibrosis and increased risk of lung cancer. Myofibroblasts contribute to the progression of asthma, COPD and IPF, leading to fibrosis in the airway and lungs. A growing body of evidence demonstrates that metabolic reprogramming is a major hallmark of fibrosis, being important in the progression of fibrosis. Using gene expression microarray, we identified and validated that the lipid metabolic pathway was upregulated in lung fibroblasts upon interleukin (IL)‐4, IL‐13 and tumour necrosis factor (TNF)‐α treatment. In this study, we described that prostaglandin E synthase (PTGES) was upregulated in lung fibroblasts after IL‐4, IL‐13 and TNF‐α treatments. PTGES increased α‐SMA levels and promoted lung fibroblast cell migration and invasion abilities. Furthermore, PTGES was upregulated in a lung fibrosis rat model in vivo. PTGES increased AKT phosphorylation, leading to activation of the HIF‐1α‐glycolysis pathway in lung fibroblast cells. HIF‐1α inhibitor or 2‐DG treatments reduced α‐SMA expression in recombinant PTGES (rPTGES)‐treated lung fibroblast cells. Targeting PGE2 signalling in PTGES‐overexpressing cells by a PTGES inhibitor reduced α‐SMA expression. In conclusion, the results of this study demonstrate that PTGES increases the expression of myofibroblast marker via HIF‐1α‐dependent glycolysis and contributes to myofibroblast differentiation. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) includes cardiovascular risk factors like obesity, dyslipidemia, hypertension, and glucose intolerance, which increase the risk of overactive bladder (OAB), characterized by urgency, frequency, urge incontinence, and nocturia. Both MetS and ovarian hormone deficiency (OHD) are linked to bladder overactivity. Nitric oxide (NO) is known to reduce inflammation and promote healing but its effect on bladder overactivity in MetS and OHD is unclear. This study aimed to investigate NO's impact on detrusor muscle hyperactivity in rats with MetS and OHD. Female Sprague-Dawley rats were divided into seven groups based on diet and treatments involving L-arginine (NO precursor) and L-NAME (NOS inhibitor). After 12 months on a high-fat, high-sugar diet with or without OVX, a cystometrogram and tracing analysis of voiding behavior were used to identify the symptoms of detrusor hyperactivity. The MetS with or without OHD group had a worse bladder contractile response while L-arginine ameliorated bladder contractile function. In summary, MetS with or without OHD decreased NO production, reduced angiogenesis, and enhanced oxidative stress to cause bladder overactivity, mediated through the NF-kB signaling pathway, whereas L-arginine ameliorated the symptoms of detrusor overactivity and lessened oxidative damage via the NRF2/HIF-1α signaling pathway in MetS with or without OHD-induced OAB. [ABSTRACT FROM AUTHOR]