RA-Det: Towards Universal Detection of AI-Generated Images via Robustness Asymmetry

Recent image generators produce photo-realistic content that undermines the reliability of downstream recognition systems. As visual appearance cues become less pronounced, appearance-driven detectors that rely on forensic cues or high-level representations lose stability. This motivates a shift from appearance to behavior, focusing on how images respond to controlled perturbations rather than how they look. In this work, we identify a simple and universal behavioral signal. Natural images preserve stable semantic representations under small, structured perturbations, whereas generated images exhibit markedly larger feature drift. We refer to this phenomenon as robustness asymmetry and provide a theoretical analysis that establishes a lower bound connecting this asymmetry to memorization tendencies in generative models, explaining its prevalence across architectures. Building on this insight, we introduce Robustness Asymmetry Detection (RA-Det), a behavior-driven detection framework that converts robustness asymmetry into a reliable decision signal. Evaluated across 14 diverse generative models and against more than 10 strong detectors, RA-Det achieves superior performance, improving the average performance by 7.81 percent. The method is data- and model-agnostic, requires no generator fingerprints, and transfers across unseen generators. Together, these results indicate that robustness asymmetry is a stable, general cue for synthetic-image detection and that carefully designed probing can turn this cue into a practical, universal detector. The source code is publicly available at Github.

Phenome-wide causal proteomics enhance systemic lupus erythematosus flare prediction: A study in Asian populations

Objective: Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by unpredictable flares. This study aimed to develop a novel proteomics-based risk prediction model specifically for Asian SLE populations to enhance personalized disease management and early intervention. Methods: A longitudinal cohort study was conducted over 48 weeks, including 139 SLE patients monitored every 12 weeks. Patients were classified into flare (n = 53) and non-flare (n = 86) groups. Baseline plasma samples underwent data-independent acquisition (DIA) proteomics analysis, and phenome-wide Mendelian randomization (PheWAS) was performed to evaluate causal relationships between proteins and clinical predictors. Logistic regression (LR) and random forest (RF) models were used to integrate proteomic and clinical data for flare risk prediction. Results: Five proteins (SAA1, B4GALT5, GIT2, NAA15, and RPIA) were significantly associated with SLE Disease Activity Index-2K (SLEDAI-2K) scores and 1-year flare risk, implicating key pathways such as B-cell receptor signaling and platelet degranulation. SAA1 demonstrated causal effects on flare-related clinical markers, including hemoglobin and red blood cell counts. A combined model integrating clinical and proteomic data achieved the highest predictive accuracy (AUC = 0.769), surpassing individual models. SAA1 was highlighted as a priority biomarker for rapid flare discrimination. Conclusion: The integration of proteomic and clinical data significantly improves flare prediction in Asian SLE patients. The identification of key proteins and their causal relationships with flare-related clinical markers provides valuable insights for proactive SLE management and personalized therapeutic approaches.