In the present study, we investigate and compare reasoning in large language models (LLMs) and humans, using a selection of cognitive psychology tools traditionally dedicated to the study of (bounded) rationality. We presented to human participants and an array of pretrained LLMs new variants of classical cognitive experiments, and cross-compared their performances. Our results showed that most of the included models presented reasoning errors akin to those frequently ascribed to error-prone, heuristic-based human reasoning. Notwithstanding this superficial similarity, an in-depth comparison between humans and LLMs indicated important differences with human-like reasoning, with models' limitations disappearing almost entirely in more recent LLMs' releases. Moreover, we show that while it is possible to devise strategies to induce better performance, humans and machines are not equally responsive to the same prompting schemes. We conclude by discussing the epistemological implications and challenges of comparing human and machine behavior for both artificial intelligence and cognitive psychology.
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http://dx.doi.org/10.1038/s44271-024-00091-8 | DOI Listing |
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School of Systems Biomedical Science, Soongsil University, 369 Sangdo-ro, Dongjak-gu, 06978, Seoul, Republic of Korea.
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Department of Statistics and Data Science, Jahangirnagar University, Dhaka, 1342, Bangladesh.
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Department of Surgery, University of California, San Francisco, San Francisco, CA, USA.
Therapeutic efficacy and safety of adeno-associated virus (AAV) liver gene therapy depend on capsid choice. To predict AAV capsid performance under near-clinical conditions, we established side-by-side comparison at single-cell resolution in human livers maintained by normothermic machine perfusion. AAV-LK03 transduced hepatocytes much more efficiently and specifically than AAV5, AAV8 and AAV6, which are most commonly used clinically, and AAV-NP59, which is better at transducing human hepatocytes engrafted in immune-deficient mice.
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Institute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.
During normal cellular homeostasis, unfolded and mislocalized proteins are recognized and removed, preventing the build-up of toxic byproducts. When protein homeostasis is perturbed during ageing, neurodegeneration or cellular stress, proteins can accumulate several forms of chemical damage through reactive metabolites. Such modifications have been proposed to trigger the selective removal of chemically marked proteins; however, identifying modifications that are sufficient to induce protein degradation has remained challenging.
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