Project description:ObjectivesAmbient clinical documentation technology uses automatic speech recognition (ASR) and natural language processing (NLP) to turn patient-clinician conversations into clinical documentation. It is a promising approach to reducing clinician burden and improving documentation quality. However, the performance of current-generation ASR remains inadequately validated. In this study, we investigated the impact of non-lexical conversational sounds (NLCS) on ASR performance. NLCS, such as Mm-hm and Uh-uh, are commonly used to convey important information in clinical conversations, for example, Mm-hm as a "yes" response from the patient to the clinician question "are you allergic to antibiotics?"Materials and methodsIn this study, we evaluated 2 contemporary ASR engines, Google Speech-to-Text Clinical Conversation ("Google ASR"), and Amazon Transcribe Medical ("Amazon ASR"), both of which have their language models specifically tailored to clinical conversations. The empirical data used were from 36 primary care encounters. We conducted a series of quantitative and qualitative analyses to examine the word error rate (WER) and the potential impact of misrecognized NLCS on the quality of clinical documentation.ResultsOut of a total of 135 647 spoken words contained in the evaluation data, 3284 (2.4%) were NLCS. Among these NLCS, 76 (0.06% of total words, 2.3% of all NLCS) were used to convey clinically relevant information. The overall WER, of all spoken words, was 11.8% for Google ASR and 12.8% for Amazon ASR. However, both ASR engines demonstrated poor performance in recognizing NLCS: the WERs across frequently used NLCS were 40.8% (Google) and 57.2% (Amazon), respectively; and among the NLCS that conveyed clinically relevant information, 94.7% and 98.7%, respectively.Discussion and conclusionCurrent ASR solutions are not capable of properly recognizing NLCS, particularly those that convey clinically relevant information. Although the volume of NLCS in our evaluation data was very small (2.4% of the total corpus; and for NLCS that conveyed clinically relevant information: 0.06%), incorrect recognition of them could result in inaccuracies in clinical documentation and introduce new patient safety risks.
Project description:People occasionally use filler phrases or pauses, such as "uh", "um", or "y'know," that interrupt the flow of a sentence and fill silent moments between ordinary (non-filler) phrases. It remains unknown which brain networks are engaged during the utterance of fillers. We addressed this question by quantifying event-related cortical high gamma activity at 70-110 Hz. During extraoperative electrocorticography recordings performed as part of the presurgical evaluation, patients with drug-resistant focal epilepsy were instructed to overtly explain, in a sentence, 'what is in the image (subject)', 'doing what (verb)', 'where (location)', and 'when (time)'. Time-frequency analysis revealed that the utterance of fillers, compared to that of ordinary words, was associated with a greater magnitude of high gamma augmentation in association and visual cortex of either hemisphere. Our preliminary results raise the hypothesis that filler utterance would often occur when large-scale networks across the association and visual cortex are engaged in cognitive processing, including lexical retrieval as well as verbal working memory and visual scene scanning.
Project description:Reprogramming of the gamete into a developmentally competent embryo identity is a fundamental aspect of preimplantation development. One of the most important processes of this reprogramming is the transcriptional awakening during embryonic genome activation (EGA), which robustly occurs in fertilized embryos but is defective in most somatic cell nuclear transfer (SCNT) embryos. However, little is known about the genome-wide underlying chromatin landscape during EGA in SCNT embryos and how it differs from a fertilized embryo. By profiling open chromatin genome-wide in both types of bovine embryos, we find that SCNT embryos fail to reprogram a subset of the EGA gene targets that are normally activated in fertilized embryos. Importantly, a small number of transcription factor (TF) motifs explain most chromatin regions that fail to open in SCNT embryos suggesting that over-expression of a limited number of TFs may provide more robust reprogramming. One such TF, the zygotically-expressed bovine gene DUXC which is a homologue of EGA factors DUX/DUX4 in mouse/human, is alone capable of activating ~84% of all EGA transcripts that fail to activate normally in SCNT embryos. Additionally, single-cell chromatin profiling revealed low intra-embryo heterogeneity but high inter-embryo heterogeneity in SCNT embryos and an uncoupling of cell division and open chromatin reprogramming during EGA. Surprisingly, our data also indicate that transcriptional defects may arise downstream of promoter chromatin opening in SCNT embryos, suggesting additional mechanistic insights into how and why transcription at EGA is dysregulated. We anticipate that our work will lead to altered SCNT protocols to increase the developmental competency of bovine SCNT embryos.
