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cs.AI, q-bio.NC updates on arXiv.org
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Assessing the Real-World Utility of Explainable AI for Arousal Diagnostics: An Application-Grounded User Study
arXiv:2510.21389v1 Announce Type: cross Abstract: Artificial intelligence (AI) systems increasingly match or surpass human experts in biomedical signal interpretation. However, their effective integration into clinical practice requires more than high predictive accuracy. Clinicians must discern \textit{when} and \textit{why} to trust algorithmic recommendations. This work presents an application-grounded user study with eight professional sleep medicine practitioners, who score nocturnal arous
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cs.AI, q-bio.NC updates on arXiv.org
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A Definition of AGI
arXiv:2510.18212v2 Announce Type: replace Abstract: The lack of a concrete definition for Artificial General Intelligence (AGI) obscures the gap between today's specialized AI and human-level cognition. This paper introduces a quantifiable framework to address this, defining AGI as matching the cognitive versatility and proficiency of a well-educated adult. To operationalize this, we ground our methodology in Cattell-Horn-Carroll theory, the most empirically validated model of human cognition.
A Definition of AGI
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(Multiomics OR Omics) AND (Pancreatic)
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Codon specific readthrough as a mechanism of BRCA2 restoration in acquired PARP inhibitor and chemotherapy resistance
Nucleic Acids Res. 2025 Oct 14;53(19):gkaf990. doi: 10.1093/nar/gkaf990.ABSTRACTBRCA2 mutations contribute to the pathogenesis and treatment sensitivity of a subset of ovarian, breast, prostate, and pancreatic cancers. When these cancers become therapy resistant, secondary mutations that restore the BRCA2 open reading frame are found in half the cases, but other causes of resistance remain incompletely understood. Here, we identified translational readthrough of a premature termination codon (PT
Codon specific readthrough as a mechanism of BRCA2 restoration in acquired PARP inhibitor and chemotherapy resistance
Nucleic Acids Res. 2025 Oct 14;53(19):gkaf990. doi: 10.1093/nar/gkaf990.
ABSTRACT
BRCA2 mutations contribute to the pathogenesis and treatment sensitivity of a subset of ovarian, breast, prostate, and pancreatic cancers. When these cancers become therapy resistant, secondary mutations that restore the BRCA2 open reading frame are found in half the cases, but other causes of resistance remain incompletely understood. Here, we identified translational readthrough of a premature termination codon (PTC) as a cause of resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) and cisplatin in cells derived from the BRCA2-mutated ovarian cancer line PEO1 by PARPi selection. Despite persistence of the signature 4965C > G (p.Y1655X) BRCA2 mutation, low-level expression of full-length BRCA2 protein was detectable in these cells by immunoblotting and tandem mass spectrometry. Either BRCA2 knockdown or gene interruption 5' or 3' to the PTC restored treatment sensitivity, implicating BRCA2 in the resistance. Reporter assays demonstrated UAG-selective readthrough in the resistant clones but not parental cells. Moreover, custom searching of global proteomic data indicated readthrough of stop codons, particularly UAGs, in additional proteins in the resistant clones. Finally, multi-omic analysis identified multiple changes in the nonsense-mediated decay and termination machineries that favor readthrough. Accordingly, the present results identify PTC readthrough as a potential mechanism of drug resistance in cells with BRCA2 nonsense mutations.
PMID:41099700 | PMC:PMC12526053 | DOI:10.1093/nar/gkaf990
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Cell Death Discovery nature.com science feeds
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Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia
Cell Death Discovery, Published online: 02 September 2022; doi:10.1038/s41420-022-01165-4Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia
Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia
Cell Death Discovery, Published online: 02 September 2022; doi:10.1038/s41420-022-01165-4
Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia