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VLM-CAD: VLM-Optimized Collaborative Agent Design Workflow for Analog Circuit Sizing

arXiv:2601.07315v4 Announce Type: replace-cross Abstract: Vision Language Models (VLMs) have demonstrated remarkable potential in multimodal reasoning, yet they inherently suffer from spatial blindness and logical hallucinations when interpreting densely structured engineering content, such as analog circuit schematics. To address these challenges, we propose a Vision Language Model-Optimized Collaborative Agent Design Workflow for Analog Circuit Sizing (VLM-CAD) designed for robust, step-by-step reasoning over multimodal evidence. VLM-CAD bridges the modality gap by integrating a neuro-symbolic structural parsing module, Image2Net, which transforms raw pixels into explicit topological graphs and structured JSON representations to anchor VLM interpretation in deterministic facts. To ensure the reliability required for engineering decisions, we further propose ExTuRBO, an Explainable Trust Region Bayesian Optimization method. ExTuRBO serves as an explainable grounding engine, employing agent-generated semantic seeds to warm-start local searches and utilizing Automatic Relevance Determination to provide quantified evidence for the VLM's decisions. Experimental results on two complex circuit benchmarks demonstrate that VLM-CAD significantly enhances spatial reasoning accuracy and maintains physics-based explainability. VLM-CAD consistently satisfies complex specification requirements while achieving low power consumption, with a total runtime under 66 minutes, marking a significant step toward robust, explainable multimodal reasoning in specialized technical domains.

A multiomics Mendelian randomization study on PANoptosis-related genes and gastric cancer risk

17 March 2026 at 18:00

J Int Med Res. 2026 Mar;54(3):3000605261430163. doi: 10.1177/03000605261430163. Epub 2026 Mar 16.

ABSTRACT

ObjectiveTo explore the potential involvement of PANoptosis-related genes in gastric cancer susceptibility through multiomics analyses.MethodsSummary-data-based Mendelian randomization was performed by integrating blood-derived methylation, gene expression, and protein quantitative trait loci data with genome-wide association study results. The findings were further evaluated in The Cancer Genome Atlas cohort, followed by protein-protein interaction analysis, drug prediction, and molecular docking.ResultsSummary-data-based Mendelian randomization and colocalization analyses identified several traits suggestively associated with gastric cancer risk. Genetically predicted higher expression of apoptosis and caspase activation inhibitor (AVEN) and hepatocyte growth factor (HGF) as well as higher HGF protein levels were associated with increased risk, whereas higher levels of protein phosphatase 2 regulatory subunit B beta (PPP2R2B) appeared to be protective. Multiomics integration suggested epigenetic regulation of HGF and PPP2R2B. The Cancer Genome Atlas analysis corroborated the dysregulation of these candidates, with high AVEN expression associated with poorer survival. Protein-protein interaction and drug prediction analyses highlighted functional networks and potential therapeutics, supported by molecular docking demonstrating strong HGF-binding affinities. However, these associations did not reach statistical significance in the independent validation cohort, possibly due to limited statistical power.ConclusionsThis study identified AVEN, HGF, and PPP2R2B as potential candidate genes for gastric cancer. These findings require further validation in larger cohorts.

PMID:41840829 | DOI:10.1177/03000605261430163

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