A patient-centered digital scribe for automatic medical documentation.

OBJECTIVE: We developed a digital scribe for automatic medical documentation by utilizing elements of patient-centered communication. Excessive time spent on medical documentation may contribute to physician burnout. Patient-centered communication may improve patient satisfaction, reduce malpractice rates, and decrease diagnostic testing expenses. We demonstrate that patient-centered communication may allow providers to simultaneously talk to patients and efficiently document relevant information. MATERIALS AND METHODS: We utilized two elements of patient-centered communication to document patient history. One element was summarizing, which involved providers recapping information to confirm an accurate understanding of the patient. Another element was signposting, which involved providers using transition questions and statements to guide the conversation. We also utilized text classification to allow providers to simultaneously perform and document the physical exam. We conducted a proof-of-concept study by simulating patient encounters with two medical students. RESULTS: For history sections, the digital scribe was about 2.7 times faster than both typing and dictation. For physical exam sections, the digital scribe was about 2.17 times faster than typing and about 3.12 times faster than dictation. Results also suggested that providers required minimal training to use the digital scribe, and that they improved at using the system to document history sections. CONCLUSION: Compared to typing and dictation, a patient-centered digital scribe may facilitate effective patient communication. It may also be more reliable compared to previous approaches that solely use machine learning. We conclude that a patient-centered digital scribe may be an effective tool for automatic medical documentation.

The roles of phosphotyrosines-294, -404, and -451 in RET/PTC1-induced thyroid tumor formation.

RET/PTC1 is a rearranged form of the RET proto-oncogene detected in human papillary thyroid carcinomas. We previously showed that thyroid-targeted expression of RET/PTC1 leads to thyroid tumor formation in Tg-PTC1 transgenic mice. Signal transduction pathways mediated by phosphotyrosine 294, 404, or 451 in RET/PTC1 have been shown to be critical for RET-induced transforming activity in vitro. To investigate the contribution of these signaling pathways in RET/PTC1-induced thyroid tumor formation in vivo, we generated and characterized transgenic mice expressing thyroid-targeted RET/PTC1 mutants carrying a site-directed mutation changing tyrosine (Y) to phenylalanine (F) at the residue 294, 404, or 451. In contrast to the 100% tumor formation rate in Tg-PTC1 transgenic mice, tumor formation rates were significantly decreased in Tg-PTC1-Y294F (6%), Tg-PTC1-Y404F (41%), and Tg-PTC1-Y451F (30%) transgenic mice. This indicates that signaling pathways mediated by pY294, pY404, and pY451 do play a role in RET/PTC1-induced tumor formation. However, as tumors are still able to form in some mice within these three mutant transgenic groups, it indicates that none of the signaling pathways mediated by pY294, pY404, or pY451, are solely essential for RET/PTC1-induced tumor formation.