Development of Technologies for the Detection of (Cyber)Bullying Actions: The BullyBuster Project

Bullying and cyberbullying are harmful social phenomena that involve the intentional, repeated use of power to intimidate or harm others. The ramifications of these actions are felt not just at the individual level but also pervasively throughout society, necessitating immediate attention and practical solutions. The BullyBuster project pioneers a multi-disciplinary approach, integrating artificial intelligence (AI) techniques with psychological models to comprehensively understand and combat these issues. In particular, employing AI in the project allows the automatic identification of potentially harmful content by analyzing linguistic patterns and behaviors in various data sources, including photos and videos. This timely detection enables alerts to relevant authorities or moderators, allowing for rapid interventions and potential harm mitigation. This paper, a culmination of previous research and advancements, details the potential for significantly enhancing cyberbullying detection and prevention by focusing on the system’s design and the novel application of AI classifiers within an integrated framework. Our primary aim is to evaluate the feasibility and applicability of such a framework in a real-world application context. The proposed approach is shown to tackle the pervasive issue of cyberbullying effectively

Regulation of the intermediate filament protein nestin at rodent neuromuscular junctions by innervation and activity

The intermediate filament nestin is localized postsynaptically at rodent neuromuscular junctions. The protein forms a filamentous network beneath and between the synaptic gutters, surrounds myofiber nuclei, and is associated with Z-discs adjacent to the junction. In situ hybridization shows that nestin mRNA is synthesized selectively by synaptic myonuclei. Although weak immunoreactivity is present in myelinating Schwann cells that wrap the preterminal axon, nestin is not detected in the terminal Schwann cells (tSCs) that cover the nerve terminal branches. However, after denervation of muscle, nestin is upregulated in tSCs and in SCs within the nerve distal to the lesion site. In contrast, immunoreactivity is strongly downregulated in the muscle fiber. Transgenic mice in which the nestin neural enhancer drives expression of a green fluorescent protein (GFP) reporter show that the regulation in SCs is transcriptional. However, the postsynaptic expression occurs through enhancer elements distinct from those responsible for regulation in SCs. Application of botulinum toxin shows that the upregulation in tSCs and the loss of immunoreactivity in muscle fibers occurs with blockade of transmitter release. Extrinsic stimulation of denervated muscle maintains the postsynaptic expression of nestin but does not affect the upregulation in SCs. Thus, a nestin-containing cytoskeleton is promoted in the postsynaptic muscle fiber by nerve-evoked muscle activity but suppressed in tSCs by transmitter release. Nestin antibodies and GFP driven by nestin promoter elements serve as excellent markers for the reactive state of SCs. Vital imaging of GFP shows that SCs grow a dynamic set of processes after denervation

Usability Evaluation of Hong Kong Hotel Websites

School of Hotel and Tourism Managemen

Clinical Relevance of Shiga Toxin Concentrations in the Blood of Patients With Hemolytic Uremic Syndrome

Background: Intestinal infections with Shiga toxin-producing Escherichia coli (STEC) in children can lead to the hemolytic uremic syndrome (HUS). Shiga toxins (Stx) released in the gut by bacteria enter the blood stream and target the kidney causing endothelial injury. Free toxins have never been detected in the blood of HUS patients, but they have been found on the surface of polymorphonuclear leukocytes (PMN). Methods: With respect to their clinical features, the clinical relevance of the amounts of serum Stx (cytotoxicity assay with human endothelial cells) and PMN-bound Stx (cytofluorimetric assay) in 46 patients with STECassociated HUS was evaluated. Results: Stx-positive PMN were found in 60% of patients, whereas negligible amounts of free Stx were detected in the sera. Patients with high amounts of Stx on PMN showed preserved or slightly impaired renal function (incomplete form of HUS), whereas cases with low amounts of Stx usually presented evidence of acute renal failure. Conclusions: These observations suggest that the extent of renal damage in children with STEC-associated HUS could depend on the concentration of Stx present on their PMN and presumably delivered by them to the kidney. As previously shown by experimental models from our laboratory, high amounts of Stx could induce a reduced release of cytokines by the renal endothelium, with a consequent lower degree of inflammation. Conversely, low toxin amounts can trigger the cytokine cascade, provoking inflammation, thereby leading to tissue damage