Project description:Reprogramming of the gamete into a developmentally competent embryo identity is a fundamental aspect of preimplantation development. One of the most important processes of this reprogramming is the transcriptional awakening during embryonic genome activation (EGA), which robustly occurs in fertilized embryos but is defective in most somatic cell nuclear transfer (SCNT) embryos. However, little is known about the genome-wide underlying chromatin landscape during EGA in SCNT embryos and how it differs from a fertilized embryo. By profiling open chromatin genome-wide in both types of bovine embryos, we find that SCNT embryos fail to reprogram a subset of the EGA gene targets that are normally activated in fertilized embryos. Importantly, a small number of transcription factor (TF) motifs explain most chromatin regions that fail to open in SCNT embryos suggesting that over-expression of a limited number of TFs may provide more robust reprogramming. One such TF, the zygotically-expressed bovine gene DUXC which is a homologue of EGA factors DUX/DUX4 in mouse/human, is alone capable of activating ~84% of all EGA transcripts that fail to activate normally in SCNT embryos. Additionally, single-cell chromatin profiling revealed low intra-embryo heterogeneity but high inter-embryo heterogeneity in SCNT embryos and an uncoupling of cell division and open chromatin reprogramming during EGA. Surprisingly, our data also indicate that transcriptional defects may arise downstream of promoter chromatin opening in SCNT embryos, suggesting additional mechanistic insights into how and why transcription at EGA is dysregulated. We anticipate that our work will lead to altered SCNT protocols to increase the developmental competency of bovine SCNT embryos.
Project description:Reprogramming of the gamete into a developmentally competent embryo identity is a fundamental aspect of preimplantation development. One of the most important processes of this reprogramming is the transcriptional awakening during embryonic genome activation (EGA), which robustly occurs in fertilized embryos but is defective in most somatic cell nuclear transfer (SCNT) embryos. However, little is known about the genome-wide underlying chromatin landscape during EGA in SCNT embryos and how it differs from a fertilized embryo. By profiling open chromatin genome-wide in both types of bovine embryos, we find that SCNT embryos fail to reprogram a subset of the EGA gene targets that are normally activated in fertilized embryos. Importantly, a small number of transcription factor (TF) motifs explain most chromatin regions that fail to open in SCNT embryos suggesting that over-expression of a limited number of TFs may provide more robust reprogramming. One such TF, the zygotically-expressed bovine gene DUXC which is a homologue of EGA factors DUX/DUX4 in mouse/human, is alone capable of activating ~84% of all EGA transcripts that fail to activate normally in SCNT embryos. Additionally, single-cell chromatin profiling revealed low intra-embryo heterogeneity but high inter-embryo heterogeneity in SCNT embryos and an uncoupling of cell division and open chromatin reprogramming during EGA. Surprisingly, our data also indicate that transcriptional defects may arise downstream of promoter chromatin opening in SCNT embryos, suggesting additional mechanistic insights into how and why transcription at EGA is dysregulated. We anticipate that our work will lead to altered SCNT protocols to increase the developmental competency of bovine SCNT embryos.
Project description:Reprogramming of the gamete into a developmentally competent embryo identity is a fundamental aspect of preimplantation development. One of the most important processes of this reprogramming is the transcriptional awakening during embryonic genome activation (EGA), which robustly occurs in fertilized embryos but is defective in most somatic cell nuclear transfer (SCNT) embryos. However, little is known about the genome-wide underlying chromatin landscape during EGA in SCNT embryos and how it differs from a fertilized embryo. By profiling open chromatin genome-wide in both types of bovine embryos, we find that SCNT embryos fail to reprogram a subset of the EGA gene targets that are normally activated in fertilized embryos. Importantly, a small number of transcription factor (TF) motifs explain most chromatin regions that fail to open in SCNT embryos suggesting that over-expression of a limited number of TFs may provide more robust reprogramming. One such TF, the zygotically-expressed bovine gene DUXC which is a homologue of EGA factors DUX/DUX4 in mouse/human, is alone capable of activating ~84% of all EGA transcripts that fail to activate normally in SCNT embryos. Additionally, single-cell chromatin profiling revealed low intra-embryo heterogeneity but high inter-embryo heterogeneity in SCNT embryos and an uncoupling of cell division and open chromatin reprogramming during EGA. Surprisingly, our data also indicate that transcriptional defects may arise downstream of promoter chromatin opening in SCNT embryos, suggesting additional mechanistic insights into how and why transcription at EGA is dysregulated. We anticipate that our work will lead to altered SCNT protocols to increase the developmental competency of bovine SCNT embryos.
Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 29 samples of primary cells or cultured primary cells of different haemopoeitc lineages from cord blood are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of EGA data sets is EGAD00001001165. Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. The mapping of samples to these EGA accessions can be found in the 'Sample Data Relationship Format' file of this ArrayExpress record. Information on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu