3 research outputs found

    The Flow of Trust: A Visualization Framework to Externalize, Explore, and Explain Trust in ML Applications

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    We present a conceptual framework for the development of visual interactive techniques to formalize and externalize trust in machine learning (ML) workflows. Currently, trust in ML applications is an implicit process that takes place in the user’s mind. As such, there is no method of feedback or communication of trust that can be acted upon. Our framework will be instrumental in developing interactive visualization approaches that will help users to efficiently and effectively build and communicate trust in ways that fit each of the ML process stages. We formulate several research questions and directions that include: 1) a typology/taxonomy of trust objects, trust issues, and possible reasons for (mis)trust; 2) formalisms to represent trust in machine-readable form; 3) means by which users can express their state of trust by interacting with a computer system (e.g., text, drawing, marking); 4) ways in which a system can facilitate users’ expression and communication of the state of trust; and 5) creation of visual interactive techniques for representation and exploration of trust over all stages of an ML pipeline

    Aberrant Function of the C-Terminal Tail of HIST1H1E Accelerates Cellular Senescence and Causes Premature Aging

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    Histones mediate dynamic packaging of nuclear DNA in chromatin, a process that is precisely controlled to guarantee efficient compaction of the genome and proper chromosomal segregation during cell division and to accomplish DNA replication, transcription, and repair. Due to the important structural and regulatory roles played by histones, it is not surprising that histone functional dysregulation or aberrant levels of histones can have severe consequences for multiple cellular processes and ultimately might affect development or contribute to cell transformation. Recently, germline frameshift mutations involving the C-terminal tail of HIST1H1E, which is a widely expressed member of the linker histone family and facilitates higher-order chromatin folding, have been causally linked to an as-yet poorly defined syndrome that includes intellectual disability. We report that these mutations result in stable proteins that reside in the nucleus, bind to chromatin, disrupt proper compaction of DNA, and are associated with a specific methylation pattern. Cells expressing these mutant proteins have a dramatically reduced proliferation rate and competence, hardly enter into the S phase, and undergo accelerated senescence. Remarkably, clinical assessment of a relatively large cohort of subjects sharing these mutations revealed a premature aging phenotype as a previously unrecognized feature of the disorder. Our findings identify a direct link between aberrant chromatin remodeling, cellular senescence, and accelerated aging
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