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Field
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the following: digital twins, cyberphysical systems, human-centred AI causal modelling, uncertainty quantification, explainable AI, or trustworthy AI agentic AI, multiagent systems, sequential decision
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learning and LLM frameworks like LangChain and agent-based LLM frameworks, Retrieval Augmented Generation (RAG). Experience with fine-tuning, deploying, and evaluating Large Language Models. Experience with
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highly complex workflows. We aim to develop optimization models and algorithms to improve wafer processing sequences across semiconductor manufacturing tools, with the objectives of reducing cycle times
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Max Planck Institute for Demographic Research (MPIDR) | Rostock, Mecklenburg Vorpommern | Germany | about 22 hours ago
for Demographic Research, Rostock This network focuses on “scientifically motivated engineering” to design, build, and test digital prototypes—such as machine learning models and large language models—that serve as
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support research in: • Transportation systems modeling and simulation, including O/D modeling, multimodal network modeling, agent-based or behavioral modeling • Large-scale computing, cloud-native analytics
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probe flavin chemistry using a powerful combination of approaches: the design of biomimetic flavin models (lumiflavin-based systems), detailed mechanistic studies in solution, and state-of-the-art gas
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of host–pathogen interactions with the development of next-generation sequencing (NGS)-based assays to create advanced tools for detecting pathogens and adventitious agents, thereby improving product safety
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, while accounting for dynamic and stochastic demand patterns. The project addresses these challenges through a combination of advanced optimization methods (e.g., flow-based models that strengthen
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of the circulation of infectious agents in populations of marine vertebrates in the Southern Territories. The main models considered are seabirds (albatrosses, penguins, petrels, wrasses) and marine mammals (elephant
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abnormal scarring of the liver in which healthy tissue is replaced by a rigid and dysfunctional extracellular matrix (ECM). It results from chronic damage, activating myofibroblasts, the main agents