Southeastern University

We propose a hierarchical, policy-aware federated learning (FL) framework that enforces strict data residency while training intrusion and anomaly detectors across jurisdictions such as the United States and the European Union. A policy engine encoded in a domain-specific YAML dialect constrains cross-border traffic to either nothing or to differentially private (DP) summaries whose privacy loss is tracked with a Renyi DP accountant; regional aggregators train local models that are fused into a global backbone through secure aggregation. Using public cybersecurity datasets partitioned into simulated US/EU sites, we benchmark ROC-AUC, macro-F1, cross-border communication cost, and cumulative privacy loss $\varepsilon$ under varying non-IID severity and temporal drift. Results indicate the proposed method preserves compliance (zero residency violations) while matching or exceeding flat FL baselines at $10 \%-30 \%$ lower cross-border bandwidth for comparable $\varepsilon$. We release an open-source reference implementation including policy schemas, enforcement hooks, and an auditable DP accountant, along with a reproducibility checklist and SDK to operationalize compliance in FL deployments.

Abstract In an era of increasing disturbances, understanding the capacity for coral reefs to recover and the drivers that underpin resilience is critical for predicting the health of future coral reefs. Traditional resilience paradigms for Western Atlantic reefs suggest that high herbivore biomass and low macroalgal cover are tenets of resilient systems. Yet, it is clear that some locations, such as Florida’s reefs, and potentially other locations, are not well explained by this paradigm. Here, we suggest that the proliferation and increased dominance of long-sediment-laden algal turfs (LSATs) create an additional negative feedback process that helps explain the compromised resilience of Florida’s reefs and further extends the existing Western Atlantic model. Collectively, coral mortality, reef flattening, and intense grazing appear to have created a series of negative feedback processes that reinforce a flat, sediment-laden benthos that impedes the recovery of already diminished coral populations. Importantly, feedbacks associated with LSATs could be strengthened in the presence of high herbivore biomass, thereby undermining foundational expectations of resilience based on grazing pressure alone. Here, we outline this destructive cycle and provide support for the mechanisms that drive these feedbacks. Although we focus on the ecological context of Florida’s reefs, our expansion of the conceptual framework will likely apply to other reef systems in the Caribbean with similar ecological attributes. Mounting evidence suggests that LSAT dominance represents a novel ecosystem state for Western Atlantic reefs.

BackgroundObesity is a multifaceted disease that dramatically impacts an individual's quality of life and, when prolonged, can lead to an increase in several inflammatory markers, leading to chronic low‐grade inflammation. This review seeks to compile scientific literature related to obesity and its associated inflammatory markers that may be related to the onset of Alzheimer's Disease (AD).MethodsLiterature was acquired using PubMed, Google Scholar, and NIH distributed from 2020‐2024. Obesity, Alzheimer's Disease, inflammatory markers, neuroinflammation, insulin resistance, and immune signaling pathways were keywords used. Inclusion criteria involved relevant peer‐reviewed studies published in English, within the last five years that also included populations characterized as obese. Exclusion criteria comprised pertinent studies that were published outside the time frame, in addition to studies that were not peer‐reviewed journals or contained non‐relevant populations.ResultsStudies suggest that low‐grade systemic and local inflammation observed in obese individuals is associated with the development of other chronic conditions, as well as an earlier onset of AD. This can be attributed to the release of pro‐inflammatory markers and hormones caused by the accumulation of adipose tissue, while M1 macrophages further induce the inflammatory state by releasing more cytokines and activating microglia. Reactive oxygen species disrupt the blood‐brain barrier, leading to ischemia and apoptosis of neuronal cells, contributing to the AD phenotype. Additional studies have shown that insulin resistance, associated with obesity, leads to amyloid deposits and plaque buildup in the brain, which impacts brain cell function, a biomarker for AD.ConclusionWhile inflammation is believed to be the primary cause of AD, to gain a deeper understanding of the relationship between obesity as an increased risk factor for developing AD, further research must be done. Obesity as a modifiable risk factor for the development of other chronic conditions emphasizes the significance of research in this area and the need for urgent intervention, especially among certain ethnic and racial groups, where African American women are the most likely to be affected by both obesity and AD.